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    1. A 35-year-old woman who was a homozygous carrier of the p.(Pro1066Arg) variant

      Case:Female, 35.

      DiseaseAssertion:Hypertrophic cardiomyopathy (HCM) with left ventricular noncompaction (LVNC) and conduction abnormalities.

      Familyinfo:The patient's father had hypertrophic cardiomyopathy and carried a heterozygous MYBPC3 p.(Pro1066Arg) variant. The patient's mother was also heterozygous for the MYBPC3 variant. The patient had one sister who did not have reported cardiac abnormalities and was heterozygous for the MYBPC3 variant. The family was initially considered non-consanguineous. Genetic analysis identified a 26 Mb region of homozygosity, suggesting distant parental relatedness.

      ParentalTesting:Both parents were tested. The father and mother were heterozygous for MYBPC3 c.3197C>G (p.Pro1066Arg). The affected daughter inherited the variant from both parents and was homozygous.

      CasePresentingHPOs:HP:0031992, HP:0001685, HP:0005157, HP:0031295, HP:0001667, HP:0001670, HP:0001712, HP:0005144, HP: 0031195, HP:0030682, HP:0005135, HP: 0006682, HP: 0004763

      CaseHPOFreeText:The patient developed severe cardiac manifestations associated with homozygous MYBPC3 p.(Pro1066Arg). Cardiac MRI showed ventricular hypertrophy, myocardial fibrosis, and features of left ventricular noncompaction. At follow-up, imaging showed asymmetric ventricular wall thickness, with a maximum diastolic thickness of 20 mm in the mid-lateral segment. She also had apical hypokinesia and left atrial enlargement. Electrocardiography and Holter monitoring showed premature ventricular complexes and a 20-beat episode of nonsustained ventricular tachycardia.

      CaseNotHPOs:No specific negative HPO findings were established for the affected daughter in the reported HPO table.

      CaseNOTHPOFreeText:not reported

      CasePreviousTesting:Cardiac MRI, echocardiography, electrocardiography, and 24-hour Holter monitoring were performed. Genetic evaluation was also conducted to identify the MYBPC3 and MYH7 variants.

      GenotypingMethod:Whole-exome sequencing (WES) trio analysis was performed using DNA from the affected daughter and both parents. Family segregation analysis was performed by Sanger sequencing using an Applied Biosystems 3130 sequencer.

      FunctionalAnalysis:No direct functional analysis of the MYBPC3 variant was reported.

      Variant:NM_000256.3 (MYBPC3): c.3197C>G; p.(Pro1066Arg).

      ClinVar: 1171602

      CAID:not reported

      gnomAD:not reported

      AdditionalInfo:The patient was homozygous for the MYBPC3 p.(Pro1066Arg) variant. Both parents carried the variant in the heterozygous state. A 26 Mb region of homozygosity was identified on chromosome 11, supporting the possibility of distant parental relatedness. The variant was initially classified as a variant of uncertain significance and was subsequently reclassified as likely pathogenic following family segregation analysis.

    1. Genome sequencing identified a heterozygous ACTC1 variant (NM_005159.5; c.325G>A, p.Glu109Lys) in Individual 1 and her mother. The variant was absent from gnomAD v2.1.1, had an AlphaMissense score of 0.99 and a REVEL score of 0.827. It was classified as likely pathogenic with ACMG criteria (PM1, PM2, PP1, PP2, PP3).

      Case:Female, born at 34 weeks of gestation, 5 years old at the first detailed examination, 8 years old during a later clinical description.

      DiseaseAssertion:Arthrogryposis multiplex congenita (AMC). Cardiomyopathy not reported.

      Familyinfo:The patient was the first child of unrelated parents. Her mother and one maternal aunt were born with bilateral clubfeet and later developed scoliosis. The mother also had a history of cleft palate. Neither the mother nor the patient had a reported history of cardiac problems.

      ParentalTesting:The patient's mother carried the same heterozygous ACTC1 c.325G>A (p.Glu109Lys) variant. The variant was therefore inherited from the mother.

      CasePresentingHPOs:Bilateral clubfeet, scoliosis, cleft palate, neck webbing, camptodactyly, joint contractures.

      CaseHPOFreeText:The patient was born by cesarean section at 34 weeks of gestation. Bilateral clubfeet, cleft palate, neck webbing, and spinal deformity were noted. At age 5, she had severe scoliosis measuring 120 degrees and severe short stature. At age 8, mild camptodactyly of both hands and mild contractures of the neck, left hip, both knees, and feet were observed. She had no significant mobility or cognitive difficulties and was independent in self-care activities.

      CaseNotHPOs:No reported cardiac problems, no significant cognitive difficulties, no significant mobility difficulties.

      CaseNOTHPOFreeText:The patient had no reported cardiac phenotype despite carrying an ACTC1 variant. Her mother also had no history of cardiac problems.

      CasePreviousTesting:Genome sequencing was performed to identify genetic variants associated with the patient's clinical presentation.

      GenotypingMethod:Genome sequencing. Plasmid sequencing was also verified by Sanger sequencing for the experimental functional studies.

      FunctionalAnalysis:In vitro functional studies were performed using MC3T3-E1 preosteoblastic cells. The p.Glu109Lys variant caused decreased ACTC1 protein levels and impaired actin filament assembly. Immunofluorescence and Western blotting were used to evaluate protein expression and actin filament organization.

      Variant:NM_005159.5 (ACTC1): c.325G>A; p.Glu109Lys.

      ClinVar:not reported

      CAID:not reported

      gnomAD:not found

      AdditionalInfo:The variant was inherited from the patient's mother, who also had bilateral clubfeet, scoliosis, and a history of cleft palate. The authors classified the variant as likely pathogenic using ACMG criteria (PM1, PM2, PP1, PP2, PP3). The functional studies demonstrated reduced ACTC1 protein levels and impaired actin filament assembly.

    2. A de novo heterozygous ACTC1 variant (NM_005159.5; c.650A>C, p.Lys217Thr) was found in Individual 2.

      Case:Male, born at 39 weeks of gestation, evaluated during infancy-age 6.

      DiseaseAssertion:Arthrogryposis multiplex congenita (AMC). The patient also had Shone's complex with coarctation of the aorta. Cardiomyopathy not reported.

      Familyinfo:The patient was the first child of unrelated parents. No family history of arthrogryposis multiplex congenita was reported.

      ParentalTesting:The ACTC1 c.650A>C (p.Lys217Thr) variant was identified as de novo. Neither parent was reported to carry the variant.

      CasePresentingHPOs:Limited range of motion in wrists, Limited range of motion in fingers, Limited range of motion in thumbs, Hip contractures, Knee contractures, Bilateral clubfeet, Clenched hands, Hypotonia, Lower extremity weakness,

      CaseHPOFreeText:The patient was born at 39 weeks of gestation. At birth, he had limited range of motion in the wrists, fingers, thumbs, hips, and knees, along with bilateral clubfeet. Echocardiography revealed Shone's complex, including coarctation of the aorta, which required surgical repair. At age 1, he had clenched hands with deep single palmar creases, overlapping toes, and hypoplastic fifth toenails. He also had truncal hypotonia, mild lower extremity weakness, and delayed gross motor milestones. At age 3, moderate wrist contractures, thumb-in-palm deformities, and mild bilateral hip contractures were observed. He began walking independently at age 4. At age 5, he underwent additional heart surgery and pacemaker insertion.

      CaseNotHPOs:Scoliosis: not identified on spine X-rays, cognitive difficulties: not reported

      CaseNOTHPOFreeText:The patient did not have reported cognitive difficulties. Spine X-rays did not reveal scoliosis.

      CasePreviousTesting:Genome sequencing was performed to identify genetic variants associated with the patient's clinical presentation. Echocardiography was used to identify Shone's complex and coarctation of the aorta.

      GenotypingMethod:Genome sequencing. Plasmid sequences used for the functional experiments were verified by Sanger sequencing.

      FunctionalAnalysis:In vitro functional studies were performed using MC3T3-E1 preosteoblastic cells. The p.Lys217Thr variant did not demonstrate a clear effect on ACTC1 protein expression or localization compared with wild-type ACTC1. The authors reported no apparent reduction in protein levels or impaired actin filament organization.

      Variant:NM_005159.5 (ACTC1): c.650A>C; p.Lys217Thr.

      ClinVar:not reported

      CAID:not reported

      gnomAD:not reported

      AdditionalInfo:The variant was identified as de novo and classified as likely pathogenic using ACMG criteria (PS2, PM1, PM2, PP2, PP3). Although functional testing did not demonstrate a clear effect on ACTC1 protein expression or localization, the authors considered the variant likely pathogenic based on the genetic and clinical evidence.

    1. woman with autosomal dominant Alport syndrome (ADAS) with a family history of left ventricular noncompaction cardiomyopathy (LVNC). Exome sequencing identified a rare heterozygous variant in COL4A4, NM_000092.5: c.2510G>C (p.G837A), and a novel heterozygous variant in ACTC1, NM_005159.5: c.922T>C (p.Y308H), as causes of ADAS and LVNC, respectively.

      Case:Female, 21.

      DiseaseAssertion:Left ventricular noncompaction cardiomyopathy (LVNC).

      Familyinfo:The patient's father had hypertrophic cardiomyopathy. Her paternal grandfather and paternal uncle also reportedly had cardiac disease, although detailed clinical information was unavailable. The patient's mother had microscopic hematuria and was diagnosed with thin basement membrane nephropathy. The maternal grandmother also had a history of kidney disease.

      ParentalTesting:The mother was tested and did not carry the ACTC1 c.922T>C variant. The father could not be tested because the patient had no contact with him. The authors presumed paternal inheritance of the ACTC1 variant based on the family history, but paternal inheritance was not genetically confirmed.

      CasePresentingHPOs:Left ventricular noncompaction cardiomyopathy, Abnormal cardiac morphology, Cardiac hypertrophy, Hematuria

      CaseHPOFreeText:The patient had microscopic hematuria beginning at age 6. At the same age, routine school screening identified cardiac dysfunction, and echocardiography revealed a myocardial densification defect. At age 21, echocardiography showed a noncompacted-to-compacted myocardial ratio greater than 2:1, consistent with LVNC. Electrocardiography showed sinus rhythm with ST-T wave flattening in leads V4–V6, indicative of cardiac hypertrophy. The patient remained without cardiac symptoms and had a normal ejection fraction. Her BNP level increased to 204 pg/mL. She had normal renal function, with a serum creatinine level of 0.58 mg/dL, and no proteinuria.

      CaseNotHPOs:Hearing impairment: not reported, Ophthalmological abnormalities: not reported, Cardiac symptoms: not reported

      CaseNOTHPOFreeText:The patient remained asymptomatic despite the cardiac findings. No hearing impairment or ophthalmological abnormalities were identified.

      CasePreviousTesting:Echocardiography identified LVNC during childhood. Further cardiac evaluation included electrocardiography and follow-up BNP measurements. Renal evaluation included serum creatinine testing, urinalysis, abdominal ultrasonography, and genetic evaluation for hereditary kidney disease.

      GenotypingMethod:Whole exome sequencing was performed using DNA extracted from the patient's blood sample. Sanger sequencing was used to confirm both identified variants. The mother's DNA was also analyzed to determine inheritance.

      FunctionalAnalysis:No direct functional studies were performed on the ACTC1 variant. The authors used AlphaFold3 protein structure prediction to examine the effect of the amino acid substitution. The variant was located near the ATP-binding site, suggesting a possible effect on ACTC1 function and ATP binding.

      Variant:NM_005159.5 (ACTC1): c.922T>C; p.(Tyr308His).

      ClinVar:accession: VCV000948806.7.

      CAID:not reported

      gnomAD:not reported

      AdditionalInfo:The patient carried two separate heterozygous variants associated with different conditions. The COL4A4 c.2510G>C (p.Gly837Ala) variant was associated with autosomal dominant Alport syndrome, while the ACTC1 c.922T>C (p.Tyr308His) variant was identified as a candidate associated with LVNC. The ACTC1 variant was classified as a variant of uncertain significance (VUS) by the authors using ACMG criteria (PM2, PP3, PP4). The authors noted that there were no functional studies confirming its effect on ACTC1 protein function.

    1. 7

      Patient7: Male, 3.8mo at ERT start, 3.3yo at study end

      CasePresentingHPOs:

      HPOsFreeText: treated with 40mg/kg/wk, patient had 10 infusion associated reactions

      CaseNotHPOs:

      NotHPOsFreeText:

      CaseAddInfo:

      CasePMIDs:

      CasePreviousTesting: same as group

      CaseGenotypingMethod: same as group

      Variant1: NC_000017.11:g.(?80118193)(80118357_?)del (c.2481 + 102_2646 + 31del)

      ClinVar: 456368, https://www.ncbi.nlm.nih.gov/clinvar/variation/456368/

      gnomAD: n/a

      Variant2: NM_000152.4(GAA):c.525delT (p.Glu176Argfs)

      ClinVar: 4033, https://www.ncbi.nlm.nih.gov/clinvar/variation/4033/

      gnomAD: 0.00009959, http://gnomad.broadinstitute.org/variant/17-78078909-CT-C

    1. GroupID: 237

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 2 members of this family were found to harbor a germline large rearrangement of the VHL gene. Member 7398 had no renal involvement. Member 645 presented with severe renal disease (RCC). Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      GroupPresentingHPOs: HP:0005584 (Renal cell carcinoma)

      GroupHPOFreeText: Severe renal disease (any solid lesion before 25 years of age, five or more solid lesions within one or two kidneys, or metastasis of renal cell carcinoma).

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: Paper states that this family is previously reported in PMID 12202531, where 12 individuals with this mutation are reported. It is unclear which of the previously reported individuals correspond to which of the currently reported families/individuals (i.e. families 40, 90, 174, 237, 264, 284, 307 or 394).

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: Rearrangement

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: rearrangement_region

      CivicName: Rearrangement

      MultipleGeneVariants: N/A

    2. PatientID: 9760

      KindredID: 415

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Mild renal disease (simple renal cyst, multicystic kidney[s], small lesion [less than 10 mm in size] of unknown significance, or small solid tumor without indication for surgical removal [less than 30 mm in size]).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: Rearrangement

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: rearrangement_region

      CivicName: Rearrangement

      MultipleGeneVariants: N/A

    1. PatientID: 251

      KindredID: 96

      Case: F, 44Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 250) presented with a CNS hemangioblastoma at 23, retinal angioma at 17, and multiple pancreatic cysts/tumors at 19. His mother (patient 251) presented with a CNS hemangioblastoma at age 43, retinal angioma at 35, renal cell carcinoma/multiple pancreatic cysts/tumors at 44.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0001737; HP:0001732; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The patient's mother presented with a CNS hemangioblastoma at age 43, retinal angioma at 35, renal cell carcinoma/multiple pancreatic cysts/tumors at 44.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    2. PatientID: 277

      KindredID: 108

      Case: M, 28Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 277, presented with a CNS hemangioblastoma at age 16, retinal angioma a 20, and renal cell carcinoma at 28. Their father who passed away before diagnosis presented with a CNS hemangioblastoma at 48.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, Renal cell carcinoma)

      CaseHPOFreeText: The proband, patient 277, presented with a CNS hemangioblastoma at age 16, retinal angioma a 20, and renal cell carcinoma at 28.

      CaseNotHPOs: HP:0002666; HP:0001737; HP:0001732 (Pheochromocytoma, Pancreatic cysts, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    3. PatientID: 253

      KindredID: 98

      Case: F, 27Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 253, presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at age 27. Their father (patient 254) was asymptomatic at the time of assessment. Their grandmother (patient 255) presented with renal cell carcinoma at 60 and multiple pancreatic cysts/tumors at 27, but passed away before diagnosis/ before the mutation could be confirmed.

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0001732; HP:0005584 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The patient presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at age 27.

      CaseNotHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    4. PatientID: 290

      KindredID: 114

      Case: M, 41Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001732; HP:0001737; HP:0005584; HP:0009711 (Hemangioblastoma, Abnormality of the pancreas, Pancreatic cysts, Renal cell carcinoma, Retinal capillary hemangioma)

      CaseHPOFreeText: The proband presented with a CNS hemangioblastoma at age 38, and at age 41 presented with a retinal angioma, renal cell carcinoma, and multiple pancreatic cysts/tumors.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    5. PatientID: 291

      KindredID: 115

      Case: M, 31Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001732; HP:0001737; HP:0005584; HP:0002666 (Hemangioblastoma, Abnormality of the pancreas, Pancreatic cysts, Renal cell carcinoma, Pheochromocytoma)

      CaseHPOFreeText: The proband, patient 291, presented with a CNS hemangioblastoma at 27, and at 31 presented with renal cell carcinoma, multiple pancreatic cysts/tumors, and pheochromocytoma.

      CaseNotHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    6. PatientID: 259

      KindredID: 100

      Case: F, 28Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 259, presented with a CNS hemangioblastoma and multiple pancreatic cysts/tumors at age 28, and a retinal angioma at age 24. The proband's son, patient 260, was asymptomatic at the time of analysis.

      CasePresentingHPOs: N/A

      CasePresentingHPOs: HP:0009711; HP:0001737; HP:0001732; HP:0005584; HP:0010797 (Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas, Hemangioblastoma)

      CaseHPOFreeText: The proband, patient 259, presented with a CNS hemangioblastoma and multiple pancreatic cysts/tumors at age 28, and a retinal angioma at age 24.

      CaseNotHPOs: HP:0002666; HP:0005584 (Pheochromocytoma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 1-2 Deletion (c.1-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-2 Deletion

      MultipleGeneVariants: N/A

    7. PatientID: 280

      KindredID: 110

      Case: M, 22Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 280, presented with a CNS hemangioblastoma at age 16, a retinal angioma at age 15, and multiple pancreatic cysts/tumors at age 22. Their father presented with a CNS hemangioblastoma at age 25, and retinal angioma at age 29.

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0001732; HP:0009711 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas, Retinal capillary hemangioma)

      CaseHPOFreeText: The proband, patient 280, presented with a CNS hemangioblastoma at age 16, a retinal angioma at age 15, and multiple pancreatic cysts/tumors at age 22.

      CaseNotHPOs: HP:0002666; HP:0005584 (Pheochromocytoma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. High-molecular-weight deoxyribonucleic acid (DNA) of the probands was isolated from peripheral blood according to standard procedures. Exons 1, 2, and 3 of the VHL gene and their immediately flanking sequences were amplified by use of polymerase chain reaction (PCR). Appropriate pairs of oligonucleotides were designed in the intronic regions flanking the three exons of the VHL gene. The flanking sequences included 75 nucleotides upstream of the start codon (the first nucleotide of the coding region is 214) and 45 nucleotides downstream of the stop codon. Amplicons were denatured at 94°C and renatured at 25°C for heteroduplex analysis. Denaturing acetonitrile gradient profiles and melting temperatures were established by the Wavemaker 3.0 software prediction. Equal amounts (50 ng) of PCR product were mixed with reference human wild-type genomic DNA and, after denaturation-renaturation, were screened for heteroduplexes by denaturing high-performance liquid chromatography (dHPLC). For amplicons exhibiting abnormal dHPLC profiles, new PCR reactions were performed from 20 ng of genomic DNA, and sequence changes were evaluated by PCR product purification and direct sequencing (Big Dye; Applied Biosystems, Foster City, CA). The positive mutation results were repeated for confirmation.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Exons 1, 2, and 3 of the VHL gene and their immediately flanking sequences were amplified by use of polymerase chain reaction (PCR). Amplicons were denatured at 94°C and renatured at 25°C for heteroduplex analysis. Denaturing acetonitrile gradient profiles and melting temperatures were established by the Wavemaker 3.0 software prediction. Equal amounts (50 ng) of PCR product were mixed with reference human wild-type genomic DNA and after denaturation-renaturation, were screened for heteroduplexes by dHPLC

      SamplingMethod: peripheral blood

    1. S 23 27 M ? ? ? - - - - VHL FLD a – BRK1, FANCD2

      PatientID: 23

      KindredID: KS

      Case: M, 27Y0M, Indian

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001737 (Hemangioblastoma, Pancreatic cysts)

      CaseHPOFreeText: CNS hemangioblastoma and multi-cystic pancreatic lesions.

      CaseNotHPOs: HP:0030393; HP:0009711; HP:0002666; HP:0005584 (Endolymphatic sac tumor, Retinal capillary hemangioma, Pheochromocytoma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: This variant is noted as a full-length deletion involving genes BRK1 and FANCD2.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. PM 30 49 M ? ? ? - - - - VHL FLD – BRK1, FANCD2

      PatientID: 30

      KindredID: PM

      Case: M, 49Y0M, Indian

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001737 (Hemangioblastoma, Pancreatic cysts)

      CaseHPOFreeText: CNS hemangioblastoma and multi-cystic pancreatic lesions.

      CaseNotHPOs: HP:0030393; HP:0009711; HP:0002666; HP:0005584 (Endolymphatic sac tumor, Retinal capillary hemangioma, Pheochromocytoma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: This variant is noted as a full-length deletion involving genes BRK1 and FANCD2.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. A deletion of exon 3 in the VHL gene was found in this family.

      PatientID: III-6

      KindredID: Family A

      Case: M, 31Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s grandfather (I-1), now deceased, and aunt (II-1) had CNS/spinal hemangioblastoma and the confirmed VHL gene mutation. His aunts II-2 and II-3 both had confirmed VHL and CNS hemangioblastoma. His dad (II-3) has confirmed VHL gene and pancreatic and renal cysts. His cousins (2 boys 1 girl: III-3; III-5; III-3) were all found with the confirmed VHL gene mutation; III-3 and III-5 with retinal hemangioblastoma and CNS/spinal hemangioblastomas and III-4 with pancreatic and ovarian cysts. Patient’s son and nephew IV-1 and IV-3, were confirmed with the VHL gene mutation although no other manifestations.

      CasePresentingHPOs: HP:0005584; HP:001079 (renal cell carcinoma, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711; HP:0002666 (retinal capillary hemangioblastoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Deletion of exon 3 (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 deletion

      MultipleGeneVariants: N/A

    2. A deletion of exon 3 in the VHL gene was found in this family.

      PatientID: IV-1

      KindredID: Family A

      Case: M, Age unknown, Ethnicity unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Patient’s great-grandfather (I-1), now deceased, and great-aunt (II-1) had CNS/spinal hemangioblastoma and the confirmed VHL gene mutation. His great-aunt II-2 and great-uncle II-3 both had confirmed VHL and (II-2) CNS hemangioblastoma; (II-3) with pancreatic and renal cysts. His dad (III-3) has confirmed VHL gene retinal and CNS hemangioblastoma, his aunt (III-4) had confirmed VHL and pancreatic and ovarian cysts. His uncle III-5 was found with the confirmed VHL gene mutation and retinal hemangioblastoma and CNS/spinal hemangioblastomas. III-6 with renal cell carcinoma and hemangioblastoma. Patient’s cousin IV-3, was confirmed with the VHL gene mutation although no other manifestations.

      CasePresentingHPOs: None

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Deletion of exon 3 (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 deletion

      MultipleGeneVariants: N/A

    3. A deletion of exon 3 in the VHL gene was found in this family.

      PatientID: III-4

      KindredID: Family A

      Case: F, 38Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s grandfather (I-1), now deceased, and aunt (II-1) had CNS/spinal hemangioblastoma and the confirmed VHL gene mutation. Her mom II-2 had confirmed VHL and CNS hemangioblastoma; and her cousin (III-6) has renal cell carcinoma and CNS/spinal hemangioblastoma and also the confirmed VHL gene mutation. Her uncle (II-3) has confirmed VHL gene and pancreatic and renal cysts. Her brother and sister (III-3; III-5) both were found with the confirmed VHL gene mutation; with retinal hemangioblastoma and CNS/spinal hemangioblastomas. IV-1 and IV-3, were confirmed with the VHL gene mutation although no other manifestations.

      CasePresentingHPOs:HP:0001737; HP:0000138 (pancreatic cyst; ovarian cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0009711; HP:0010797 (renal cell carcinoma, pheochromocytoma, retinal capillary hemangioblastoma, CNS hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Deletion of exon 3 (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 deletion

      MultipleGeneVariants: N/A

    1. Written informed consent was obtained from all family members who participated in the study. Genomic DNA was extracted from peripheral blood leukocytes using DNA isolation kit for mammalian blood samples (Boehringer Mannheim Corporation, Indianapolis, IN). Mutation analysis of the VHL gene was performed as previously described [16].

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Mutation analysis of exons 1, 2 and 3 of the VHL gene was performed using direct sequencing of the PCR-amplified DNA.

      SamplingMethod: peripheral blood

    1. PatientID: None

      KindredID: VHL25

      Case: M, 31Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: A total of 190 patients recruited by the COMETE network over 15 years were included in the study.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: The patient had one benign pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHC/SDHD

      PreviouslyPublished: N/A

      SupplementalData: Table 1 of Supplementary

      Variant: Complete Deletion (c.1-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: The patient had no LOH found in the BAC array CGH data. No variants were found in the tumor tissue.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. PatientID: None

      KindredID: VHL24

      Case: M, 22Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: A total of 190 patients recruited by the COMETE network over 15 years were included in the study.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: The patient had one benign pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHC/SDHD

      PreviouslyPublished: N/A

      SupplementalData: Table 1 of Supplementary

      Variant: Complete Deletion (c.1-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: The patient had no LOH found in the BAC array CGH data. Somatic VHL variant c.250G>C was found in the tumor tissue.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. PatientID: 122

      KindredID: 122

      Case: Sex Unknown, 31Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0001732 (Hemangioblastoma, Retinal capillary hemangioma, Abnormality of the pancreas)

      CaseHPOFreeText: CNS hemangioblastoma, retinal hemangioblastoma and pancreatic cyst or tumor.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0000107 (Clear cell renal cell carcinoma, Pheochromocytoma, Renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Partial Deletion (8.2kb)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Partial deletion of 8.2kb

      MultipleGeneVariants: N/A

    2. PatientID: 65

      KindredID: 65

      Case: Sex Unknown, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history is positive but no details provided.

      CasePresentingHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: CNS hemangioblastoma and retinal hemangioblastoma.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0000107; HP:0001732 (Clear cell renal cell carcinoma, Pheochromocytoma, Renal cyst, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Complete deletion)

      MultipleGeneVariants: N/A

    3. High-molecular-weight genomic DNA was extracted from peripheral blood leucocytes by standard protocols. Mutation scanning of the VHL gene for identification of point- or small-size mutations was conducted on the entire coding sequence and intron–exon boundaries by polymerase chain reaction (PCR) amplification, denaturating high-performance liquid chromatography (DHPLC), and direct sequence analysis, as follows.

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: Polymerase chain reaction (PCR) amplification, denaturating high-performance liquid chromatography (DHPLC), and direct sequence analysis were used to analyze the entire coding sequence and intron-exon boundaries.

      SamplingMethod: peripheral blood

    4. PatientID: 254

      KindredID: 254

      Case: Sex Unknown, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history is positive but no details provided.

      CasePresentingHPOs: HP:0009711; HP:0001732 (Retinal capillary hemangioma, Abnormality of the pancreas)

      CaseHPOFreeText: Retinal hemangioblastoma and pancreatic cyst or tumor.

      CaseNotHPOs: HP:0010797; HP:0002666; HP:0000107; HP:0006770 (Hemangioblastoma, Pheochromocytoma, Renal cyst, Clear cell renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant; deletion

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    5. PatientID: 121

      KindredID: 121

      Case: Sex Unknown, 14Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: CNS hemangioblastoma and retinal hemangioblastoma.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0000107; HP:0001732 (Clear cell renal cell carcinoma, Pheochromocytoma, Renal cyst, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Partial Deletion (11kb)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Partial deletion of 11kb

      MultipleGeneVariants: N/A

    6. PatientID: 204

      KindredID: 204

      Case: Sex Unknown, 45Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history is positive but no details provided.

      CasePresentingHPOs: HP:0010797; HP:0000107; HP:0001732 (Hemangioblastoma, Renal cyst, Abnormality of the pancreas)

      CaseHPOFreeText: CNS hemangioblastoma, renal cyst and pancreatic cyst or tumor.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0009711 (Clear cell renal cell carcinoma, Pheochromocytoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Complete deletion)

      MultipleGeneVariants: N/A

    1. DNA extraction, genotyping of coding sequences and deletion search Venous blood samples were drawn from all participants and DNA was extracted from whole blood (DNA purification kit, Gentra). The different exons and intron-exon boundaries of SDHD, SDHB, SDHC, and VHL genes were amplified by polymerase chain reaction (PCR). Screening for mutations was performed by single strand conformation polymorphism (SSCP), and heteroduplex analysis, as previously described [10] or by denaturing high performance liquid chromatography (dHPLC) analysis, using the WAVE 3500 HT system (Transgenomic, Inc., Omaha, NE, USA). Fragments showing abnormal migration were re-amplified and sequenced on a CEQ2000 capillary sequencer (Beckman Coulter). Search for large rearrangement (deletion/duplication) was performed by Quantitative multiplex PCR of short fluorescent fragments (QMPSF) [11] or Multiplex Ligation-dependent Probe Amplification (MLPA) (SALSA MLPA kit P226; MRC-Holland, Amsterdam, The Netherlands). The functionality of observed genetic changes was assessed in silico as previously described

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: The different exons and intron-exon boundaries of SDHD, SDHB, SDHC, and VHL genes were amplified by polymerase chain reaction (PCR). Screening for mutations was performed by single strand conformation polymorphism (SSCP), and heteroduplex analysis, as previously described [10] or by denaturing high performance liquid chromatography (dHPLC) analysis, using the WAVE 3500 HT system

      SamplingMethod: whole blood

    1. We studied six patients with VHL disease and their relatives. Loss of heterozygosity (LOH) was determined by five flanking microsatellite polymorphic markers in the VHL locus.

      PatientID: 16

      KindredID: F01

      Case: F, Age Unknown, Taiwanese

      DiseaseAssertion: VHL

      FamilyInfo: A total of 10 members of this family (F01) had a complete deletion of the VHL gene. Four of these patients (16, 18, 21, 33) presented with clinical features of VHL.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: Brain hemangioblastoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 19288063

      SupplementalData: Figure 1

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of 142.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. We studied six patients with VHL disease and their relatives. Loss of heterozygosity (LOH) was determined by five flanking microsatellite polymorphic markers in the VHL locus.

      PatientID: 31

      KindredID: F01

      Case: M, Age Unknown, Taiwanese

      DiseaseAssertion: Asymptomatic

      FamilyInfo: A total of 10 members of this family (F01) had a complete deletion of the VHL gene. Four of these patients (16, 18, 21, 33) presented with clinical features of VHL.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 19288063

      SupplementalData: Figure 1

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of 142.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. Supplementary Data: Table 2

      Case B: proband, Female

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7, LMNA)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    2. Supplementary Data: Table 2

      Case K:

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

      MultipleGeneVariants:

      (1) VCL Variant:

      Variant: NM_014000.2(VCL):c.688C>T (p.Arg230Cys)

      ClinVar: 45620, https://www.ncbi.nlm.nih.gov/clinvar/variation/45620/

      gnomAD: 0.00008137, https://gnomad.broadinstitute.org/variant/10-75834566-C-T

    3. Supplementary Data: Table 2

      Case A: proband, female

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7, LMNA)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    4. Supplementary Data: Table 2

      Case L:

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    5. Supplementary Data: Table 2

      Case N:

      DiseaseAssertion: left ventricular noncompaction

      CasePresentingHPOs: HP:0030682 (left ventricular noncompaction)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7, MYBPC3)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    6. Supplementary Data: Table 2

      Case H: proband, Female

      DiseaseAssertion: left ventricular noncompaction

      CasePresentingHPOs: HP:0030682 (left ventricular noncompaction)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    7. Supplementary Data: Table 2

      Case F: proband, Female

      DiseaseAssertion: Left ventricular noncompaction

      CasePresentingHPOs: HP:0030682 (left ventricular noncompaction)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    8. Supplementary Data: Table 2

      Case J: proband, Male

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    9. Supplementary Data: Table 2

      Case D: proband, female

      DiseaseAssertion: Hypertrophic cardiomyopathy

      CasePresentingHPOs: HP:0001639 (hypertrophic cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

      MultipleGeneVariants:

      (1) DSC2 Variant:

      Variant: NM_004949.4(DSC2):c.2194T>G (p.Leu732Val)

      ClinVar: 36005, https://www.ncbi.nlm.nih.gov/clinvar/variation/36005/

      gnomAD: 0.001181, https://gnomad.broadinstitute.org/variant/18-28650748-A-C

      (2) DSG2 Variant:

      Variant: NM_001943.4(DSG2):c.1174G>A (p.Val392Ile)

      ClinVar: 36009, https://www.ncbi.nlm.nih.gov/clinvar/variation/36009/

      gnomAD: 0.002137, https://gnomad.broadinstitute.org/variant/18-29111109-G-A

      (3) DSP Variant:

      Variant: NM_001008844.2(DSP):c.1778A>G (p.Asn593Ser)

      ClinVar: 44867, https://www.ncbi.nlm.nih.gov/clinvar/variation/44867/

      gnomAD: 0.0005695, https://gnomad.broadinstitute.org/variant/6-7571692-A-G

    10. Supplementary Data: Table 2

      Case 3:

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: WES, Cytoscan HD SNP array (performed on proband, 3 additional carriers, and parents)

      Variant - paternal: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    11. Supplementary Data: Table 2

      Case 2:

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: WES, Cytoscan HD SNP array (performed on proband, 3 additional carriers, and parents)

      Variant - maternal: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    12. Supplementary Data: Table 2

      Case M:

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7, MYBPC3)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    13. Supplementary Data: Table 2

      Case C: proband, Male

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7, CSRP3, DES, LMNA, MYBPC3, TNNT2, TNNI3)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    14. Supplementary Data: Table 2

      Case E: proband, male

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

      MultipleGeneVariants:

      (1) PRDM16 Variant:

      Variant: NM_022114.3(PRDM16):c.2666C>T (p.Pro889Leu)

      ClinVar: 487607, https://www.ncbi.nlm.nih.gov/clinvar/variation/487607/

      gnomAD: 0.0001771, https://gnomad.broadinstitute.org/variant/1-3331186-C-T

    15. Supplementary Data: Table 2

      Case G: proband, Male

      DiseaseAssertion: left ventricular noncompaction

      CasePresentingHPOs: HP:0030682 (left ventricular noncompaction)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, partial testing (MYH7)

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    16. Supplementary Data: Table 2

      Case I: proband, Male

      DiseaseAssertion: Dilated Cardiomyopathy

      CasePresentingHPOs: HP:0001644 (dilated cardiomyopathy)

      CasePreviousTesting: 12-lead electrocardiogram (ECG), echocardiography, exercise test and 24-hour (or 48-hour) Holter monitoring, cardiac MRI, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplemental table 2

      CaseGenotypingMethod: genomic DNA isolated from peripheral blood, initially analyzed via Sanger Sequencing then by next-generation sequencing using targeted gene panels, variant pathogenicity assed using in silico prediction tools, Haplotype analysis was performed using 16 microsatellite markers around MYH7 (DNA from the 14 probands was analysed, and DNA samples of 6 family members carrying the mutation were used to verify the phase and reconstruct the haplotype Supplementary Data: Table 1)

      Variant: NM_000257.2(MYH7):c.5754C>R (p.Asn1918Lys)

      ClinVar: 66082, https://www.ncbi.nlm.nih.gov/clinvar/variation/66082/

      gnomAD: n/a

    1. Supplementary Material 4

      Case M-31: Japanese

      DiseaseAssertion: idiopathic cardiomyopathy (HCM and DCM)

      CasePreviousTesting: Clinical evaluation, chest radiography, electrocardiography, echocardiography, cardiac catheterization, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1)

      CaseGenotypingMethod: 8 sarcomeric genes amplified from genomic DNA via PCR then screened using bidirectional direct sequencing

      Variant: NM_000257.3(MYH7):c.4721G>A (p.Arg1574Gln)

      ClinVar: 228912, https://www.ncbi.nlm.nih.gov/clinvar/variation/228912/

      gnomAD: 0.00001989, https://gnomad.broadinstitute.org/variant/14-23885445-C-T

    1. 19

      Case: Patient 19, female, 33yo, symptom onset in childhood

      CasePresentingHPOs: HP:0009027, HP:0008959, HP:0009053, HP:0008997, HP:0008994, HP:0002650, HP:0003458 (foot drop, Distal upper limb muscle weakness, Distal lower limb muscle weakness, Proximal muscle weakness in upper limbs, Proximal muscle weakness in lower limbs, scoliosis, EMG: myopathic abnormalities)

      HPOsFreeText: respiratory involvement - restrictive from 25yo, normal CK levels, minicores present on muscle biopsy

      CaseNotHPOs: no cardiac involvement

      FamilyInfo: family history

      DiseaseEntity: no assertion

      InheritancePattern: no assertion

      CasePreviousTesting: see below

      CaseGenotypingMethod: 9 cases underwent targeted Sanger sequencing of MYH7, 12 cases underwent Motorplex analysis (NGS of 93 myopathy-related genes - PMID:25214167), all MYH7 variants confirmed via Sanger sequencing, segregation analysis performed on available family members, which cases received which sequencing technique is not specified

      Variant: NM_000257.4(MYH7):c.4844_4846AGA[2] (p.Lys1617del)

      ClinVar: 190401, https://www.ncbi.nlm.nih.gov/clinvar/variation/190401/

      gnomAD: absent

    2. 6

      Case: 6, femaly, 16yo, congenital onset of symptoms

      CasePresentingHPOs: HP:0003327, HP:0008959, HP:0009053, HP:0002650 (axial muscle weakness, distal upper limb muscle weakness, distal lower limb muscle weakness, scoliosis)

      HPOsFreeText: normal CK

      CaseNotHPOs:

      NotHPOsFreeText: no respiratory or cardiac involvement

      FamilyInfo: family history, pedigree in Figure 1

      DiseaseEntity: no assertion

      InheritancePattern: no assertion

      CasePreviousTesting: see below

      CaseGenotypingMethod: 9 cases underwent targeted Sanger sequencing of MYH7, 12 cases underwent Motorplex analysis (NGS of 93 myopathy-related genes - PMID:25214167), all MYH7 variants confirmed via Sanger sequencing, segregation analysis performed on available family members, which cases received which sequencing technique is not specified

      Variant: NM_000257.4(MYH7):c.4807G>C (p.Ala1603Pro)

      ClinVar: 190407, https://www.ncbi.nlm.nih.gov/clinvar/variation/190407/

      gnomAD: absent

    3. 4

      Case: Patient 4, male, 22yo, symptom onset in childhood

      CasePresentingHPOs: HP:0009027, HP:0003327, HP:0008959, HP:0009053, HP:0001701, HP:0030682 (foot drop, axial muscle weakness, distal upper limb muscle weakness, distal lower limb muscle weakness, pericarditis, left ventricular noncompaction)

      CaseNotHPOs: HP:0003306 (rigid spine)

      HPOsFreeText: restrictive respiratory involvement from age 16, CK = 711U/l, minicores present on muscle biopsy, hypertrophy of gastrocnemii

      FamilyInfo: no family history

      DiseaseEntity: no assertion

      InheritancePattern: no assertion

      CasePreviousTesting: see below; variants in SEPN1 and LMNA rules out

      CaseGenotypingMethod: 9 cases underwent targeted Sanger sequencing of MYH7, 12 cases underwent Motorplex analysis (NGS of 93 myopathy-related genes - PMID:25214167), all MYH7 variants confirmed via Sanger sequencing, segregation analysis performed on available family members, which cases received which sequencing technique is not specified

      Variant: NM_000257.4(MYH7):c.4844_4846AGA[2] (p.Lys1617del)

      ClinVar: 190401, https://www.ncbi.nlm.nih.gov/clinvar/variation/190401/

      gnomAD: absent

    4. 13

      Case: Patient 13, female, 59yo, symptom onset in adulthood

      CasePresentingHPOs: HP:0003701, HP:0003306, HP:0003458 (proximal muscle weakness, rigid spine, EMG: myopathic abnormalities)

      HPOsFreeText: normal CK levels, cores present on muscle biopsy

      CaseNotHPOs: no respiratory or cardiac involvement

      FamilyInfo: family history

      DiseaseEntity: no assertion

      InheritancePattern: no assertion

      CasePreviousTesting: see below

      CaseGenotypingMethod: 9 cases underwent targeted Sanger sequencing of MYH7, 12 cases underwent Motorplex analysis (NGS of 93 myopathy-related genes - PMID:25214167), all MYH7 variants confirmed via Sanger sequencing, segregation analysis performed on available family members, which cases received which sequencing technique is not specified

      Variant: NM_000257.4(MYH7):c.4315G>C (p.Ala1439Pro)

      ClinVar: 190404, https://www.ncbi.nlm.nih.gov/clinvar/variation/190404/

      gnomAD: absent

    5. 8

      Case: Patient 8, male, 35yo, symptom onset in childhood

      CasePresentingHPOs: HP:0009027, HP:0003327, HP:0002460, HP:0002650, HP:0003458 (foot drop, axial muscle weakness, distal muscle weakness, scoliosis, EMG: myopathic abnormalities)

      HPOsFreeText: CK = 720U/l, neurogenic EMG, cores present on muscle biopsy

      CaseNotHPOs:

      NotHPOsFreeText: no respiratory or cardiac involvement

      FamilyInfo: pedigree in Figure 1

      DiseaseEntity: no assertion

      InheritancePattern: no assertion

      CasePreviousTesting: see below

      CaseGenotypingMethod: 9 cases underwent targeted Sanger sequencing of MYH7, 12 cases underwent Motorplex analysis (NGS of 93 myopathy-related genes - PMID:25214167), all MYH7 variants confirmed via Sanger sequencing, segregation analysis performed on available family members, which cases received which sequencing technique is not specified

      Variant 1: NM_000257.4(MYH7):c.4844_4846AGA[2] (p.Lys1617del)

      ClinVar: 190401, https://www.ncbi.nlm.nih.gov/clinvar/variation/190401/

      gnomAD: absent

      Variant 2: NM_000257.4(MYH7):c.4855G>A(p.Glu1619Lys)

      ClinVar: 181268, https://www.ncbi.nlm.nih.gov/clinvar/variation/181268/

      gnomAD: absent

    1. The proband

      Case: Patient UK1-IV:1, female, 31yo, Caucasian, Irish ancestry

      CasePresentingHPOs: HP:0040083, HP:0002650, HP:0001508, HP:0011471, HP:0002093, HP:0002877, HP:0001620 (toe-walking, scoliosis, poor weight gain, Feeding problem necessitating gastrostomy tube feeding, respiratory impairment, nocturnal hypoventilation, high-pitched voice)

      HPOsFreeText: scoliosis required spinal fusion surgery, required nocturnal BiPAP ventilation in adolescence, reduced muscle bulk

      Muscle biopsy showed variability in myofiber size, uniformity of type I myofibers on ATPase, moth-eaten appearance of myofibers

      CaseNotHPOs:

      FamilyInfo: non-consanguineous family

      CasePreviousTesting: 32 Illumina genes

      CaseGenotypingMethod: NGS (Illumina gene panel) or 32 genes previously associated with congenital myopathies, Sanger sequencing to confirm recessive inheritance

      InheritancePattern: autosomal recessive

      DiseaseEntity:

      Variant 1: NM_000257.3:c.4699C>T (p.Gln1657Ter), maternal

      CAID: CA389037829, http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA389037829

      gnomAD: n/a

      Variant 2: NM_000257.4(MYH7):c.4664A>G (p.Glu1555Gly), paternal

      ClinVar: 181261, https://www.ncbi.nlm.nih.gov/clinvar/variation/181261/

      gnomAD: n/a

    1. Supplementary Data: Table S3

      Case 56:

      DiseaseAssertion: left ventricular noncompaction

      CasePresentingHPOs: HP:0030682 (left ventricular noncompaction)

      CaseHPOFreeText: >7yo, able to hold breath, non compacted segment = distinct 2-layered appearance of trabeculated and compacted myocardium, NC/C ratio > 2.3:1

      CasePreviousTesting: Cardiac MRI using 17-segment model of LV segmentation, ECG, transthoracic echocardiography, full testing (MYBPC3, TNNT2, TNNI3, MYL2, MYL3, TPM1, ACTC1), additional testing listed in supplementary data tables S1 and S2.

      CaseGenotypingMethod: WES, variant enrichment analysis

      Variant: NM_000257.3(MYH7):c.4717G>A (p.Glu1573Lys)

      ClinVar: 222729, https://www.ncbi.nlm.nih.gov/clinvar/variation/222729/

      gnomAD: 0.00005967, https://gnomad.broadinstitute.org/variant/14-23885449-C-T

      MultipleGeneVariants:

      (1) TMPO Variant:

      Variant: NM_003276.2(TMPO):c.821G>A (p.Arg274Lys)

      ClinVar: 44673, https://www.ncbi.nlm.nih.gov/clinvar/variation/44673/

      gnomAD: 0.002714, https://gnomad.broadinstitute.org/variant/12-98926856-G-A

    1. 25

      CaseVIII: Brazil, Caucasian

      DiseaseAssertion: Hypertrophic cardiomyopathy

      FamilyInfo: Family history of HCM, 1 other relative without phenotypes

      CasePresentingHPOs: HP:0001712, HP:0001639, HP:0011103 (Left ventricular hypertrophy, Hypertrophic cardiomyopathy, Abnormality of the left ventricular outflow tract)

      HPOsFreeText: N/A

      CaseNotHPOs: N/A

      NotHPOsFreeText: N/A

      CaseAddInfo: Cosegregation confirmed for MYH7

      CasePreviousTesting: Only MYH7, MYBPC3, and TNNT2 were tested.

      CaseGenotypingMethod: DNA was extracted from peripheral blood and the above genes were subject to PCR amplification and directly sequenced. The resulting sequences were compared with the reference and filtered for pathogenicity.

      Variant: NM_000257.3:c.4402G>A (p.Glu1468Lys)

      ClinVar: 235033 https://www.ncbi.nlm.nih.gov/clinvar/variation/235033/

      gnomAD: Not in gnomAD

      Multiple Gene Variants

      MYBPC3 Variant

      Variant: NM_000256.3:c.2686G>A (p.Val896Met)

      ClinVar: 42652 https://www.ncbi.nlm.nih.gov/clinvar/variation/42652/

      gnomAD: European (Finnish) 0.02794, Overall 0.006194 https://gnomad.broadinstitute.org/variant/11-47357479-C-T

    1. HCM014

      CaseHCM014: 43 yrs report, Vietnam, Asian

      DiseaseAssertion: Hypertrophic Cardiomyopathy

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0100749, HP:0001712, HP:0031295 (Chest pain, Left ventricular hypertrophy)

      HPOsFreeText: Maximal LV thickness 27 mm

      CaseNotHPOs: HP:0005110, HP:0001297, HP:0004756 (Atrial fibrillation, Stroke, Ventricular tachycardia)

      NotHPOsFreeText: N/A

      CaseAddInfo: N/A

      CasePreviousTesting: The gene panel included 10 sarcomeric genes (MYH7, MYBPC3, TNNT2, TNNI3, TPM1, MYL2, MYL3, ACTC1, TNNC1, MYH6), 9 genes encoding Z-disk components and Ca2+ homeostasis factors (LDB3, CSRP3, TCAP, VCL, ACTN2, MYOZ2, NEXN, JPH2, PLN), and 4 genes involved in HCM phenocopies (GLA, LAMP2, PRKAG2, TTR), All probands had left ventricular wall thickness >= 15 mm and no other diseases that can cause secondary hypertrophy

      CaseGenotypingMethod: The coding region, flanking sequences, and untranslated regions of each gene were enriched by LC-PCR, amplified, and sequenced on the Illumina MiSeq or MiniSeq platform. Identified variants were then filtered for pathogenicity and confirmed by Sanger sequencing.

      Variant: NM_000257.4(MYH7):c.5135G>A (p.Arg1712Gln)

      ClinVar: 36642 https://www.ncbi.nlm.nih.gov/clinvar/variation/36642/

      gnomAD: 0.00004657, http://gnomad.broadinstitute.org/variant/14-23884860-C-T

    1. DiseaseAssertion: None

      VariantPreviousTesting: Some combination of ACTC1, ACTN2, CSRP3, LAMP2, MYBPC3, MYH7, NEXN, PLN, TNNC1, TNNI3, TNNT2, TPM1, ABCC9, CTF1, DES, EMD, LDB3, LMNA, MYH6, RBM20, SGCD, TAZ, TCAP, TTN, VCL, CAV3, GLA, MYL2, MYL3, MYOZ2, PRKAG2, TTR, DSC2, DSG2, DSP, JUP, PKP2, RYR2, TMEM43, CASQ2 and RYR2 were tested via NGS.

      VariantGenotypingMethod: Next-generation sequencing panels were used to sequence and read the genetic information of probands for variants within exons and in +/- 10 nucleotides within the flanking introns of the genes provided above. These variants were then interpreted and filtered for pathogenicity.

      Variant: NM_000257.4(MYH7):c.4668C>A (p.Gly1556=)

      ClinVar: 626810 https://www.ncbi.nlm.nih.gov/clinvar/variation/626810/

      gnomAD: 0.0009022, http://gnomad.broadinstitute.org/variant/14-23885498-G-T

    1. Case#: Consequence 16 Table 1 in Data Supplement (1 cases)

      DiseaseAssertion: HCM

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Cardiac magnetic resonance imaging, BSA, NYHA functional class, obstructive HCM, atrial fibrillation, coronary artery disease, NSVT, Syncope, SCD family hitory, wall thickness

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Additional oligonucleotide hybridization–based DNA sequencing and dideoxy-based DNA sequencing for MYBPC3, TMP1, TNNC1, TNNI2, TNNI3, TNNT2, ACTC1, MYL3

      CaseGenotypingMethod: oligonucleotide hybridization–based DNA sequencing and dideoxy-based DNA sequencing

      Variant: NM_000257.4(MYH7):c.5135G>A (p.Arg1712Gln)

      ClinVar: 36642 https://www.ncbi.nlm.nih.gov/clinvar/variation/36642/

      CAID: n/a

      gnomAD: 0.00004657 European (non-Finnish) https://gnomad.broadinstitute.org/variant/14-23884860-C-T

    2. Case#: Consequence 2 Table 1 in Data Supplement (1 case)

      DiseaseAssertion: HCM

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Cardiac magnetic resonance imaging, BSA, NYHA functional class, obstructive HCM, atrial fibrillation, coronary artery disease, NSVT, Syncope, SCD family hitory, wall thickness

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Additional oligonucleotide hybridization–based DNA sequencing and dideoxy-based DNA sequencing for MYBPC3, TMP1, TNNC1, TNNI2, TNNI3, TNNT2, ACTC1, MYL3

      CaseGenotypingMethod: oligonucleotide hybridization–based DNA sequencing and dideoxy-based DNA sequencing

      Variant: NM_000257.4(MYH7):c.5135G>A (p.Arg1712Gln)

      ClinVar: 36642 https://www.ncbi.nlm.nih.gov/clinvar/variation/36642/

      CAID: n/a

      gnomAD: 0.00004657 European (non-Finnish) https://gnomad.broadinstitute.org/variant/14-23884860-C-T

    1. PatientID: 43

      KindredID: F01

      Case: M, Age Unknown, Unknown Ethnicity

      DiseaseAssertion: VHL

      FamilyInfo: A total of 12 members of this family (F01) had a complete deletion of the VHL gene. Five of these patients (16, 18, 21, 33, 43) presented with clinical features of VHL. This family was previously published except for patients 43 and 48 which were newly diagnosed with VHL disease in the current study.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 17537157

      SupplementalData: Figure 2.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of ~250.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. PatientID: 21

      KindredID: F01

      Case: F, Age Unknown, Unknown Ethnicity

      DiseaseAssertion: VHL

      FamilyInfo: A total of 12 members of this family (F01) had a complete deletion of the VHL gene. Five of these patients (16, 18, 21, 33, 43) presented with clinical features of VHL. This family was previously published except for patients 43 and 48 which were newly diagnosed with VHL disease in the current study.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 17537157

      SupplementalData: Figure 2.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of ~250.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families

      GroupID: 9

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0000107; HP:0002666; HP:0009711; HP:0010797; HP:0009713; HP:0030424; HP:0001737 (Renal cell carcinoma, Renal cyst, Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma, Epididymal cyst, Pancreatic cysts)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (2), Renal cyst (2), Pheochromocytoma (1), Retinal capillary hemangioma (2), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (2), Epididymal cyst (1), Pancreatic cysts (2)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 1-2 Deletion (c.1-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-2 Deletion

      MultipleGeneVariants: N/A

    2. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 45

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0000107; HP:0009711; HP:0010797; HP:0009713; HP:0030393; HP:0001737; HP:0030424 (Renal cell carcinoma, Renal cyst, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma, Endolymphatic sac tumor, Pancreatic cysts, Epididymal cyst)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Renal cyst (1), Retinal capillary hemangioma (1), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (1), Endolymphatic sac tumor (1), Pancreatic cysts/single cyst (1), Epididymal cyst (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 1-3 Deletion (c.1-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: Germline, HSPC300, partial deletion

      MultipleGeneVariants: Germline, ENST197804, deletion

      MultipleGeneVariants: Germline, IRAK2, deletion

      MultipleGeneVariants: Germline, TATDN2, partial deletion

    3. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 26

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0000107; HP:0009711; HP:0010797; HP:0009713; HP:0030393; HP:0001737; HP:0030424 (Renal cell carcinoma, Renal cyst, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma, Endolymphatic sac tumor, Pancreatic cysts, Epididymal cyst)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Renal cyst (1), Retinal capillary hemangioma (1), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (1), Endolymphatic sac tumor (1), Pancreatic cysts (1), Epididymal cyst (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    4. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 51

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0010797; HP:0030393; HP:0030424 (Renal cell carcinoma, Hemangioblastoma, Endolymphatic sac tumor, Epididymal cysts)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Hemangioblastoma/brain/cerebellum (1), Endolymphatic sac tumor (1), Epididymal cysts (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 1-3 Deletion (c.1-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: Germline, IRAK2, deletion

      MultipleGeneVariants: Germline, FANCD2, deletion

    5. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families

      GroupID: 4

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0002666; HP:0009711; HP:0001737 (Renal cell carcinoma, Pheochromocytoma, Retinal capillary hemangioma, Pancreatic cysts)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Pheochromocytoma (1), Retinal capillary hemangioma (1), Pancreatic cysts (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    6. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 20

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: 0 GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0009711; HP:0010797; HP:0009713 (Renal cell carcinoma, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Retinal capillary hemangioma (1), Hemangioblastoma/brain/cerebellum (4), Spinal hemangioblastoma (2)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    1. F60yellowFemale60Trp117Cys3rd R (prior L radical)Never24.76No

      PatientID: None

      KindredID: 4

      Case: F, 60Y0M, Ethnicity Unknown

      DiseaseAssertion: Clear Cell Renal Cell Carcinoma

      FamilyInfo: N/A

      CohortInfo: The National Cancer Institute has a frozen tumour bank of ccRCC tumours that have been removed from VHL patients. We selected six patients, three males and three females, with at least five tumours from a single surgery from one kidney.

      CasePresentingHPOs: HP:0006770 (clear cell renal cell carcinoma)

      CaseHPOFreeText: The patient presented with ccRCC at age 60.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W117C(c.351G>X)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: This protein change corresponds to both c.351G>C or c.351G>T.

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:W117C(c.351G>X)

      MultipleGeneVariants: N/A

    1. Mutational analysis of the VHL gene, performed using DNA extracted from her peripheral blood cells according to a previously reported method [4], revealed a G-to-A point mutation at nucleotide 500 (exon 1) resulting in an Arg167Glu amino acid substitution.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: N/A

      SamplingMethod: peripheral blood

    1. 13MProbandExon2, 3 deletion1324444, B–41–4

      PatientID: Proband

      KindredID: 13

      Case: M, 44Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Son and brother presented with the same VHL variant. Son is asymptomatic. Brother presented with CNS hemangioblastoma at 29Y, retinal hemangioblastoma at 52Y, bilateral RCC at 43Y, multiple pancreatic lesions (pancreatic cyst or tumor, unspecified) at 43Y and bilateral renal cysts at 43Y. Nephew presented with CNS hemangioblastoma at 22Y, retinal hemangioblastoma at 18Y, bilateral RCC at 29Y and multiple pancreatic lesions (pancreatic cyst or tumor, unspecified) at 18Y but was not genetically confirmed.

      CohortInfo: Thirteen unrelated patients with germline VHL mutations who were diagnosed with VHL disease were evaluated.

      CasePresentingHPOs: HP:0001732; HP:0010797; HP:0005584; HP:0009711 (Abnormality of the pancreas, Hemangioblastoma, Renal cell carcinoma, Retinal capillary hemangioma)

      CaseHPOFreeText: CNS hemangioblastoma at 32Y, retinal hemangioblastoma at 44Y, bilateral RCC at 44Y and multiple pancreatic lesions (pancreatic cyst or tumor, unspecified) at 41Y. Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0000107; HP:0002666 (Renal cyst, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    2. Genomic DNA was extracted from peripheral blood using the Gentra Puregene Blood kit (Gentra Systems, Minneapolis, MN, USA), according to the manufacturer’s instructions. All coding exons and flanking intronic regions were amplified by PCR using primers specific for VHL exons 1–3. The amplified product was directly sequenced with an ABI PRISM 3730xl DNA Analyzer (Applied Biosystems, Foster City, CA, USA) using the BigDye Terminator v.3.1 Cycle Sequencing Kit (Applied Biosystems).For screening exon deletions and duplications, multiplex ligation-dependent probe amplification (MLPA) P016-C1/P16-C2 kits (MRC-Holland, Amsterdam, Netherlands) were used. DNA denaturation, probe-target sequence hybridization, probe ligation, and PCR amplification of ligated probes were performed according to the manufacturer’s instructions. The products were loaded onto ABI PRISM 3130xl DNA Analyzer (Applied Biosystems) and analyzed by GeneMarker software version 1.51 (SoftGenetics, LLC, State College, PA, USA).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Direct sequencing uaing an ABI PRISM 3730xl DNA Analyzer (Applied Biosystems, Foster City, CA, USA) using the BigDye Terminator v.3.1 Cycle Sequencing Kit (Applied Biosystems). and multiplex ligation-dependent probe amplification.

      SamplingMethod: peripheral blood

    1. Genetic subdivision All patients who fulfilled clinical criteria of VHL (Schmid et al. 2014) were included in the analyses, regardless of the presence of a positive genetic test result. Molecular genetic testing was conducted by DNA sequencing and gene dosage analysis. Since a molecular genetic testing has often already been performed close to patient's home and since the patients live all over Germany, the molecular genetic data not performed in our internal human genetic laboratory originate from several different external laboratories all over Germany. For molecular genetic testing, DNA sequencing and gene dosage analysis of the VHL gene (NCBI/Ensembl gene ID: 7428; reference genome: GRCh37.p13) were conducted. The pathogenicity of the VHL gene variant was reviewed via the human gene mutation database (HGMD®). If the genetic test result was known, patients were divided into two groups, patients with a truncating variant or a complete deletion of the VHL gene, and patients with a single amino-acid substitution/deletion. If the pathogenicity of detected VHL gene variant was uncertain, the patient was not assigned to either of the above groups.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: DNA sequencing and gene dosage analysis

      SamplingMethod: Not stated

    2. 1 (100)

      GroupID: 4

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      CohortInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: This individual patient did NOT have retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes - Supplementary Table S1

      Variant: Exon 2-3 deletion

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 deletion

      MultipleGeneVariants: N/A

    3. 10 (67)

      GroupID: 2a

      DiseaseAssertion: VHL

      GroupSize: 10

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      GroupPresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      GroupHPOFreeText: These 10/15 patients with a VHL gene deletion had retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes - Supplementary Table S1

      Variant: VHL gene deletion

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Complete Deletion)

      MultipleGeneVariants: N/A

    4. 1 (100)

      GroupID: 3

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      CohortInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: This individual patient did NOT have retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes - Supplementary Table S1

      Variant: Exon 1-2 deletion

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-2 deletion

      MultipleGeneVariants: N/A

    1. Case report: We present a case of a compound heterozygote patient with von Hippel-Lindau disease and familial erythrocytosis type 2. One of the mutations found in our patient, c.416C>G (p.Ser139Cys) of the VHL gene, has not been previously reported. This case is the second one reported where von Hippel-Lindau disease and familial erythrocytosis type 2 coexist in the same individual.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: MLPA complete VHL gene sequencing.

      SamplingMethod: peripheral blood

    1. gross deletions (4/16)

      PatientID: 15

      KindredID: 15

      Case: 34Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: Positive family history

      CasePresentingHPOs: HP:0006770; HP:0001737; HP:0000107; HP:0030393 (clear cell renal cell carcinoma; pancreatic cysts; renal cyst; endolymphatic sac tumor)

      CaseHPOFreeText: Aged 34Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. ccRCC, pancreatic cysts, renal cysts, and endolymphatic sac tumors were all diagnosed at 34Y (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: exon 3 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. Sequencing of the VHL gene Blood samples were collected from the patients. The genomic DNA was isolated from the peripheral blood leukocytes using a Wizard genomic DNA purification kit according to the manufacturer's instructions (Promega, Madison, WI, U.S.A.).

      ArticleReferenceSequence: NM_000551.2

      GenotypingMethod: PCR and multiple ligation-dependent probe amplification (MLPA) analysis; re-PCR and resequencing with alliquot of stored DNA was additionally done.

      SamplingMethod: peripheral blood leukocytes

    2. Partial deletions were heterozygous in size and position: one removed exon 3

      PatientID: 14

      KindredID: 14

      Case: M, 51Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0010797; HP:0005584 (hemangioblastoma, renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database) [Refer to table 2].

      SupplementalData: N/A

      Variant: Exon 3 deletion (c.464-?_642+?del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 deletion

      MultipleGeneVariants: N/A

    3. Multiplex ligation-dependent probe amplification (MLPA) analysis of VHL exons 1-3. Signal intensity reveals only a single copy of VHL exon 2 and 3 in a patient with VHL due to deletion of VHL exon 2 and 3 (A) and only a single copy of each VHL exon in a patient with VHL due to deletion of whole VHL gene deletion (B) when compared to a healthy control (C).

      PatientID: None (sister)

      KindredID: 10

      Case: F, 38Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Patient had a positive family history: Her father was died of RCC (no mutation availible), and her older sister who presented with spinal HB and multiple cysts in pancreas and both kidneys, harbored the same exon deletion

      CasePresentingHPOs: HP:0010797; HP:0005584 (hemangioblastoma, renal cell carcinoma)

      CaseHPOFreeText: presented with medullary HB at the age of 37 and multiple RCC in both kidneys at the age of 38

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-3 deletion (c.1-?_642+?del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: N/A

    1. 1 France delEx2

      GroupID: 37

      Case: Sex unknown, Age unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: Unknown. 1 registrant was found with this variant; no family info was mentioned

      CasePresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    2. 1 Netherlands delEx1

      GroupID: 36

      Case: Sex unknown, Age unknown, Dutch (The Netherlands)

      DiseaseAssertion: VHL

      FamilyInfo: Unknown. 1 registrant was found with this variant; no family info was mentioned

      CasePresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    1. ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: MLPA. Those cases that were found in the MLPA assay to have deletions affecting VHL exon 1 but not FANCD2, were further characterized by means of a user-designed multiplex-PCR analysis in order to establish the retention of HSPC300 band ENST197804. The presence of. VHL point mutations were evaluated in apparently sporadic ccRRCs by PCR amplification and sequencing, and loss of heterozygosity (LOH) was analyzed by commercial multiplex ligation-dependent probe amplification (MLPA).

      SamplingMethod: peripheral blood, tissue resection

    2. PatientID: None

      KindredID: 36

      Case: M, 31Y0M, Spanish

      DiseaseAssertion: VHL

      FamilyInfo: Positive for familial antecedents. No known familial tumors.

      CohortInfo: Probands belonging to 18 unrelated Spanish VHL families carrying germline VHL deletions.

      CasePresentingHPOs: HP:0006880; HP:0001737 (Cerebellar hemangioblastoma, Pancreatic cysts)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Germline HSPC300, ENST197804 and FANCD2 (unclear if partial or complete) gene deletions. Study provides evidence to show that loss of HSPC300 highly correlates with the absence of ccRCC in VHL patients.

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: Germline, HSPC300, Deletion MultipleGeneVariants: Germline, ENST197804, Deletion MultipleGeneVariants: Germline, FANCD2, Deletion

    3. PatientID: None (Proband)

      KindredID: 53

      Case: F, 18Y0M, Spanish

      DiseaseAssertion: VHL

      FamilyInfo: Positive for familial antecedents. Family history of clear cell renal cell carcinoma.

      CohortInfo: Probands belonging to 18 unrelated Spanish VHL families carrying germline VHL deletions.

      CasePresentingHPOs: HP:0006880; HP:0001737; HP:0009711 (Cerebellar hemangioblastoma, Pancreatic cysts, Retinal capillary hemangioma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Germline HSPC300 (Figure 2 appears to indicate an exon 2-3 deletion of this gene since it spans the same left-most distance as the mutation in patient 108 which is stated to be an exon 2-3 deletion) and ENST197804 deletion. Study provides evidence to show that loss of HSPC300 highly correlates with the absence of ccRCC in VHL patients.

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: Germline, HSPC300, Exon 2-3 Deletion MultipleGeneVariants: Germline, ENST197804, Deletion

    1. 2 Partial deletion Deletion of exon 1 and 2 1 0

      GroupID: 2

      DiseaseAssertion: VHL

      Group size: 1

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      Group Info: Retrospective analysis of a longitudinal cohort of 21 VHL germline mutation carriers and retinal haemangioblastomas. All patients were categorized in two genotypic categories: missense mutations and truncating mutations.

      GroupPresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      GroupHPOFreeText: The patient presented with retinal capillary hemangioma.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1

      Variant: Exon 1-2 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: cDNA level information: c.(?_1)_463+?del

      MutationType: exon_loss_deletion

      CivicName: Exon 1-2 deletion

      MultipleGeneVariants: N/A

    1. We previously reported a case of VHL with a germline VHL mutation, 233 A > T, who underwent total pancreatectomy for multiple SCNs and right nephrectomy for renal cell carcinoma [8]. Herein, we report that this case developed multiple metachronous liver metastases of the SCN after the initial operation and underwent surgical resections for the metastases. This patient has been alive without any recurrence more than 6 years after the metastasectomies.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: N/A - Genetic testing done previously (PMID: 21673464)

      SamplingMethod: N/A

    1. We present the case of a 22-year-old woman who was diagnosed in childhood with type IIb VHL, with known multiple retinal angiomas, pancreatic cysts, and spinal and cerebellar hemangioblastomas. She was admitted to our hospital complaining of progressive dyspnea and palpitations. On examination, her blood pressure was 159/119 mm Hg and her pulse was 123 bpm. Physical examination revealed a systolic murmur at the mitral focus with irradiation to the axilla and pulmonary rales. Electrocardiography revealed no remarkable findings, except for sinus tachycardia. Laboratory tests showed an elevated N-terminal pro-brain natriuretic peptide and chest X-ray showed signs of pulmonary interstitial edema. The patient was admitted to the Department of Cardiology with the diagnosis of acute decompensated heart failure. Transthoracic echocardiography showed a dilated left ventricle with severely depressed ejection fraction due to generalized hypokinesia and a mild mitral regurgitation (fig. ​(fig.1a).1a). During admission, the patient had several episodes of paroxysmal dyspnea despite treatment with β-blockers and diuretics. Due to the clinical suspicion of adrenal gland disease, 24-hour urinary catecholamine and metanephrine tests were requested. Cardiac MRI was performed in order to complete the cardiomyopathy study, and confirmed the echocardiographic findings as well as revealed an incidental finding of a great left renal mass. The 24-hour urine laboratory tests showed markedly elevated levels of norepinephrine, total catecholamines, normetanephrine and metanephrine with normal epinephrine values: 24-hour norepinephrine 468 μg (normal range: 23-105), 24-hour epinephrine 13 μg (normal range: 4-20), 24-hour total catecholamines 658 μg (normal range: 217-575), 24-hour normetanephrine 2,988 μg (normal range: 105-354), 24-hour total metanephrine 3,013 μg (normal range: 0-1,000). Therefore, an abdominal MRI was performed, which showed the presence of two cystic masses (fig. ​(fig.2)2) located at the left hypochondrium. Surgical resection of both masses was performed (after α-blockade with phenoxybenzamine and β-blockade with propranolol) through a laparoscopic approach, confirming the diagnosis of pheochromocytoma and clear cell renal carcinoma on histology. During follow-up, blood pressure and heart rate values normalized (124/77 mm Hg, 78 bpm), 24-hour urinary catecholamine values returned to normal range (norepinephrine 69 μg/24 h, total catecholamine 221 μg/24 h, normetanephrine 202 μg/24 h and total metanephrine 259 μg/24 h) and the patient had no new episodes of palpitations or dyspnea. Six months after surgical resection, echocardiography was repeated and showed a left ventricle with normal diameters and preserved ejection fraction (fig. ​(fig.1b).1b). Genetic analysis revealed a germline mutation (exon 3 deletion) of the VHL tumor suppressor gene on the short arm of chromosome 3. As the patient had no family history of VHL, it was concluded that it was a de novo mutation.

      PatientID: None

      KindredID: 1

      Case: F, 22Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL, it was concluded that it was a de novo mutation.

      CasePresentingHPOs: HP:0009711; HP:0001737; HP:0009713; HP:0006880; HP:0002094; HP:0001962; HP:0011703; HP:0031664; HP:0001635; HP:0002375; HP:0001653; HP:0002666; HP:0006770 (Retinal capillary hemangioma, Pancreatic cysts, Spinal hemangioblastoma, Cerebellar hemangioblastoma, Dyspnea, Palpitations, Sinus tachycardia, Systolic heart murmur, Congestive heart failure, Hypokinesia, Mitral regurgitation, Pheochromocytoma, Clear cell renal cell carcinoma)

      CaseHPOFreeText: 22-year-old woman who was diagnosed in childhood with type IIb VHL, with known multiple retinal angiomas, pancreatic cysts, and spinal and cerebellar hemangioblastomas. She was admitted to our hospital complaining of progressive dyspnea and palpitations. Physical examination revealed a systolic murmur at the mitral focus with irradiation to the axilla and pulmonary rales. Electrocardiography revealed no remarkable findings, except for sinus tachycardia. Chest X-ray showed signs of pulmonary interstitial edema. The patient was admitted to the Department of Cardiology with the diagnosis of acute decompensated heart failure. Transthoracic echocardiography showed a dilated left ventricle with severely depressed ejection fraction due to generalized hypokinesia and a mild mitral regurgitation. During admission, the patient had several episodes of paroxysmal dyspnea. Cardiac MRI was performed in order to complete the cardiomyopathy study, and confirmed the echocardiographic findings as well as revealed an incidental finding of a great left renal mass. Abdominal MRI was performed, which showed the presence of two cystic masses located at the left hypochondrium confirming the diagnosis of pheochromocytoma and clear cell renal carcinoma on histology.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. A two-month-old infant

      case1: male, 40 weeks,

      DiseaseAssertion: sudden-onset acute heart failure

      FamilyInfo: Both parents suspected of being heterozygous carriers of a pathogenic MYBPC3 variant

      ParentalTesting: Both parents were identified as heterozygous carriers of a pathogenic MYBPC3 variant

      CasePresentingHPOs: HP: 0001639, HP: 0001631, HP: 0001635

      “Hypertrophic cardiomyopathy, atrial septal defect, acute heart failure”

      CaseHPOFreeText: Absence of significant interstitial fibrosis, extensive myocardial disarray and contraction band necrosis

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: normal fetal growth and anatomy reported

      CasePreviousTesting: Targeted gene panel for pathogenic variants in MYBPC3

      Genotyping Method: Whole-exome sequencing (WES)

      FunctionalAnalysis: N/A

      Variant: NM_000256.3:c.2905+1G>A

    1. Genomic DNA was extracted from the patient’s peripheral blood leukocytes using a DNA extraction kit, and VHL gene coding sequence analysis was performed by direct sequencing of PCR-amplified products using Sanger sequencing technology with an Applied Biosystems 3500 Dx Series Genetic Analyzer (ThermoFisher Scientific, USA) at Beijing Shengguzhi Medical Laboratory (Beijing, China) following the manufacturer’s instructions. It was found that a deletion mutation (Fig. 4) occurred in the patient’s VHL gene at the c530-536delGACTGGA region in exon 3. This deletion caused a change in the amino acid at position 177 (Arg-177, Fig. 4). Based on the results of genetic tests, the patient was diagnosed with VHL syndrome with renal carcinoma, bilateral lung metastases, multiple nephrotic cysts and multiple cysts of the liver, cerebellar hemangioblastoma and cystadenoma of the head (Fig. 5). The patient’s conditions were informed to his family members, and a family medical census was proposed but was ultimately declined. The application of vascular endothelial growth factor inhibitors to treat the disease was also refused. Other symptomatic and supportive treatments for anaemia and hypoproteinaemia were also declined. On August 26, 2017, CT examinations showed that the renal tumours and lung metastatic lesions increased compared with previous conditions. The patient discontinued treatments and died in 2018. Fig. 4VHL gene and testing results of case 1. a The top row shows the wild-type human VHL DNA sequence segment of 721–770 from the NCBI database (NM_000551.3). The nucleotide database includes EST and GSS sequences. The bottom row shows the deletion of the GACTGGA sequence in the VHL gene of the subject. b Genetic testing results of the patient’s VHL gene, indicating the deletion of the GACTGGA sequence, leading to an amino acid Arg-177 change in case 1

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: Sanger sequencing of PCR-amplified coding sequences of the VHL gene.

      SamplingMethod: peripheral blood

    1. PatientID: 47 (Uncle)

      KindredID: 18

      Case: M, 39Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 11 members of this family tested positive for the c.712C>T/c.499C>T germline variant of the VHL gene. 14 members of this family were assumed to carry this variant due to family history/personal medical history. Members of this family range from asymptomatic to multi-organ involvement (pheochromocytoma, pancreatic and renal cysts/tumors and hemangioblastomas). The family was previously reported in PMID 3942913.

      CasePresentingHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (30 and 42Y) and retinal angioma (26Y). Patient died at 39Y.

      CaseNotHPOs: HP:0005584; HP:0000077; HP:0001732; HP:0002666 (Renal cell carcinoma, Abnormality of the kidney, Abnormality of the pancreas, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 3942913 (some members of this family are previously reported (phenotypes only) but unable to match patients across papers with confidence)

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.712C>T germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing was done on this patient to confirm this. Being that this familial variant is out of bound with respect to the NM_000551.3 reference sequence, it was concluded that this variant is noted in the Latif et al. (1993) reference and was translated to c.499C>T (NM_000551.3).

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    2. PatientID: 3 (Father)

      KindredID: 13

      Case: M, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 5 members of this family were found to harbour the deletion of one VHL allele. The proband (ID 1), sister (ID 2) and uncle (ID 5) were all asymptomatic. The grandmother (ID 9) presented with CNS hemangioblastoma (34Y).

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (34Y).

      CaseNotHPOs: HP:0002666; HP:0005584; HP:0009711; HP:0000077; HP:0001732 (Pheochromocytoma, Renal cell carcinoma, Retinal capillary hemangioma, Abnormality of the kidney, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Reported as “del one vHL allele”.

      MutationType: deletion

      CivicName: Null (del one VHL allele)

      MultipleGeneVariants: N/A

    3. PatientID: 1 (Proband)

      KindredID: 3

      Case: M, 3Y0M, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: 3 members of this family were genetically confirmed to be carriers of a germline partial deletion of exon 2 of the VHL gene. ID 8 presented with CNS hemangioblastoma and ID 2 presented with retinal angioma and pancreatic abnormality. ID 16 presented with a retinal angioma (33Y), CNS hemangioblastoma at (32Y) and died at age 42. ID 16 was stated as having the germline variant but this was inferred from family/personal history and was not genetically confirmed.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584; HP:0001732; HP:0000077; HP:0002666; HP:0009711; HP:0010797 (Renal cell carcinoma, Abnormality of the pancreas, Abnormality of the kidney, Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: Exon 2 Partial Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Partial deletion of Exon 2)

      MultipleGeneVariants: N/A

    4. PatientID: 149 (Half first cousin once removed)

      KindredID: 18

      Case: M, 57Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 11 members of this family tested positive for the c.712C>T/c.499C>T germline variant of the VHL gene. 14 members of this family were assumed to carry this variant due to family history/personal medical history. Members of this family range from asymptomatic to multi-organ involvement (pheochromocytoma, pancreatic and renal cysts/tumors and hemangioblastomas). The family was previously reported in PMID 3942913.

      CasePresentingHPOs: HP:0009711; HP:0002666 (Retinal capillary hemangioma, Pheochromocytoma)

      CaseHPOFreeText: This patient presented with retinal angioma (21Y) and pheochromocytoma (21Y).

      CaseNotHPOs: HP:0005584; HP:0000077; HP:0001732; HP:0010797 (Renal cell carcinoma, Abnormality of the kidney, Abnormality of the pancreas, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 3942913 (some members of this family are previously reported (phenotypes only) but unable to match patients across papers with confidence)

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.712C>T germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing was done on this patient to confirm this. Being that this familial variant is out of bound with respect to the NM_000551.3 reference sequence, it was concluded that this variant is noted in the Latif et al. (1993) reference and was translated to c.499C>T (NM_000551.3).

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    5. PatientID: 20 (Great aunt)

      KindredID: 17

      Case: F, 70Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 6 members of this family tested positive for the c.496_506del germline variant of the VHL gene. ID 4 presented with CNS hemangioblastoma, retinal angioma and renal and pancreatic abnormalities. ID 1, 25 and 8 were asymptomatic.ID 22 presented with CNS hemangioblastoma. ID 5 presented with retinal angioma. 2 members were assumed to have the variant but were not genetically confirmed (ID 20 and ID 11). ID 11 presented with CNS hemangioblastoma.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (43Y).

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0000077; HP:0001732; HP:0009711 (Renal cell carcinoma, Pheochromocytoma, Abnormality of the kidney, Abnormality of the pancreas, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.496_506del germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing is done to confirm this. It is unclear from the publication if this variant is reported according to legacy (AF010238.1) or NM_000551.3 reference sequence. Clinical notes from the case confirm the reference sequence to be NM_000551.3.

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. GroupID: 1

      DiseaseAssertion: assumed VHL

      GroupSize: 113

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 113 of the 573 patients discussed in this paper were found to have the following mutation belonging to 39 families altogether

      GroupPresentingHPOs: HP:0005584; HP:0006880; HP:0009711; HP:0002666 (renal cell carcinoma; cerebellar hemangioblastoma; retinal capillary hemangioma; pheochromocytoma)

      GroupHPOFreeText: 68 patients had retinal angiomas diagnosed at a mean age of 25Y, 61 had cerebellar hemangioblastomas diagnosed ad a mean age of 31Y, 34 had RCC diagnosed at a mean age of 45Y, and 4 had pheochromocytoma diagnosed at a mean age of 33Y

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: exonic deletions

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Exon Deletion

      MultipleGeneVariants: N/A

    1. Case 8In 1997, a 19-yr-old man with a familial history for VHL presented with headaches. MRI of the CNS was normal, but ophthalmological examination showed a right retinal hemangioblastoma that was treated by laser. In 2002, he had right nephrectomy and left nephron-sparing surgery for renal cell carcinoma. At age 27, a palpable mass on the left side of the neck was diagnosed during dental care. CT and MRI revealed a 4-cm carotid body tumor that was removed after selective embolization. Histology revealed a paraganglioma. The patient also has pancreatic cysts. Molecular genetics identified the deletion of exons 2 and 3 of the VHL gene.

      PatientID: 8

      KindredID: 8

      Case: M, 27Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Positive family history for VHL.

      CohortInfo: An international consortium registered patients with head and neck paragangliomas with VHL or RET gene mutations.

      CasePresentingHPOs: HP:0009711; HP:0005584; HP:0002668; HP:0001737; HP:0002666 (retinal capillary hemangioma, renal cell carcinoma, paraganglioma, pancreatic cysts, pheochromocytoma)

      CaseHPOFreeText: At 19Y (in 1997), he presented with headaches, ophthalmological examination showed a right retinal hemangioblastoma (treated by laser). 5 years later (age 24Y) he had a right nephrectomy and left nephron-sparing surgery for renal cell carcinoma. Age 27, a palpable mass on the left side of the neck. CT and MRI revealed a 4-cm carotid body tumor (paraganglioma). The patient also has pancreatic cysts. 

      CaseNotHPOs: HP:0010797 (hemangioblastoma)

      CaseNotHPOFreeText: MRI scan from case presenting headaches showed a normal CNS

      CasePreviousTesting: RET

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: exon 2-3 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: EXON 2-3 DELETION

      MultipleGeneVariants: N/A

    1. patients with VHL disease

      PatientID: 2

      KindredID: 1

      Case: F, 47Y0M, Japanese

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s son had retinal capillary hemangioma of right eye at 19Y0M, and of both eyes by 24Y0M, he was also found with numerous tumors in the spinal cord, kidney, pancreas, and liver at age 25Y0M; patient's mother lost her eyesight and died from renal cancer and brain tumors at 58Y0M. No mutation was clearly outlined in mother but the c.233A>G recorded in son. According to family history, the patient was considered to carry type I VHL disease

      CasePresentingHPOs: HP:0001737; HP:0000107; HP:0009711 (pancreatic cysts; renal cyst; retinal capillary hemangioma)

      CaseHPOFreeText: had pancreatic and renal cysts at 37Y0M, and retinal angiomas at 47Y0M

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: unknown

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: unknown

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. Family 17−Exon 2 DeletionNo2A––292929–

      PatientID: None

      KindredID: 17

      Case: Sex Unknown, 29Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0005584, HP:0001732, HP:0002666 ( renal cell carcinoma, abnormality of the pancreas, pheochromocytoma)

      CaseHPOFreeText: The patient presented with pheochromocytoma, renal cell carcinoma, and pancreatic cysts or tumours at age 29.

      CaseNotHPOs: HP:0009711, HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      CaseNotHPOFreeText: The patient did not have an epididymal or ovarian cystadenoma.

      CasePreviousTesting: N/A

      PreviouslyPublished: 29330336

      Variant: Exon 2 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    2. Using polymerase chain reaction (PCR)-direct sequencing and universal primer quantitative fluorescent multiplex–PCR, we examined mutations in VHL gene in 19 VHL disease families recruited from the Department of Urology, Peking University First Hospital in the period from 2009 to 2012.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Polymerase chain reaction direct sequencing and universal primer quantitative fluorescent multiplex–PCR to detect point mutations, small and large indels.

      SamplingMethod:N/A

    1. Genetic linkage and haplotype analysesPeripheral blood leukocytes were collected from 33 of the 38 living family members, and human genomic DNA was extracted using the DNA Isolation Kit for Mammalian Blood (Tiangen Biotech Co., Ltd., Beijing, China). We genotyped three polymorphic microsatellite markers that flanked VHL on chromosome 3p25 (D3S3691, D3S1597 and D3S1263). The microsatellite markers were amplified by PCR using fluorescently labeled primers. The products were analyzed with an Applied Biosystems 3730 Genetic Analyzer (Applied Biosystem, Foster City, CA, USA). LOD scores were calculated using the MLINK program of the LINKAGE package 5.1 (Perkin Elmer, Waltham, USA). The parameters used for linkage analysis were autosomal dominant inheritance, complete penetrance, a mutation rate of 0, equal male-female recombination rates, equal allele frequency, and the disease allele frequency of 1 in 10,000.[17]Von Hippel-Lindau sequence analysisMutation screening was performed by directly analyzing the DNA sequence output. The exons of VHL were amplified with primers flanking the exon-intron boundaries [Table 1]. The PCR thermal cycling program was as follows: One cycle of 2 minutes for denaturation at 95°C, 35 cycles for 30 seconds at 95°C, 35 seconds at 57°C, 45 seconds at 72°C, and one 7 minutes extension step at 72°C. The PCR products were sequenced on an Applied Biosystems 3730 Genetic Analyzer.[17,18]

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: genotyped three polymorphic microsatellite markers that flanked VHL on chromosome 3p25 (D3S3691, D3S1597 and D3S1263). The microsatellite markers were amplified by PCR using fluorescently labeled primers. Mutation screening was performed by directly analyzing the DNA sequence output. The exons of VHL were amplified with primers flanking the exon‑intron boundaries

      SamplingMethod: peripheral blood leukocytes

    1. 136MIntron 2Splice g. 8665, A > G; c.DNA 463,+2A > C1 peripheral-1 peripheralGreat exudationNo changesNo exudation

      PatientID: 1

      KindredID: 1

      Case: M, 36Y0M, Spanish

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: CohortInfo: 7 VHL patients, from different regions of Spain, affected from juxtapapillary or peripheral haemangioblastomas were administered 120 mg propranolol daily.

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Patient 1 presented with one peripheral tumor in the left eye and one peripheral tumor in the right eye with great exudation. Ophthalmologist wrote in his clinical history “no new lesions/no active lesions” during the visits he attended from January 2015 until December 2015. Moreover, his retinal exudation decreased during the months of treatment with the administration of propranolol.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Information obtained from Table 2.

      Variant: c.463+2A>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: Amino acid does not coincide with position, declared by the authors. Variant c.463+2A>C could be translated to c.463+2T>C or c.463+3A>C. Needs to be confirmed with the authors.

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: c.463+2A>C

      MultipleGeneVariants: N/A

    1. PatientID: 2

      KindredID: 4

      Case: F, 41Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Thirteen patients with a supratentorial hemangioblastoma.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: The patient had a right temporal hemangioblastoma at age 25. After surgery the patient was disease free. The patient was followed up 16 years later.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2-3 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType:exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    1. case 10: deletion in exons 2 and 3

      PatientID: 10

      KindredID: 1

      Case: M, 35Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666; HP:0010797; HP:0006770 (pheochromocytoma; hemangioblastoma; clear cell renal cell carcinoma)

      CaseHPOFreeText: bilateral pheochromocytoma sized R: 3.0(cm), L: 1.0(cm); Grade 2 cystic clear cell renal cell carcinoma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: SDHB/TMEM127

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: See table 4 for SDHB information; See table 6 for TMEM127 information

      MutationType: exon_loss_variant

      CivicName: EXON 2-3 DELETION

      MultipleGeneVariants: N/A

    1. Clinical Case This is a 32 year-old Thai male with VHL diagnosed at age 20 when he was found to have a cerebellar hemangioblastoma. Genetic testing revealed a large deletion of exon 3 and poly A sites of VHL gene. Abdominal CT obtained as part of routine surveillance demonstrated multiple cystic lesions with rim enhancement in the pancreas. Based on CT characteristics, these lesions were presumed benign thus regular follow-up abdominal imagings were not performed. 10 years later, he developed abdominal discomfort. CT abdomen showed multiple solid and cystic enhancing lesions involving the entire pancreas with a hypervascular mass at segment 7 of liver. Given radiological findings, he was diagnosed with malignant pancreatic neuroendocrine tumor (PNET) with liver metastasis, thereupon underwent total pancreactomy with wedge resection of the liver mass. Surprisingly, the histopathology revealed a serous cystadenocarcinoma in the pancreas measuring 28 x 11.5 x 7 cm and a 4.5 x 4.5 x 3 cm metastatic lesion in the liver with hepatic capsular invasion. Since then annual abdominal CTs have been performed. Until present, there has been no evidence of tumor recurrence.

      PatientID: N/A (Case)

      KindredID: 1

      Case: M, 32Y0M, Thai (South Asian)

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006880; HP:0030405 (cerebellar hemangioblastoma; pancreatic endocrine tumor)

      CaseHPOFreeText: This male was diagnosed with VHL at 20Y when he was found to have a cerebellar hemangioblastoma. Abdominal CT obtained as part of routine surveillance demonstrated multiple cystic lesions with rim enhancement in the pancreas. 10 years later, he developed abdominal discomfort, and an abdomen CT showed multiple solid and cystic enhancing lesions involving the entire pancreas with a hypervascular mass at segment 7 of liver. Given radiological findings, he was diagnosed with malignant pancreatic neuroendocrine tumor (PNET) with liver metastasis, thereupon underwent total pancreactomy with wedge resection of the liver mass. Surprisingly, the histopathology revealed a serous cystadenocarcinoma in the pancreas measuring 28 x 11.5 x 7 cm and a 4.5 x 4.5 x 3 cm metastatic lesion in the liver with hepatic capsular invasion. 

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Genetic testing revealed a large deletion of exon 3 and poly A sites of VHL gene.

      MutationType: exon_loss_variant

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. 42 c.1-?_642+? Genomic deletion of exons 1 to 3 Familial VHL

      GroupID/ KindredID: 42

      DiseaseAssertion: VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 5 registrants belonging to the same family (42) have the germline VHL deletion.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0001737; HP:0000107; HP:0030393 (hemangioblastoma, retinal capillary hemangioma, pancreatic cysts, renal cyst, endolymphatic sac tumor)

      GroupHPOFreeText: 4/5 members had hemangioblastomas, 1 had retinal capillary hemangiomas and renal cysts, 2 had pancreatic cysts, 2 had endolymphatic sac tumors, and 1 had an adnexal papillary tumor of probably mesonephric origin

      GroupNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-3 deletion (c.1-?_642+?)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-3 deletion

      MultipleGeneVariants: N/A

    2. 37 c.1-?_340+? Genomic deletion of exon 1 Familial VHL

      GroupID/ KindredID: 37

      DiseaseAssertion: VHL

      GroupSize: 8

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 8 registrants belonging to the same family (37) have the germline VHL deletion.

      GroupPresentingHPOs: HP:0009711; HP:0010797; HP:0005584; HP:0001737 (retinal capillary hemangioma, hemangioblastoma, renal cell carcinoma, pancreatic cysts)

      GroupHPOFreeText: all 8 members had hemangioblastomas, 7 had retinal capillary hemangiomas. 7 had renal cell carcinoma, 1 had pancreatic cysts, and 1 had hepatic carcinoma

      GroupNotHPOs: HP:0002666; HP:0000107 (pheochromocytoma, renal cyst)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 deletion (c.1-?_340+?)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 deletion

      MultipleGeneVariants: N/A

    1. PatientID: N/A

      KindredID: 195

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Paper states familial VHL

      CasePresentingHPOs: unknown

      CaseHPOFreeText: Patient had VHL, but no specific phenotypes were described

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: exon 3 deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion 

      MultipleGeneVariants: N/A

    2. PatientID: N/A

      KindredID: 193

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Paper states familial VHL; no obvious relation (family surnames, location) but could be distantly related

      CasePresentingHPOs: Unknown

      CaseHPOFreeText: Patient was said to have VHL, however their specific phenotypes are unknown

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: Exon 2 Deletion (c.341-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    1. Additionally, one uncle had succumbed to RCC

      PatientID: None (proband’s uncle)

      KindredID: 1

      Case: M, Age unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Recorded family history of VHL disease, with the patient’s 4 sisters, mother, and brother suffering from the disease. 5 of these individuals in the family had succumbed to cerebral hemangioblastomas. No mutation was stated. The 34Y old proband (nephew) had cerebellar hemangioblastoma, renal cell carcinoma and pancreatic endocrine tumour and a confirmed c.473T>C mutation.

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: unknown

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: N/A

      CivicName: N/A - (L158P (c.473T>C))

      MultipleGeneVariants: N/A

    1. 19 I 0 5 No manifestations T c.464-?_642 + ?del

      PatientID: I

      KindredID: 19

      Case: Sex Unknown, 5Y0M, Danish

      DiseaseAssertion: Asymptomatic

      FamilyInfo: 3 other family members presented with this VHL variant. Patients 19-II and 19-III were asymptomatic. Patient 19-IV presented with 2 retinal hemangioblastomas (10Y and 12Y) and kidney disease (17Y).

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Diagnosed with VHL at age 0Y. Age at the end of study: 5Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Null (c.464-?_642+?del)

      MultipleGeneVariants: N/A

    1. VHL mutation analysis was performed in 3 laboratories participating in the French VHL network (Lyon, Villejuif, and Paris) after approval from our local ethics committee. Individual written consent for molecular analysis was obtained from all sampled individuals or their legal guardians. DNA was isolated from peripheral blood lymphocytes using standard protocols. Direct sequencing of the 3 exons of VHL was performed for all the DNA. If no mutation was detected, Southern blot analysis was performed to detect large rearrangements. Mutations are named according to international recommendations. Nucleotide is numbered according to GenBank accession number AF010238.1, nucleotide 1 corresponds to A of ATG initiation codon, and the codon for initiator methionine is codon 1. For DNA sequencing, polymerase chain reaction was performed according to a previously reported protocol.39 Southern blot analysis was performed according to previously reported procedures.10

      ArticleReferenceSequence: Specified to follow AF010238.1, although reference sequence appears to follow NM_000551.3

      GenotypingMethod: Direct sequencing of the 3 exons of VHL was performed for all the DNA using PCR. If no mutation was detected, Southern blot analysis was performed to detect large rearrangements.

      SamplingMethod: peripheral blood leukocytes

    1. PatientID: None

      KindredID: 1

      Case: F, 24Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Third child of healthy unrelated parents; she has two healthy older sisters.

      CasePresentingHPOs: HP:0001511; HP:0001999; HP:0000952; HP:0001943; HP:0001508; HP:0000851; HP:0001250; HP:0002650; HP:0001332; HP:0001263; HP:0006880 (Intrauterine growth retardation, Abnormal facial shape, Jaundice, Hypoglycemia, Failure to thrive, Congenital hypothyroidism, Seizure, Scoliosis, Dystonia, Global developmental delay, Cerebellar hemangioblastoma)

      CaseHPOFreeText: Normally born after 37 weeks pregnancy. During the prenatal period, she showed intrauterine growth retardation of unknown cause. At birth, dysmorphic features were noted (full list in table 1). After birth, she was treated for physiological jaundice and hypoglycemia. In addition, she has problem for failure to thrive and feeding difficulties associated with poor sucking and regurgitation. Furthermore, she was diagnosed with a congenital hypothyroidism in the neonatal screening. At 26 months old, she developed epilepsy. At 7Y, was considered to have Rett syndrome because of stereotypic hand movements since 2 years old, scoliosis and dystonia. Her psychomotor development was severely delayed: she had no ability to move by herself, visual contact, or social interaction. Brain MRI was performed at 1 year old and 6 years old. Both of these showed no abnormal findings. At 16 years old, follow-up MRI unexpectedly demonstrated a solid tumor with peritumoral edema at right cerebellum; diagnosed a cerebellar hemangioblastoma and confirmed through histopathology.

      CaseNotHPOs: HP:0002012 (Abnormality of the abdominal organs)

      CaseNotHPOFreeText: Repeat brain MRI, fundoscopy, abdominal echography and CT, blood and urine testing revealed no other tumors associated with VHL.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: No mutation was detected in MECP2 on chromosome Xq28. At 5 months old, her chromosome analysis of the white blood cells revealed a distal deletion of the short arm of chromosome 3. Genomic DNA from the patient and her parents revealed a de novo 11.0-Mb deletion at 3p26.3-25.3 that included VHL and a paternally inherited 740-kb gain at Xp22.2-22.13, which was predicted to be a benign copy number variation. Unfortunately, since the mutation analysis of VHL was not performed using resected tumor tissues in the present case, “the second hit” could not be confirmed. Thus, the reason remains unclear why a cerebellar hemangioblastoma developed in her.

      MutationType: deletion

      CivicName: 3p26.3-25.3 11Mb del

      MultipleGeneVariants: see VariantEvidence.

    1. Chromosomal analysis confirmed the presence of 384delT of frame-shift mutation in exon 2 of the tumor suppressor, E3 ubiquitin protein ligase, vHL gene.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Chromosomal analysis not specified further

      SamplingMethod: N/A - Not stated

    1. 2 complete deletions

      27 index patients suspected of having VHL disease from unrelated Chinese families and their relatives were studied. The nucleotide were numbered according to the sequence numbering by Latif et al, 1993 and this was converted to NM_000551.3. The paper did not differentiate between a pancreatic cysts and tumor and presented these together as a 'pancreatic lesion'. The paper summarized the phenotypes of the families together. Family 21 and 25 were each one member (proband) each and were found with complete VHL deletions. Proband 21 had only hemangioblastoma and genetic testing of her parents confirmed a de novo mutation. Proband 25 was found with hemangioblastoma, retinal angioma and pancreatic lesion. Proband 25 had no family history of VHL but parents were not available for genetic testing so de novo mutation cannot be assessed. ACMG PVS1

    1. The second daughter (IV‐5) is the index case

      Case1: 14 month, female

      DiseaseAssertion: dilated cardiomyopathy

      FamilyInfo:The three siblings' cases were born to consanguineous parents. They had DCM and died from decompensated heart failure around the age of 12 months

      ParentalTesting: Sanger Sequencing determined the parents carried the variant at the heterozygous state (Figure 1)

      CasePresentingHPOs: HP:0002094, HP:0002099, HP:0002098, HP:0002090,

      CaseHPOFreeText:productive cough, and whining, wheezing, mitral and tricuspid regurgitation

      CaseNotHPOs: NR

      CaseNotHPOFreeText:no sign of ischemia,

      CasePreviousTesting: cardiac ultrasound

      Genotyping Method: sanger sequencing

      FunctionalAnalysis: NR

      Variant: TNNI3 (NM_000363.5): c.204delG;p.(Arg69AlafsTer8)

      ClinVar: 179447

      gnomAD: not found

    1. 12-year-old boy

      Case1: Male, 12, China

      DiseaseAssertion: Hypertrophic cardiomyopathy

      FamilyInfo: parents where not consanguineous, both carried variants.

      ParentalTesting: sanger sequencing showed c.1789C>T variant in patients paternal grandmother, and c.3033delG from maternal grandmother

      CasePresentingHPOs: HP:0001962 HP:0002094 HP:0001279 HP:0001712 “Palpitations, Dyspnea, Syncope, Left ventricular hypertrophy”

      CaseHPOFreeText: symptoms lasted about a year, ECG showed sinus arrhythmia, high left ventricle voltage

      CaseNotHPOs: “the patient had no skeletal muscle disease or mental retardation. The diagnosis of glycogen storage disease was also excluded.”

      CaseNotHPOFreeText: no other family members diagnosed with heart disease

      CasePreviousTesting: diagnosed 3 months before presentation with HCM, no prior genetic testing, but there was echocardiogram and ecg testing.

      Genotyping Method: Sanger and NGS

      FunctionalAnalysis: no functional analysis preformed

      Variant: c.1789C>T (p.Arg597Trp), c.3033delG (p.Gln1012Serfs*8)

      ClinVar: NM_000256.3(MYBPC3):c.1789C>T (p.Arg597Trp),

      CAID: no results

      gnomAD: no results

      AdditionalInfo: treated with metoprolol, at 3 moth follow up lvot decreased

    1. All registrants provided 10 ml EDTA-anticoagulated blood for molecular genetic analyses. The analyses comprised testing of all exons including the splice sites of the VHL (RefSeq:NM_000551.2) and MEN1 (RefSeq:NM_130803.1) genes for germline mutations. DNA extraction, primers, PCR conditions, and sequencing methods followed published protocols of international standards (Lemmens et al. 1997, Franke et al. 2009). The primers are available on request. Of note, analyses also included screening for large deletions or rearrangements of the VHL and MEN1 genes. For screening for intragenic mutations, we used the PCR-based denaturing HPLC. For detection of large deletions/rearrangements, we used two commercially available kits for multiplex ligation-dependent probe amplification, the SALSA MLPA KIT P016 VHL, and the SALSA MLPA KIT P017-B1 MEN1 respectively (MLPA, MRC Holland, Amsterdam, The Netherlands). The primers are available on request. All analyses for the VHL gene and the analyses for intragenic mutations in the MEN1 gene have been performed in Freiburg. The analyses for the large deletions and rearrangements of the MEN1 gene have been performed in Madrid.

      ArticleReferenceSequence: NM_000551.2

      GenotypingMethod: PCR; and the SALSA MLPA KIT P016 VHL for detection of large deletions/rearrangements.

      SamplingMethod: blood (EDTA-anticoagulated blood).

    1. Genomic DNA samples were extracted from 10 mL of ethylenediaminetetraacetic acid (EDTA)-treated peripheral blood samples using the Nucleosopin Blood Mini Kit (MACHEREY–NAGEL GmbH & Co. KG, Düren, Germany) according to the manufacturer’s instructions. The following seven genes were analysed: MAX ({"type":"entrez-nucleotide","attrs":{"text":"NM_002382.5","term_id":"1653960896","term_text":"NM_002382.5"}}NM_002382.5), SDHB ({"type":"entrez-nucleotide","attrs":{"text":"NM_003000.3","term_id":"1732746310","term_text":"NM_003000.3"}}NM_003000.3), SDHC ({"type":"entrez-nucleotide","attrs":{"text":"NM_003001.5","term_id":"1779948875","term_text":"NM_003001.5"}}NM_003001.5), SDHD ({"type":"entrez-nucleotide","attrs":{"text":"NM_003002.4","term_id":"1519245278","term_text":"NM_003002.4"}}NM_003002.4), TMEM127 ({"type":"entrez-nucleotide","attrs":{"text":"NM_017849.4","term_id":"1777425445","term_text":"NM_017849.4"}}NM_017849.4), VHL ({"type":"entrez-nucleotide","attrs":{"text":"NM_000551.3","term_id":"319655736","term_text":"NM_000551.3"}}NM_000551.3), and exons 10, 11 and 13–16 of the RET ({"type":"entrez-nucleotide","attrs":{"text":"NM_020630.4","term_id":"126273513","term_text":"NM_020630.4"}}NM_020630.4) proto-oncogene. A priority order was used for genetic analysis according to previous recommendations [5,6]. For instance, VHL and RET genes were analysed with priority for bilateral PCC, SDHB gene for retroperitoneum PGL or metastatic PCC/PGL, and SDHD gene for head and neck PGL. When a pathogenic variant was found in one of these genes, no further testing was performed in the remaining genes. After performing PCR using gel electrophoresis for each primer pair, Sanger sequencing was outsourced to a commercial service provider (Eurofins Genomics, Ota-ku, Tokyo, Japan) to detect variants, and the results were analysed at our department. The primers used for the PCR amplification are listed in Table S5. When no P/LP variant was found by the Sanger sequencing, all exons of the SDHB, SDHC, and SDHD gene were reanalysed using multiplex ligation-dependent probe amplification (MLPA) to examine copy number variation. The MLPA assay was carried out by a commercial service provider (FALCO Biosystems Ltd., Kumiyama, Kyoto, Japan). The sequence results were analysed using Sequence Scanner Software v2.0 (Thermo Fisher Scientific, Waltham, MA, USA) and CLC Sequence Viewer 8.0 software (QIAGEN, Aarhus C, Denmark).

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: Seven genes were analysed (MAX, SDHB, SDHC, SDHD, TMEM127, VHL, and exons 10, 11 and 13–16 of RET. After PCR for each primer pair, Sanger sequencing was outsourced to detect variants, followed by the analysis of the results internally.

      SamplingMethod: peripheral blood

    1. Genetic testingThe proband’s maternal aunt, who lived a significant distance away had genetic testing; no pathogenic mutation was detected in either BRCA 1 or BRCA2 genes. A variant identified in the VHL gene c.74C>T(p.Pro25Leu) was thought to be pathogenic at the time, and the extended family was advised that family testing was available. On this basis, our proband was offered testing for the family-specific variant. The DNA sample obtained from the patient was independently amplified and sequenced in opposite directions from exon 1 of the VHL gene. Analysis of this exon has not detected the c.74C>T variant. Soon thereafter, this variant was revised as unlikely to be pathogenic.Subsequently, his aunt had next-generation sequencing (NGS) for MAX, RET, SDHAF2, SDHB, SDHC, SDHD, TMEM127 and multiplex ligation-dependent probe amplification (MLPA) for VHL, SDHA, MAX, SDHB, SDHC and SDHC. No pathogenic mutation was detected.Our proband was offered MLPA and NGS for VHL and TP53. Complete sequence screening of all coding exons and intron–exon boundaries of the TP53 gene did not reveal the presence of a pathogenic variant. In MLPA, none of the tested exons showed a significant deviation from the normal range of the tested population, and duplicate tests were concordantly indicating a normal copy number.Following his disease progression and with the recent diagnosis of papillary thyroid cancer as well as papillary urothelial cancer and the availability of broader panel testing, testing of72 cancer predisposition genes was offered for him. The heterozygous pathogenic variant, CHEK21100delC was found.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: next-generation sequencing (NGS) for MAX, RET, SDHAF2, SDHB, SDHC, SDHD, TMEM127 and multiplex ligation-dependent probe amplification (MLPA) for VHL, SDHA, MAX, SDHB, SDHC and SDHC.

      SamplingMethod: N/A

    1. VHL-25c.1 − ?_463 + ?Del ex 1 + 2[11]noA2Multiple–+––Renal

      PatientID: VHL-25

      KindredID: 25

      Case: Sex Unknown, Age Unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL.

      CohortInfo: Forty-three index cases were referred to the Service of Medical Genetics, Genova, for germline mutation analysis in the VHL gene between 1995 and 2008.

      CasePresentingHPOs: HP:0010797; HP:0000107; HP:0001732 (Hemangioblastoma, Renal cyst, Abnormality of the pancreas)

      CaseHPOFreeText: Multiple CNS hemangioblastomas. Clinical classification: A2.

      CaseNotHPOs: HP:0002666; HP:0005584; HP:0009711 (Pheochromocytoma, Renal cell carcinoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-2 Deletion (c.1-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-2 Deletion

      MultipleGeneVariants: N/A

    1. Patients and Methods The patients were recruited through the French VHL database, which was created in 1992. During the period of the study (1996–1999), 610 patients with VHL were registered in the database. Detailed systemic follow-up data were available for 211 patients from 111 distinct pedigrees. The patients were divided into two groups: one group of 103 (48.8%) patients from 60 pedigrees with ocular involvement and a second group of 108 (51.2%) from 66 pedigrees with no ophthalmic manifestation reported on the last follow-up. Fifteen families were involved in both groups.  To be included, the patient had to meet the diagnostic criteria for VHL defined by the presence of two major manifestations, including at least one CNS or retinal hemangioblastoma, one major manifestation and a positive family history, or an isolated clinical feature with mutation in the VHL gene. 6 Patients with solitary retinal hemangioblastoma and no mutation detected in the VHL gene were excluded from the study. 

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: To detect the presence of a mutation, PCR and single-strand conformation polymorphism (SSCP) were used systematically.

      SamplingMethod: Blood

    1. Genomic DNA was extracted from whole blood samples for genetic testing of SDHB, SDHC, SDHD, and VHL. Polymerase chain reaction–based bidirectional sequencing was performed by Mayo Medical Laboratories, Rochester, MN, or by the Division of Molecular Diagnostics, University of Pittsburgh Medical Center, as previously described [13]. Large deletions were detected using multiplex ligation-dependent probe amplification and Luminex Flex-Map Technologies [14]. None of the patients had clinical presentations suggestive of RET or NF1 mutations. Testing for MAX, TMEM127, SDHA, and SDHAF2 genes was not performed.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: PCR–based bidirectional sequencing was performed. Large deletions were detected using multiplex ligation-dependent probe amplification (MLPA) and Luminex Flex-Map Technologies.

      SamplingMethod: whole blood

    1. 13 (17%) had large deletions,

      PatientID: 38

      KindredID: 38

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0006770; HP:0100634; HP:0030405 (hemangioblastoma; clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711; HP:0030421 (retinal capillary hemangioma, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867 (Family 4 - mother - see here for more info)

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: Deletion of Exon 2

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 deletion

      MultipleGeneVariants: N/A

    2. 13 (17%) had large deletions,

      PatientID: 67

      KindredID: 67

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711 (hemangioblastoma; retinal capillary hemangioma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0006770; HP:0100634; HP:0030405; HP:0030421 (clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867 (Likely family 3 - grandmother - see here for more info)

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: Deletion of Exon 2

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 deletion

      MultipleGeneVariants: N/A

    3. 13 (17%) had large deletions,

      PatientID: 74

      KindredID: 74 *

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: * 3 patients (IDs: 74, 75, 76) were previously reported in Aronoff et al, 2018 as family 13.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0006770; HP:0100634; HP:0030405; HP:0009711; HP:0030421 (clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm, retinal capillary hemangioma, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: complete deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. DIP–22–22Renal cysts, pancreatic cyst, and accessory spleen1

      PatientID: IP (Proband)

      KindredID: D

      Case: F, 22Y0M, Hungarian

      DiseaseAssertion: VHL

      FamilyInfo: Index patient was a young woman who presented with cerebellar hemangioblastoma, multiple renal cysts, retinal detachment with vitreous hemorrhage, pancreatic cyst, spinal cord hemangiomas, and recurrence of the cerebellar lesion. Family members were not available for clinical and genetic screening, but family history revealed that the patient's father died of metastatic renal cell carcinoma.

      CasePresentingHPOs: HP:0006880; HP:0005562; HP:0001737; HP:0000541; HP:0007902; HP:0009713 (Cerebellar hemangioblastoma, Multiple renal cysts, Pancreatic cysts, Retinal detachment, Vitreous hemorrhage, Spinal hemangioblastoma)

      CaseHPOFreeText: Patient underwent surgery for cerebellar hemangioblastoma at the age of 22 years. Multiple renal cysts and retinal detachment with vitreous hemorrhage were also observed. At the age of 26 years, pancreatic cyst, spinal cord hemangiomas, and recurrence of the cerebellar lesion were found. Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0002666; HP:0009711; HP:0005584 (Pheochromocytoma, Retinal capillary hemangioma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 Deletion (c.341-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    1. Gene copy number analysis based on quantitative PCR revealed partial deletion of Exon 1 in VHL gene in the peripheral blood, brainstem hemangioblastoma and meningiomas.

      ArticleReferenceSequence: Not specified- Assumption: Nucleotide change is not specified in the paper, nor protein coding change. Reported based on VHL reference sequence NM_000551.3

      GenotypingMethod: Gene copy number analysis based on quantitative PCR

      SamplingMethod: Peripheral blood and tumor tissue

    1. The coding exons and flanking regions of genes implicated in PHEO/PGL (MYC associated factor X (MAX; {"type":"entrez-nucleotide","attrs":{"text":"NM_002382.3","term_id":"21704260","term_text":"NM_002382.3"}}NM_002382.3), rearranged during transfection tyrosine kinase receptor gene (RET; {"type":"entrez-nucleotide","attrs":{"text":"NM_020975.4","term_id":"126273511","term_text":"NM_020975.4"}}NM_020975.4), succinate dehydrogenase subunit A (SDHA; {"type":"entrez-nucleotide","attrs":{"text":"NM_004168.3","term_id":"661567358","term_text":"NM_004168.3"}}NM_004168.3), succinate dehydrogenase complex assembly factor 2 (SDHAF2; {"type":"entrez-nucleotide","attrs":{"text":"NM_017841.2","term_id":"300795354","term_text":"NM_017841.2"}}NM_017841.2), succinate dehydrogenase subunit B (SDHB; {"type":"entrez-nucleotide","attrs":{"text":"NM_003000.2","term_id":"115387093","term_text":"NM_003000.2"}}NM_003000.2), succinate dehydrogenase subunit C (SDHC; {"type":"entrez-nucleotide","attrs":{"text":"NM_003001.3","term_id":"78711818","term_text":"NM_003001.3"}}NM_003001.3), succinate dehydrogenase subunit D (SDHD; {"type":"entrez-nucleotide","attrs":{"text":"NM_003002.2","term_id":"222352156","term_text":"NM_003002.2"}}NM_003002.2), transmembrane protein 127 (TMEM127; {"type":"entrez-nucleotide","attrs":{"text":"NM_017849.3","term_id":"305682550","term_text":"NM_017849.3"}}NM_017849.3), fumarate hydratase (FH; {"type":"entrez-nucleotide","attrs":{"text":"NM_000143.3","term_id":"299758401","term_text":"NM_000143.3"}}NM_000143.3), neurofibromatosis type I (NF1; {"type":"entrez-nucleotide","attrs":{"text":"NM_001042492.2","term_id":"270132520","term_text":"NM_001042492.2"}}NM_001042492.2), malate dehydrogenase 2 (MDH2; {"type":"entrez-nucleotide","attrs":{"text":"NM_005918.3","term_id":"538919612","term_text":"NM_005918.3"}}NM_005918.3), Endothelial PAS domain protein 1 (EPAS1; exon 9 and 12, {"type":"entrez-nucleotide","attrs":{"text":"NM_001430","term_id":"1519312014","term_text":"NM_001430"}}NM_001430) and von Hippel-Lindau gene (VHL; {"type":"entrez-nucleotide","attrs":{"text":"NM_000551.3","term_id":"319655736","term_text":"NM_000551.3"}}NM_000551.3)) were analyzed using a combination of next-generation sequencing (NGS, Illumina Miseq TSCA Librairies) and multiplex ligand probe assay (MLPA). The allelic variants found by NGS were confirmed using Sanger method. In silico analysis of variants was performed using Polyphen2 (http://genetics.bwh.harvard.edu/pph2/), UMD-predictor® [4], and ALAMUT 2.2.0 (http://www.interactive-biosoftware.com/) software. Blood samples for genomic DNA analysis were taken after written informed consent and patient gave written (signed) informed consent after being given a detailed explanation of the publication. Genetic researches were carried out according to The Code of Ethics of the World Medical Association (Declaration of Helsinki).

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: A combination of next-generation sequencing (NGS, Illumina Miseq TSCA Librairies) and multiplex ligand probe assay (MLPA) analyzed a gene panel. The allelic variants found by NGS were confirmed using Sanger method. In silico analysis of variants was performed using Polyphen2 (http://genetics.bwh.harvard.edu/pph2/), UMD-predictor® [4], and ALAMUT 2.2.0 (http://www.interactive-biosoftware.com/) software.

      SamplingMethod: Blood

    1. Genomic DNA was isolated from peripheral blood lymphocytes of all subjects using the standard phenol-chloroform method (17). VHL was amplified via polymerase chain reaction (PCR). Three pairs of primers were designed to cover all of the exons and splicing junctions of VHL (Table I). The thermocycling conditions of PCR used were as follows: Initial Denaturation at 95°C for 30 sec; followed by 30 cycles of denaturation at 95°C for 30 sec, annealing at 58°C for 30 sec and elongation 72°C for 30 sec; and a final extension at 75°C for 5 min. PCR amplification was performed using an ABI 2720 PCR system (Thermo Fisher Scientific, Inc., Waltham, MA, USA) using a 10 µl mixture containing premixed DNA polymerase (5 µl; Takara Biotechnology Co., Ltd., Dalian, China), primers (2 µl), genomic DNA (1 µl) and double distilled H2O (2 µl). PCR products were detected using 6% polyacrylamide gel electrophoresis with silver staining. Sanger sequencing was performed using an ABI 3100/3130 Genetic Analyzer automated sequencer (Applied Biosystems; Thermo Fisher Scientific, Inc.), according to the manufacturer's protocol. The sequencing results were analyzed using SeqMan 3.0 (DNASTAR, Inc., Madison, WI, USA), and compared with the reference sequences listed in the National Center for Biotechnology Information database (https://www.ncbi.nlm.nih.gov/). Mutation naming followed the nomenclature recommended by the Human Genomic Variation Society (http://www.hgvs.org/).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Sanger sequencing of all VHL exons and splice junctions

      SamplingMethod: peripheral blood

    1. 3.2. Molecular analysisSNP Array Assay: Samples were processed with a formalin-fixed, paraffin-embedded optimized protocol based on the GeneChip Mapping 10 K Xba or 250 K Nsp Assay Kits (Affymetrix, Santa Clara, CA). For quality control, polymerase chain reaction products were analyzed by capillary electrophoresis with the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). All samples passed quality control. The samples were then hybridized on GeneChip Mapping 10 K 2.0 or 250 K Nsp arrays (Affymetrix), for 16 hours at 48°C in a GeneChip 450 hybridization oven (Affymetrix) at 60 rpm. The arrays were washed and stained according to the manufacturer’s genotyping protocol for each array type.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: SNP Array Assay was used for molecular analysis. PCR was also used for analysis.

      SamplingMethod: formalin-fixed, paraffin-embedded tissue samples

    1. large partial deletions encompassing one or 2 vhl gene exons in 6 patients

      PatientID: 5

      KindredID: 5

      Case: 22Y0M, sex unknown, ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0009711 (hemangioblastoma; renal cell carcinoma; retinal capillary hemangioma)

      CaseHPOFreeText: See Table 1&2 for retinal capillary hemangioma information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2-3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Stated in paper as “del ex 2.3”

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    1. Targeted next-generation sequencing (NGS) was performed from 2014 using a library designed to capture all exons from the FH, FLCN, MET, SDHB and VHL genes. Sequencing was performed on a MiSeq (Illumina) to an average depth of at least 100×. Sequencing data (FASTQ files) were analyzed using Sequence Pilot SeqNext software (v4.0 JSI medical systems), where variants were called if the non-reference base frequency was above 25%. The coding sequences of BAP1 and CDKN2B (and FH, FLCN, MET, SDHB and VHL genes up to 2014) were amplified by PCR using primer pairs flanking each exon followed by sequencing on an ABI3730 DNA analyzer (Applied Biosystems). MITF was screened for the E318K variant by TaqMan analysis as recently described [25]. Moreover, genomic DNA was examined for large genomic rearrangements in the FH, FLCN, SDHB, and VHL genes by multiplex ligation-dependent probe amplification (MLPA) analysis using SALSA MLPA kits from MRC-Holland. BAP1, MITF and VHL variants are numbered according to accession number NM_004656.3, NM_000248.3 and NM_000551.3, respectively, following the guidelines from the Human Genome Variation Society (http://www.hgvs.org/varnomen). These techniques are not able to detect large rearrangements.

      ArticleReferenceSequence: NM_000551.3 (Standard)

      GenotypingMethod: Targeted next-generation sequencing (NGS), MLPA, PCR.

      SamplingMethod: peripheral blood

    1. Patients were identified through the clinical cancer genetics service in the National Cancer Centre Singapore. Before informed consent was provided to obtain blood samples for genetic testing, patients were provided genetic counseling by specialized clinical cancer geneticists. Patients and their families with confirmed VHL mutations were selected for the study and registered in a database.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Not stated. Paper states simply "local patient selection gave blood samples for genetic testing".

      SamplingMethod: blood

    1. All three exons of the VHL gene, all eight exons of the SDHB gene, all six exons of the SDHC gene, all four exons of the SDHD gene and exons 10, 11, and 13 of the RET gene were amplified by polymerase chain reaction (PCR) using the HotStar Taq DNA polymerase (Qiagen, Hilden, Germany). PCR reaction conditions are available upon request. Every amplicon was analyzed by direct sequencing with the ABI3130 sequencing analyzer according to manufacturer recommendations.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: All three exons of the VHL gene, all eight exons of the SDHB gene, all six exons of the SDHC gene, all four exons of the SDHD gene and exons 10, 11, and 13 of the RET gene were amplified by polymerase chain reaction (PCR) using the HotStar Taq DNA polymerase (Qiagen, Hilden, Germany). Every amplicon was analyzed by direct sequencing with the ABI3130 sequencing analyzer.

      SamplingMethod: tumour tissue resection and whole blood leukocytes

    1. his aunt (Patient II‐5) died of a ruptured CH

      PatientID: II-5

      KindredID: 1

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: All three of the patient’s brothers (Patient II-4, II-3, and II-1) and the patient’s nephew (III-3) were clinically diagnosed with VHL disease. Patient II-1 presented with RCCC at age 33 and CH at age 41. He carried the mutation NM_000551.3:c.269A>T. Patient II-4 presented with RCCC at age 53, and carried the same mutation. Patient III-3 presented with CH and carried the same mutation. The patient’s deceased brother (Patient II‐3) died of advanced RCCC and had an undetermined mutation. The patient’s parents (Patient I-1 and I-2) were also deceased from other causes. The patient’s grand-nephew (Patient IV‐1) was healthy and did not carry the mutation.

      CasePresentingHPOs: HP:0006880 (Cerebellar hemangioblastoma)

      CaseHPOFreeText: The patient died of a ruptured cerebellar hemangioblastoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: N/A

      CivicName:N/A

      MultipleGeneVariants: N/A

    1. exon 2 deletion

      PatientID: Daughter (of proband)

      KindredID: 6

      Case: F, age unknown, Chinese

      DiseaseAssertion: asymptomatic

      FamilyInfo: Her parent (proband 6) had the same deletion and presented with VHL disease type 1, and had CNS hemangioblastoma first presenting at age 15Y and RCC at age 22Y and EC (papillary cystadenoma of the epididymis) at 30Y. Her aunt had the same exon 2 deletion and presented with CNS hemangioblastomas at 21Y, and her other aunt had no mutation and was asymptomatic.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: patient was asymptomatic however may have been too young for manifestations to present.

      CaseNotHPOs: HP:0002666; HP:0009715; HP:0005584; HP:0010797 (pheochromocytoma, Papillary cystadenoma of the epididymis, renal cell carcinoma, hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 deletion

      MultipleGeneVariants: N/A

    1. Whole-Exome SequencingA total of 25 participants from 3 families including 9 hemangioblastoma patients who were hospitalized in Guizhou Medical University during 2014–2020,14 immediate and collateral relatives and spouses, and 2 randomly selected healthy volunteers who had no lesions and family histories were investigated. The pedigrees of the 3 families are shown in Figure 1, and the clinical dates are shown in Table 1, Table 2, Table 3. The genomic deoxyribonucleic acid (DNA) samples extracted from peripheral blood of participants were randomly fragmented in the range of 150–250 bp by Covaris technology, and the end repair of DNA was done by adding an A base at the 3′ end of each strand. Adapters were then added to the fragmented DNA followed by amplification using ligation-mediated PCR, purification, and hybridization to the exome array for enrichment while nonhybridized fragments were then washed out. The qualified captured library was then sequenced in paired-end mode using BGISEQ-500 platform. BGISEQ-500 base calling software with default parameters was used to process sequencing-derived raw images

      ArticleReferenceSequence: ex. Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: whole exome sequencing

      SamplingMethod: peripheral blood

    1. A germline truncating TMEM127 mutation, c.532_533dupT; p.Y178LfsX48, hereafter referred to as TMEM127-532dupT, was identified after a targeted, exome-based next generation sequencing screening (Fig.1C). No other pathogenic germline mutation was detected in other 35 pheochromocytoma and/or renal cancer susceptibility genes screened. Furthermore, no somatic mutations were found at high-depth sequencing (average 180x) of the proband’s frozen PHEO using Illumina TruSeq Cancer Panel screening of 42 cancer genes. The TMEM127-532dupT mutation was also detected in germline DNA from one affected sister (Fig.1A, ​,1B)1B) and three other family members, their mother and two brothers, who have no evidence of PHEO or RCC (Fig. 1A).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: targeted, exome-based next-generation sequencing screening

      SamplingMethod: N/A

    1. Read the full text

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: germline DNA was extracted, and PCR products were purified with Microcon 50 (Millipore, Billerica, MA) and sequenced using BigDyeTerminator v1.1 Sequencing Kit (Applied Biosystems, Foster City, CA). After a purification step performed with CentriSep Spin Columns (Princeton Separations, Adelphia, NJ), the products were analyzed on a 310 DNA Analyzer (Applied Biosystems).

      SamplingMethod: peripheral blood

    1. PatientID: 52

      KindredID: 52

      Case: F, 29Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Family history negative for VHL.

      CohortInfo: 26 Korean patients with more than one HAB in the CNS or eye, a single HAB in the CNS or retina plus a visceral manifestation (multiple renal, pancreatic or hepatic cysts, pheochromocytoma and RCC) and positive family history plus any one of the above manifestations.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastomas. Other phenotypes presented but not specified (one or more of: pancreatic cyst or tumor, renal or hepatic cyst). Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0002666; HP:0009711; HP:0005584 (Pheochromocytoma, Retinal capillary hemangioma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 19270817

      SupplementalData: N/A

      Variant: Exon 2-3 Deletion (c.341-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

  2. Oct 2026
    1. PatientID: 38

      KindredID: F01

      Case: M, Age Unknown, Unknown Ethnicity

      DiseaseAssertion: Asymptomatic

      FamilyInfo: A total of 12 members of this family (F01) had a complete deletion of the VHL gene. Five of these patients (16, 18, 21, 33, 43) presented with clinical features of VHL. This family was previously published except for patients 43 and 48 which were newly diagnosed with VHL disease in the current study.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 17537157

      SupplementalData: Figure 2.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of ~250.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. PatientID: 18

      KindredID: F01

      Case: M, Age Unknown, Unknown Ethnicity

      DiseaseAssertion: VHL

      FamilyInfo: A total of 12 members of this family (F01) had a complete deletion of the VHL gene. Five of these patients (16, 18, 21, 33, 43) presented with clinical features of VHL. This family was previously published except for patients 43 and 48 which were newly diagnosed with VHL disease in the current study.

      CasePresentingHPOs: HP:0010797; HP:0001737 (Hemangioblastoma, Pancreatic cysts)

      CaseHPOFreeText: CNS hemangioblastoma and pancreatic cyst.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 17537157

      SupplementalData: Figure 2.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of ~250.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. The second patient, an incidental finding, was practically asymptomatic and had a de novo germline point mutation in the VHL gene (Arg167Trp).

      ArticleReferenceSequence: Not specified- Assumption: Nucleotide change is not specified in the paper, only protein coding change is. cDNA variant was inferred based on protein coding change, and reported based on VHL reference sequence NM_000551.3

      GenotypingMethod: N/A

      SamplingMethod: N/A

    1. PatientID: 29

      KindredID: 19

      Case: F, 37Y0M, Indian

      DiseaseAssertion: VHL

      FamilyInfo: Relevant family history but details are not made available.

      CohortInfo: This retrospective study was conducted at Department of Endocrinology of a tertiary care health centre in Western India. Patients presented to our institute between 2008 and 2016 were included in the study. During the study period a total of 33 patients were suspected to have VHL syndrome based on clinical features among whom 31 patients were found to have mutation in VHL gene. All patients are of Asian Indian descent.

      CasePresentingHPOs: HP:0002666; HP:0009711; HP:0001737; HP:0030405 (Pheochromocytoma, Renal cell carcinoma, Pancreatic cysts, Pancreatic endocrine tumor)

      CaseHPOFreeText: Unilateral pheochromocytoma. Metastasis found at age 37. Cause of death: metastatic PNET.

      CaseNotHPOs: HP:0010797; HP:0002668; HP:0005584 (Hemangioblastoma, Paraganglioma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    1. PatientID: 135

      KindredID: 135

      Case: Sex Unknown, 53Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Positive family history but no details provided.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0001732; HP:0000107 (Hemangioblastoma, Retinal capillary hemangioma, Abnormality of the pancreas, Renal cyst)

      CaseHPOFreeText: CNS and retinal hemangioblastoma, pancreatic cyst or tumor and renal cystic lesion.

      CaseNotHPOs: HP:0002666; HP:0006770 (Pheochromocytoma, Clear cell renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Partial Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Partial deletion)

      MultipleGeneVariants: N/A

    2. PatientID: 396

      KindredID: 396

      Case: Sex Unknown, 29Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history is positive but no details are provided.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma.

      CaseNotHPOs: HP:0002666; HP:0006770; HP:0001732; HP:0000107; HP:0009711 (Pheochromocytoma, Clear cell renal cell carcinoma, Abnormality of the pancreas, Renal cyst, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Exon 2 Deletion (c.341-?_463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant; deletion

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    1. VHL-24c.-678 − ?_340 + ?Del 5′-UTR + ex 1[1]yesA1MultipleBilateral+–+Renal

      PatientID: VHL-24

      KindredID: 24

      Case: Sex Unknown, Age Unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: Family history of VHL. No further details provided.

      CohortInfo: Forty-three index cases were referred to the Service of Medical Genetics, Genova, for germline mutation analysis in the VHL gene between 1995 and 2008.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0005584; HP:0000107; HP:0001732 (Hemangioblastoma, Retinal capillary hemangioma, Renal cell carcinoma, Renal cyst, Abnormality of the pancreas)

      CaseHPOFreeText: Multiple CNS hemangioblastomas, bilateral RCC. Clinical classification: A1.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Large Deletion (c.-678-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of 5’ UTR and exon 1 of VHL: c.-678-?_340+?del

      MutationType: deletion; 5_prime_UTR_variant

      CivicName: Null (c.-678-?_340+?del)

      MultipleGeneVariants: N/A

    1. We studied six patients with VHL disease and their relatives. Loss of heterozygosity (LOH) was determined by five flanking microsatellite polymorphic markers in the VHL locus.

      PatientID: 28

      KindredID: F01

      Case: F, Age Unknown, Taiwanese

      DiseaseAssertion: Asymptomatic

      FamilyInfo: A total of 10 members of this family (F01) had a complete deletion of the VHL gene. Four of these patients (16, 18, 21, 33) presented with clinical features of VHL.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 19288063

      SupplementalData: Figure 1

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of 142.9kb resulted in deletion of the VHL gene.

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    2. We studied six patients with VHL disease and their relatives. Loss of heterozygosity (LOH) was determined by five flanking microsatellite polymorphic markers in the VHL locus.

      PatientID: 5

      KindredID: F03

      Case: M, Age Unknown, Taiwanese

      DiseaseAssertion: VHL

      FamilyInfo: A total of 2 members of this family (F02) had a complete deletion of the VHL gene. One of these patients (3) presented with clinical features of VHL.

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737 (Hemangioblastoma, Renal cell carcinoma, Pancreatic cysts)

      CaseHPOFreeText: Brain hemangioblastoma, pancreatic cyst, renal cell carcinoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Figure 1

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Deletion of 3.3kb resulted in deletion of Exon 3 in the VHL gene.

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: Germline, FANCD2, deletion

    1. For the matched blood and tumor samples, germline DNA (gDNA) was isolated using the DNeasy Blood & Tissue Kit (Qiagen, 69504) according to the manufacturer's instruction. 100 ng of gDNA was sheared with a Covaris E210 system (Covaris, Inc.) to target fragment sizes of 200 bp. We performed library preparation for tumor gDNA and matched germline gDNA using the Accel-NGS 2S DNA Library Kit (Swift Biosciences, Inc.) and target enrichment using the xGen Lockdown Probe kit (IDT, Inc.). The custom xGen Lockdown Probe was synthesized by IDT, Inc. for the exons and parts of introns of 618 genes of interest (Supplementary Table S2). Samples underwent paired-end sequencing on an Illumina Nextseq CN500 platform (Illumina Inc.) with a 150 bp read length and mean coverage of 1000x at a 95% capture rate and 40% dup rate.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: The exons and parts of introns of 618 genes of interest (Supplementary Table S2) underwent paired-end next generation sequencing.

      SamplingMethod: Germline DNA was extracted from whole blood. Matched tumor samples were also collected.

    1. He was diagnosed with bilateral pheochromocytoma. The patient was started on phenoxybenzamine 10 mg twice daily which was titrated up to 60 mg twice daily; propranolol 40 mg twice daily was added once appropriate alpha blockade was achieved. Metyrosine was added prior to surgery. He underwent successful laparoscopic bilateral adrenalectomy, and the histopathologic features were consistent with pheochromocytoma (Figure 2). Staining for synaptophysin, chromogranin A, and S-100 protein were all positive. Subsequent referral for genetic testing and sequencing of the von Hippel-Lindau gene showed a deleterious mutation (R167Q). Additional genetic testing was not performed. No hemangioblastomas were seen on imaging, and he had no significant neurologic or ophthalmic findings. Following surgery, he recovered well and his hypertension has resolved.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Unclear as to how VHL diagnosis was conducted. Authors state: 'referral for genetic testing and sequencing of the von Hippel-Lindau gene showed a deleterious mutation (R167Q)'.

      SamplingMethod: Unclear - N/A

    1. PatientID: 24 (Aunt)

      KindredID: 18

      Case: F, 80Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 11 members of this family tested positive for the c.712C>T/c.499C>T germline variant of the VHL gene. 14 members of this family were assumed to carry this variant due to family history/personal medical history. Members of this family range from asymptomatic to multi-organ involvement (pheochromocytoma, pancreatic and renal cysts/tumors and hemangioblastomas). The family was previously reported in PMID 3942913.

      CasePresentingHPOs: HP:0010797; HP:0002666; HP:0009711 (Hemangioblastoma, Pheochromocytoma, Retinal capillary hemangioma)

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (36Y), pheochromocytoma (36Y) and retinal angioma (22Y).

      CaseNotHPOs: HP:0005584; HP:0000077; HP:0001732 (Renal cell carcinoma, Abnormality of the kidney, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 3942913 (some members of this family are previously reported (phenotypes only) but unable to match patients across papers with confidence)

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.712C>T germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing was done on this patient to confirm this. Being that this familial variant is out of bound with respect to the NM_000551.3 reference sequence, it was concluded that this variant is noted in the Latif et al. (1993) reference and was translated to c.499C>T (NM_000551.3).

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    2. PatientID: 9 (Grandmother)

      KindredID: 13

      Case: F, 67Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 5 members of this family were found to harbour the deletion of one VHL allele. The proband (ID 1), sister (ID 2) and uncle (ID 5) were all asymptomatic. The father (ID 3) presented with CNS hemangioblastoma (34Y).

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (57Y).

      CaseNotHPOs: HP:0002666; HP:0005584; HP:0009711; HP:0000077; HP:0001732 (Pheochromocytoma, Renal cell carcinoma, Retinal capillary hemangioma, Abnormality of the kidney, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Reported as “del one vHL allele”.

      MutationType: deletion

      CivicName: Null (del one VHL allele)

      MultipleGeneVariants: N/A

    1. large partial deletions encompassing one or 2 vhl gene exons in 6 patients

      PatientID: 4

      KindredID: 4

      Case: 29Y0M, sex unknown, ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0030405; HP:0009711 (hemangioblastoma; renal cell carcinoma; pancreatic endocrine tumor; retinal capillary hemangioma)

      CaseHPOFreeText: See Table 1&2 for retinal capillary hemangioma information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2-3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Stated in paper as “del ex 2.3”

      MutationType: exon_loss_variant

      CivicName: Exon 2-3 Deletion

      MultipleGeneVariants: N/A

    1. PatientID: None

      KindredID: 330

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Paper states familial VHL

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    1. Patients & methods: Total 450 cases of histologically and clinically verified ccRCC and 490 controls were included in our study. Genotyping was performed using a TaqMan PCR allelic discrimination method. Kaplan-Meier method of statistical analysis was implemented to analyze the overall patient survival rate.

      ArticleReferenceSequence: Not specified – reference SNPs were used. Further assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: 8 polymorphisms of the VHL-HIF1α pathway genes (including involvement in miRNA binding sites), are as follows: CDCP1 rs6773576, DEC1 rs10982724, TFRC rs406271, MAPK1 rs743409, MAPK1 rs9607241, TSC1 rs10491534, VHL rs1642742, VEGFA rs3025033. Genotyping was performed using TaqMan PCR with a Bio-Rad CFX96 (Bio-Rad, CA USA) instrument.

      SamplingMethod: peripheral blood leukocytes

    1. Exons of VHL were amplified from genomic DNA by polymerase chain reaction. The primer sets for exon amplification were as follows: exon 1, forward 5′-GCGAAGACTACGGAGGTC-3′ and reverse 5′-ATGTGTCCTGCCTCAAGG-3′; exon 2, forward 5′-CCTAGACCTCATGATCCGC-3′ and reverse 5′-TTGGATAACGTGCCTGACATC-3′; and exon 3, forward 5′-GGTAGTTGTTGGCAAAGCCTC-3′ and reverse 5′-GAAACTAAGGAAGGAACCAGTCC-3′ Sanger DNA sequencing was performed. Each exon was identified and confirmed by both forward and reverse directional analyses.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Exons of VHL were amplified from genomic DNA by polymerase chain reaction and Sanger DNA sequencing was performed.

      SamplingMethod: peripheral blood

    1. HIGH GRADE VON HIPPEL-LINDAU SYNDROME PRESENTING WITH BILATERAL PHEOCHROMOCYTOMA IN A CHILD

      ArticleReferenceSequence: Not specified- Assumption: Nucleotide change is not specified in the paper, only protein coding change is. cDNA variant was inferred based on protein coding change, and reported based on VHL reference sequence NM_000551.3

      GenotypingMethod: Genetics testing was unspecified

      SamplingMethod: N/A - not stated

    1. nitial genetic testing resultsThe patient underwent germline testing on DNA isolated from peripheral blood leukocytes with a panel of genes targeted at hereditary renal cell cancer and a hereditary paraganglioma-pheochromocytoma. The patient tested negative for any pathogenic, likely pathogenic, or uncertain DNA sequence or copy number variants in FH, FLCN, MET, MITF, MLH1, MSH2, MSH6, PMS2, PTEN, SDHA, SDHB, SDHC, SDHD, TP53, TSC1, TSC2, MAX, MEN1, NF1, RET, SDHAF2, TMEM127, and VHL. Variant allele threshold for review on the germline panel was 10% or greater VAF.

      ArticleReferenceSequence: NM_000551.3 (Standard)

      GenotypingMethod: panel of genes targeted at hereditary renal cell cancer and a hereditary paraganglioma-pheochromocytoma: FH, FLCN, MET, MITF, MLH1, MSH2, MSH6, PMS2, PTEN, SDHA, SDHB, SDHC, SDHD, TP53, TSC1, TSC2, MAX, MEN1, NF1, RET, SDHAF2, TMEM127, and VHL.

      SamplingMethod: peripheral blood

    1. PatientID: 252

      KindredID: 97

      Case: M, 46Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0001737; HP:0001732; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The patient presented with a CNS hemangioblastoma, retinal angioma, renal cell carcinoma, and multiple pancreatic cysts/tumors at age 46.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 1 Deletion (c.1-?_340+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    2. PatientID: 288

      KindredID: 113

      Case: M, 24Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 288) presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at 23, and a retinal angioma at 24. Their sister (patient 289) presented with a CNS hemangioblastoma, retinal angioma, and renal cell carcinoma at 30.

      CasePresentingHPOs: HP:0010797; HP:0001732; HP:0001737; HP:0005584; HP:0009711 (Hemangioblastoma, Abnormality of the pancreas, Pancreatic cysts, Renal cell carcinoma, Retinal capillary hemangioma)

      CaseHPOFreeText: The proband (patient 288) presented with a CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at 23, and a retinal angioma at 24.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. Mutation Analysis of the VHL GeneGenomic DNA was isolated from samples of venous blood, anti-coagulated in EDTA. DNA-purification was performed using the PuregeneR DNA Isolation Kit (Gentra Systems, Minneapolis, MN) according to the manufacturer’s recommendations. Mutation screening for VHL was performed by DNA sequencing and MLPA46Schouten JP, McElgunn CJ, Waaijer R, et al. Relative quantification of 40 nucleic acid sequences by multiplex ligation-dependent probe amplification. Nucleic Acids Res 2002;30:e57 [Crossref], [PubMed], [Web of Science ®], [Google Scholar] or Southern blot analysis.47Richards FM, Crossey PA, Phipps ME, et al. Detailed mapping of germline deletions of the von Hippel-Lindau disease tumor suppressor gene. Hum Mol Genet 1994;3:595–598 [Google Scholar] DNA sequencing of all three exons was performed on PCR products purified with ExoSAP-IT (USB, Cleveland, OH). Sequence reactions were carried out using the ABI Prism Big Dye Terminator Cycle Sequencing kit (Applied Biosystems, Foster City, CA), and analyzed with the ABI Prism 3100xl Genetic Analyzer (Applied Biosystems), according to the manufacturer’s protocol. MLPA was used to detect deletions/duplications of one or more exons, and was performed as described by Meuller and co-authors.48Meuller J, Kanter-Smoler G, Nygren AOH, et al. Identification of genomic deletions of the APC gene in familial adenomatous polyposis by two independent quantitative techniques. Genetic Testing 2004;8:248–256 [Google Scholar] MLPA VHL probe mix, SALSA MLPA P016 version C2 was used. All MLPA analysis were carried out in duplicate and normalized against two different control individuals. All mutations described in this study were verified in a second independent analysis using, as far as possible, an alternative mutation-detection technique. The reference sequence used for the VHL gene was NM_000551.3.

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: performed by DNA sequencing and MLPA46 or Southern blot analysis.47 DNA sequencing of all three exons was performed on PCR products purified with ExoSAP-IT (USB, Cleveland, OH). MLPA was used to detect deletions/duplications of one or more exons.

      SamplingMethod: venous blood (anti-coagulated in EDTA)

    1. P 22 25 F ? ? ? ? - - - Exon 3 del – a, distal b

      PatientID: 22

      KindredID: P

      Case: F, 25Y0M, Indian

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0001737; HP:0009711; HP:0010797 (Pancreatic cysts, Retinal capillary hemangioma, Hemangioblastoma)

      CaseHPOFreeText: Multi-cystic pancreatic lesions, retinal angioma and CNS hemangioblastoma.

      CaseNotHPOs: HP:0030393; HP:0002666; HP:0005584 (Endolymphatic sac tumor, Pheochromocytoma, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 16

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0000107; HP:0010797; HP:0009713; HP:0001737 (Renal cyst, Hemangioblastoma, Spinal hemangioblastoma, Pancreatic cysts)

      GroupHPOFreeText: # of affected individuals: Renal cyst (1), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (1), Pancreatic cysts (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 2 Deletion (c.341-?-463+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A

    2. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 32

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0000107; HP:0009711; HP:0010797; HP:0009713; HP:0001737 (Renal cyst, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma, Pancreatic cysts)

      GroupHPOFreeText: # of affected individuals: Renal cyst (1), Retinal capillary hemangioma (1), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (1), Pancreatic cysts/single cyst (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 3 Deletion (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. Genomic DNA was isolated from peripheral blood by using a blood DNA extraction kit (Tiangene).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Telomere length measurement by Southern blot analysis after genomic DNA was isolated by using a blood DNA extraction kit (Tiangene)

      SamplingMethod: peripheral blood

    1. Multiplex ligation-dependent probe amplification (MLPA) analysis of VHL exons 1-3. Signal intensity reveals only a single copy of VHL exon 2 and 3 in a patient with VHL due to deletion of VHL exon 2 and 3 (A) and only a single copy of each VHL exon in a patient with VHL due to deletion of whole VHL gene deletion (B) when compared to a healthy control (C).

      PatientID: 10

      KindredID: 10

      Case: F, 44Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Patient had a positive family history: Her father was died of RCC (no mutation availible), and her younger sister presented with medullary HB at the age of 37 and multiple RCC in both kidneys at the age of 38, harbored the same exon deletion

      CasePresentingHPOs: HP:0009713; HP:0001737; HP:0000107 (spinal hemangioblastoma, pancreatic cysts, renal cyst)

      CaseHPOFreeText: patient had CNS hemangioblastoma (of multiple spinal hemangioblastomas), and multiple cysts in pancreas and both kidneys were identified by abdomen-pelvis CT.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database) [Refer to table 2].

      SupplementalData: N/A

      Variant: Exon 1-3 deletion (c.1-?_642+?del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: N/A

    1. P12F6M2410ynOU20/200nn20/20nnn

      PatientID: 12

      KindredID: 6

      Case: M, 12Y0M, Ethnicity Unknown

      DiseaseAssertion: Hemangioblastom

      FamilyInfo: A family pedigree is provided in figure 1. The patient’s father carried the same mutation as patient 12, but the father’s occurred de novo, as neither of the father’s parents carried the mutation. The patient’s father had cerebellar, retinal and bulbar hemangioblastomas, and retinal detachment. The patient’s 14-year-old brother (patient 11) was asymptomatic.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: Patient had a CNS hemangioblastoma.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: Patient did not have Retinal capillary hemangiomas.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.341+1_341–1(463*1_?)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: delins

      CivicName: Null (c.341+1_341–1)

      MultipleGeneVariants: N/A

    1. 13 (17%) had large deletions,

      PatientID: 76

      KindredID: 76 *

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL (asymptomatic)

      FamilyInfo: * 3 patients (IDs: 74, 75, 76) were previously reported in Aronoff et al, 2018 as family 13.

      CasePresentingHPOs: None

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0006770; HP:0100634; HP:0030405; HP:0009711; HP:0030421 (hemangioblastoma; clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm, retinal capillary hemangioma, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: complete deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. PatientID: 3194

      KindredID: 229

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Severe renal disease (any solid lesion before 25 years of age, five or more solid lesions within one or two kidneys, or metastasis of renal cell carcinoma). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: Rearrangement

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: rearrangement_region

      CivicName: Rearrangement

      MultipleGeneVariants: N/A

    1.  II1(Ca01)+−−−−

      PatientID: II1(Ca01)

      KindredID: C

      Case: F, 37Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s father (I-2) presented with hemangioblastoma and possessed the same exon 2 deletion. The patient’s two siblings also possessed the deletion. The sister (II-3) had retinoblastoma, pancreatic cyst and pheochromocytoma, while the other sibling (II-5) had hemangioblastoma, pancreatic cyst, and clear cell renal carcinoma. The patient and her two siblings each had a child and all possessed the same deletion, but did not exhibit phenotypes (Please see Figure 1. Family C matches with Pedigree B).

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: Patient presented with a CNS hemangioblastoma and had surgery one time.

      CaseNotHPOs: HP:0001737; HP:0006770; HP:0002666; HP:0009919 (Pancreatic cysts; Clear cell renal cell carcinoma, pheochromocytoma, retinoblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: large fragment deletion in exon 2

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as GRCh37 chr3:10188300ATATCACACTGCCA>T in paper

      MutationType: minus_2_frameshift_variant; deletion

      CivicName: Exon 2 (deletion)

      MultipleGeneVariants: N/A

    2. I2 (Cd01)+−−−−Male (81)0

      PatientID: I2(Cd01)

      KindredID: C

      Case: M, 81Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: All the patient’s 3 children possess the same exon 2 deletion. One daughter (II-1) presented with a CNS hemangioblastoma, the other daughter (II-3) had retinoblastoma, pancreatic cyst and pheochromocytoma, the other child (II-5) had hemangioblastoma, pancreatic cyst, and clear cell renal carcinoma. Each of the three children of the patient had a child each. All three grandchildren possessed the same deletion, but did not exhibit phenotypes (Please see Figure 1. Family C matches with Pedigree B).

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: Patient presented with a CNS hemangioblastoma.

      CaseNotHPOs: HP:0001737; HP:0006770; HP:0002666; HP:0009919 (Pancreatic cysts; Clear cell renal cell carcinoma, pheochromocytoma, retinoblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: large fragment deletion in exon 2

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as GRCh37 chr3:10188300ATATCACACTGCCA>T in paper

      MutationType: minus_2_frameshift_variant; deletion

      CivicName: Exon 2 (deletion)

      MultipleGeneVariants: N/A

    1. MethodsStudy subjectsParaffin-embedded normal and tumor tissue samples from RCC patients were provided by the Tumor Tissue Bank of the Koo Foundation Sun Yat-Sen Cancer Center, which is funded by the National Science and Technology Program for Pharmaceuticals and Biotechnology (#NSC89-2323-B-368-001). The control group consisted of 616 unrelated individuals and has been described in our previous report [21]. DNA sample collection for the VHL SNP study protocol was approved by the Institutional Review Board of Chung Shan Medical University Hospital and informed consent was obtained from each subject.Preparation of Genomic DNAThe tissues were deparaffinized using standard xylene-deparaffin procedure. Genomic DNA was isolated from normal and tumor tissues using QIAamp DNA kit (Qiagen). The concentration of nucleic acids was estimated by GeneQuant II RNA/DNA calculator (Amersham Pharmacia Biotech). Each genomic DNA sample was adjusted to 100 ng/ml and served as a template for subsequent analyses.Polymerase chain reaction (PCR)VHL rs779805A > G and rs1642742A > G were detected on polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) assays according to the methods described by Gail et al. and Payne et al. [22, 23]. Slight modifications were made in the PCR primers for rs779805 and rs1642742 as follows: rs779805-F, 5′-AGCCTCGCCTCCGTTACCAC-3′; rs779805-R, 5′-GTAGAGGATGGAACGCGCT-3′; rs1642742-F, 5′-CTGCCCATTAGAGAAGTATTT-3′; rs1642742-R, 5′-AATTCCCACTGAATTACGTATA-3′. PCR fragments were amplified in a Perkin-Elmer 2400 DNA thermal cycler in a final volume of 15 to 30 µl that contained one-fold Qiagen PCR buffer [Tris–HCl, KCl, (NH4)2SO4, 15 mM MgCl2; pH 8.7 at 20°C], one-fold Q-solution, 0.015 units/µl Taq DNA polymerase supplied from Taq DNA polymerase kit (Qiagen), 500 nM for each primer, 200 mM dGTP, dATP, dCTP and dTTP (Promega) and 300 ng/µl template. PCR conditions included initial denaturation for 5 min at 95°C, followed by 35 cycles consisting of 1 min at 95°C, 1 min at 60°C for rs779805 or 50°C for rs1642742, and 2 min at 72°C, with final extension for 10 min at 72°C.Digestion of restriction enzymeAn aliquot of 10 µl of PCR product was digested with 2.5 units BsaJ I (New England Biolabs) for rs779805 or 2.5 units Acc I (New England Biolabs) for rs1642742 in a total volume of 20 µl that contained one-fold NEBuffer 2 or NEBuffer 4. The samples were digested at 60°C for rs779805 or 37°C for rs1642742 for 4 hrs followed by heat inactivation of the restriction enzyme at 80°C for 20 min. After digestion, the products were separated onto 3% agarose gels. To avoid genotyping errors, analysis was repeated at least twice for each sample. Portions of the PCR products were sent for direct sequencing and the data were consistent with the genotyping.Direct sequencingThe A/G polymorphisms at nucleotides 19 (rs779805) and 1149 (rs1642742) in the VHL gene were analyzed by PCR amplification using published primers and experimental protocols [8, 20, 24]. The PCR products were purified using QIAquick PCR Purification kits (Qiagen). Then, the purified PCR products were sequenced by the cycle-sequencing method with fluorescently labeled dideoxy chain terminators from ABI Prism kit (Applied Biosystems) in an ABI Model 377 automated DNA sequencer. The sequencing primers were the same as those for the preceding PCRs. The nucleotide sequence was confirmed on both strands.Statistical analysisStandard normal deviate (z) test or chi-square test was used to compare the genotype and allelic frequencies between the control and patient groups. p values of less than 0.05 were considered statistically significant and p values of less than 0.01 were considered highly significant.Go to:

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: VHL rs779805A>G and rs1642742A>G were detected on polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) assays according to previous methods. The PCR products were purified using QIAquick PCR Purification kits (Qiagen).

      SamplingMethod: Paraffin-embedded normal and tumor tissues

    1. Case 1Nine years old, Twin 1 presented with no audiovestibular symptoms. Peripheral hearing assessment and screening MRI of brain/spine were normal. Vestibular assessment highlighted an abnormal cVEMP showing a left-sided weakness (42% asymmetry, Figure 2).

      PatientID: N/A (Case 1)

      KindredID: 1

      Case: Sex Unknown, 9Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s twin and 16Y0M sibling possessed the same VHL variant and had abnormal vestibular assessments.

      CasePresentingHPOs: HP:0001756 (Vestibular hypofunction)

      CaseHPOFreeText: Following a genetic VHL diagnosis, patient presented with no audiovestibular symptoms. Vestibular assessment highlighted an abnormal cVEMP showing a left-sided weakness.

      CaseNotHPOs: HP:0009713; HP:0006880 (spinal hemangioblastoma; cerebellar hemangioblastoma)

      CaseNotHPOFreeText: peripheral hearing assessment and screening MRI of brain/spine were normal.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-3 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: N/A

    1. Family 16+Exon 1 DeletionNo118–3131––

      PatientID: None

      KindredID: 16

      Case: Sex Unknown, 31Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The patient's father had a hemangioblastoma of the central nervous system at age 45. He was deceased before diagnosis could occur. The patient's sister, daughter, and nephew were all confirmed to have the same genetic mutation but were asymptomatic.

      CasePresentingHPOs: HP:0010797, HP:0005584, HP:0001732 (hemangioblastoma, renal cell carcinoma, abnormality of the pancreas)

      CaseHPOFreeText: The patient presented with hemangioblastoma at age 18. Later at age 31, he/she presented with renal cell carcinoma and pancreatic cysts or tumours.

      CaseNotHPOs: HP:0009711, HP:0002666, HP:0009715 (retinal capillary hemangioma, pheochromocytoma)

      CaseNotHPOFreeText: The patient did not have epididymal or ovarian cystadenoma.

      CasePreviousTesting: N/A

      PreviouslyPublished:29330336

      Variant: Exon 1 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    1. 10 Complete deletion VHL gene deletion 1 2

      GroupID: 10

      DiseaseAssertion: VHL

      Group size: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      Group Info: Retrospective analysis of a longitudinal cohort of 21 VHL germline mutation carriers and retinal haemangioblastomas. All patients were categorized in two genotypic categories: missense mutations and truncating mutations. From this family, 3 individuals were suspected of VHL disease. 1/3 individuals developed RH, while 2/3 did not.

      GroupPresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      GroupHPOFreeText: One patient presented with retinal capillary hemangioma.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1

      Variant: Complete VHL Deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Deletion

      MultipleGeneVariants: N/A

    1. All patients with pheochromocytoma and without previously recognized monogenetic etiology were offered genetic screening in the five genes included for the systematic genetic screening program in 2006–2013. VHL, RET, SDHB, SDHC, and SDHD were analyzed with sequencing of all coding regions and subsequently analyzed for deletions and duplications.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: screened patients for germline mutations, further info not provided.

      SamplingMethod: N/A

    1. PatientID: 17

      KindredID: 17

      Case: M, 18Y0M, Ethnicity Unknown

      DiseaseAssertion: Adrenal pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: The patient was found to have multiple benign tumours 2 cm in size in her adrenal gland.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHC/SDHB/SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 Loss

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: The patient had LOH of SDHC as indicated by Table 1.

      MutationType: exon_loss_variant

      CivicName: Exon 2 Deletion

      MultipleGeneVariants: N/A