Genomic and clinical insights into MYBPC3-related hypertrophic cardiomyopathy in Ecuadorian patients: implications for sudden cardiac death risk
PMID: 41647802
Gene: MYBPC3
HGNC ID: 7551
Genomic and clinical insights into MYBPC3-related hypertrophic cardiomyopathy in Ecuadorian patients: implications for sudden cardiac death risk
PMID: 41647802
Gene: MYBPC3
HGNC ID: 7551
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
Family M29
Case6: 48 year old male
DiseaseAssertion: Carried the MYBPC3 E619K mutation
FamilyInfo:Three unaffected children were examined (IV:1, IV:2 and IV:3), all with normal echocardiography without signs of hypertrophy or dilatation. Both affected individuals as well as a 26-year-old unaffected daughter (M29, IV:3) carried the MYBPC3 E619K mutation
ParentalTesting:NR
CasePresentingHPOs: HP:0034307, HP:0012666, HP:0011713, HP:0001635
CaseHPOFreeText: Onset of symptoms in their third decade; the index case required heart transplantation 3 years after the onset of symptoms. Has onset at the age of 37. Has left ventricular end diastolic diameter (in mm and indexed by body surface area (cm/m2)) with the value of 79 mm and 3.2 cm/m2. They have a 20% of left ventricular ejection fraction. ECG as left bundle branch block. Clinical status as DCM/ congestive heart failure. CAG as normal.
CaseNotHPOs:NR
CaseNotHPOFreeText:NR
CasePreviousTesting:NR
Genotyping Method:Genetically screened, also using GenBank with PCR by amplifying the coding region
FunctionalAnalysis:NR
Variant: NM_000256.3:c.1855G>A
ClinVar:161303
CAID:CA011336
gnomAD: gnomAD v2: 11:47362731 C / T gnomAD v3: 11:47341180 C / T gnomAD v4: chr11-47341180-C-T
AdditionalInfo:NR
nonsense mutations (6/16)
PatientID: 11
KindredID: 11
Case: 30Y0M, Sex Unknown, Argentinian
DiseaseAssertion: VHL
FamilyInfo: No family history
CasePresentingHPOs: HP:0010797; HP:0009711; HP:0000107; HP:0001737 (hemangioblastoma; retinal capillary hemangioma; renal cyst; pancreatic cysts)
CaseHPOFreeText: Aged 30Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. CNS angiomas, retinal angiomas, renal cysts and pancreatic cysts all diagnosed at 30Y (See Table 1 & 2).
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.W88* (c.263G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 182978 https://www.ncbi.nlm.nih.gov/clinvar/variation/182978/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: stop_gained
CivicName: W88* (c.263G>A)
MultipleGeneVariants: N/A
one nonsense VHL mutation was detected in a young patient with a solitary central nervous system hemangioblastoma without familial history.
PatientID: 22
KindredID: 22
Case: 13Y0M, Sex Unknown, Argentinian
DiseaseAssertion: hemangioblastoma
FamilyInfo: No family history
CasePresentingHPOs: HP:0010797 (hemangioblastoma)
CaseHPOFreeText: Aged 13Y at diagnosis (genetic testing); does not fulfil type 1 VHL clinical diagnosis. Solitary CNS angiomas diagnosed at 13Y (See Table 1 & 2).
CaseNotHPOs: N/A
CaseNotHPOFreeText: did not develop other manifestations of the disease during a 5- year follow-up.
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.W88* (c.264G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 936684 https://www.ncbi.nlm.nih.gov/clinvar/variation/936684/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: stop_gained
CivicName: W88* (c.264G>A)
MultipleGeneVariants: N/A
The other SDHA variant was identified in a patient with a VHL mutation and PA (patient 21)
PatientID: 21
KindredID: 12
Case: F, 27Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CohortInfo: Thirty-nine cases of sporadic or familial pheo/PGL and pituitary adenomas were investigated.
CasePresentingHPOs: HP:0002893; HP:0002666 (Pituitary adenoma, Pheochromocytoma)
CaseHPOFreeText: Pituitary adenoma presented at age 27. Pheochromocytoma age of presentation unknown.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: MAX/RET/TMEM127/SDHA/SDHB/SDHC/SDHD/SDHAF2
PreviouslyPublished: N/A
SupplementalData: Table 1, Supplementary Table 6
Variant: p.D197N (c.589G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA351756524, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA351756524
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: D197N (c.589G>A)
MultipleGeneVariants: Germline, SDHA, c.91C>T (p.Arg31*)
GroupID: 23
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CohortInfo: 41 non-related patients with retinal angiomatosis between 1988 and 1999 were evaluated.
CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R161* (c.481C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: R161* (c.694C>T)
ClinVarID: 2217 https://www.ncbi.nlm.nih.gov/clinvar/variation/2217/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: stop_gained
CivicName: R161* (c.481C>T)
MultipleGeneVariants: N/A
41 non-related patients with retinal capillary hemangioma presenting in the Benjamin Franklin University Eye Clinic between 1988 to 1999 Germany were evaluated for the presence of other VHL lesions. VHL disease was diagnosed in 33 patients based on the presence of other severe VHL lesions (spinal hemangioblastoma, cerebellar hemangioblastoma, renal cysts, pancreatic cyst, renal carcinoma, and pheochromocytoma), molecular genetic testing, and/or family history. VHL germline mutations were identified in 27 out of 29 VHL families screened with molecular genetics. Blood samples were genetically tested using PCR-SSCP sequencing. One patient with VHL-related retinal angiomatosis was found to have germline splicing mutation (c.464-1G>C) mutation in the VHL gene. This variant was reported as c.677-1G>C (AF010238.1) and mapped to c.464-1G>C (NM_000551.3).
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
AD 9 38 F ? ? - - - - - c.340 ? 1 G[A p.G114D b
PatientID: 9
KindredID: AD
Case: F, 38Y0M, Indian
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0001737 (Pancreatic cysts)
CaseHPOFreeText: Multi-cystic pancreatic lesions.
CaseNotHPOs: HP:0005584; HP:0002666; HP:0030393; HP:0009711; HP:0010797 (Renal cell carcinoma, Pheochromocytoma, Endolymphatic sac tumor, Retinal capillary hemangioma, Hemangioblastoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.G114D (c.340+1G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223190, https://www.ncbi.nlm.nih.gov/clinvar/variation/223190/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: splice_site_variant; missense_variant;transition
CivicName: G114D (c.340+1G>A) and c.340+5G>C
MultipleGeneVariants: N/A
PMID: 29813026
Germline sequencing of the VHL gene was performed on patients who presented with VHL syndromic hemangioblastomas, and germline results were compared to sequencing results from matched tumor tissue samples. Patients were only identified by their tumor sample number. Sample 1 (patient 1) had a Gln96_Pro102 deletion (c.287_307del) in the VHL gene. Genetic analysis was conducted as follows: peripheral blood samples were collected from patients, and genomic DNA was extracted, amplified, and purified using ExoSAP IT (ExoSAP IT (Thermo Scientific Inc., MA, USA). Sanger sequencing was performed on samples (Bigdye direct cycle sequencing v3.1, Life Technologies, CS, USA) and capillary electrophoresis was performed on an ABI Genetic Analyzer (ABI 3130xl, Life technologies, CS, USA). Deletion and duplication analysis of the VHL gene spanning the chr3p.25.3 locus was tested by the Multiplex Ligation-dependant Probe Amplification (MLPA) procedure. VHL gene locus-specific probes (P016-C2 VHL) were purchased from MRC Holland (MRC Holland, Amsterdam, Netherlands). ACMG evidence codes: PP4- Patient’s phenotype or family history is highly specific for a disease with a single genetic etiology.
III - 4
PatientID: III:4
KindredID: 1
Case: M, 56Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: A 5-generation family with VHL in 15 members. Both second generation children (presumed), 5 third generation, and 8 further generation individuals were affected and haplotyping was conducted using three polymorphic microsatellite markers. All of the 5th generation children (9 total at time of publication) had been sequenced and haplotyped as unaffected.
CasePresentingHPOs: HP:0006880; HP:0002666 (cerebellar hemangioblastoma; pheochromocytoma)
CaseHPOFreeText: patent had a combination of cerebellar HB and bilateral pheo, age of onset at 38Y, and operated on the same year
CaseNotHPOs: HP:0006880; HP:0002666; HP:0030405; HP:0001737; HP:0000107; HP:0002668 (pancreatic endocrine tumor, pancreatic cysts, renal cysts, paraganglioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: genotyped three polymorphic microsatellite markers that flanked VHL on chromosome 3p25 (D3S3691, D3S1597 and D3S1263).
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
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
Genotype-phenotype correlations of 573 VHL patients from 200 kindreds were analyzed. Higher risk of pheochromocytoma was associated with missense mutations that result in substitution of a surface amino acid (p<=0.004) than for patients with missense mutations that disrupt the structural integrity of the VHL gene product (pVHL) or other loss of function mutations (either germline deletions or truncating mutations). This missense mutation (c.395A>C), affecting a residue on surface of pVHL, was found in a VHL family of 2, 1 with retinal angiomas diagnosed at 18Y, 1 with cerebellar hemangioblastomas at 37Y, and 1 with renal cell carcinoma at 49Y.
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
GroupID: 80
DiseaseAssertion: assumed VHL
GroupSize: 33
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: 33 of the 573 patients discussed in this paper were found to have identical variants. This mutation (R161Q (c.500G>A)) was found in 7 VHL families with 33 patients altogether.
GroupPresentingHPOs: HP:0009711; HP:0006880; HP:0005584; HP:0002666 (retinal capillary hemangioma, cerebellar hemangioblastoma, renal cell carcinoma, pheochromocytoma)
GroupHPOFreeText: 17 had retinal hemangioblastoma, 9 had cerebellar hemangioblastomas, 5 had renal cell carcinoma, and 15 had pheochromcytoma. Mean ages for each diagnosis follows: 28 (RH), 23 (CHB), 41 (RCC), 17 (Pheo)
GroupNotHPOs: N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Supplementary Table S1.
Variant: p.R161Q (c.500G>A)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R161Q (c.500G>A)
MultipleGeneVariants: N/A
GroupID: 61
Case: Age Unknown, Sex Unknown, Ethnicity Unknown
DiseaseAssertion: assumed VHL
FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.262T>A) was found in 1 VHL family with a single patient.
CasePresentingHPOs: HP:0005584; HP:0009711; HP:0006880 (renal cell carcinoma; retinal capillary hemangioma; cerebellar hemangioblastoma)
CaseHPOFreeText: patient had retinal angioma diagnosed at 23Y, cerebellar hemangioblastoma diagnosed at 54Y, and RCC at 54Y.
CaseNotHPOs: HP:0002666 (pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Supplementary Table S1.
Variant: p.W88R (c.262T>A)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 456577 https://www.ncbi.nlm.nih.gov/clinvar/variation/456577/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: W88R (c.262T>A)
MultipleGeneVariants: N/A
Genotype-phenotype correlations of 573 VHL patients from 200 kindreds were analyzed and confirmed that higher risk of pheochromocytoma is associated with missense mutations that result in substitution of a surface amino acid or that disrupt the structural integrity of the VHL gene product (pVHL). Age-related risks of retinal hemangoblastomas and renal cell carcinoma were higher in patients with nonsense or frameshift mutations. Southern blot and/or MLPA analysis by whole blood detected this nonsense mutation. c.529A>T was found in 3 VHL families total. 2 families were grouped and detailed as affected with a total of 10 patients, 8 with retinal angioma, 4 with cerebellar hemangioblastoma, 1 with renal cell carcinoma (diagnosed at 50Y), and 1 with pheochromocytoma (diagnosed at 27Y). Another individual belonging to a separate family was written with the same nonsense mutation and retinal angiomas diagnosed at 28Y, cerebellar hemangioblastomas diagnosed at 22Y, and renal cell carcinoma diagnosed at 37Y.
Genotype-phenotype correlations of 573 VHL patients were analyzed and confirmed that higher risk of pheochromocytoma is associated with missense mutations that result in substitution of a surface amino acid or that disrupt the structural integrity of the VHL gene product (pVHL). Age-related risks of retinal hemangoblastomas and renal cell carcinoma were higher in patients with nonsense or frameshift mutations. Southern blot and/or MLPA analysis by whole blood detected this nonsense mutation (c.375insT: p.Glu55*) in a VHL family with 2 affected members. They both had hemangioblatomas. No other info was given.
The mutation was written as follows: AFO10238:375_376insT; NM_000551.2:c.162_163insT; p.54MetX. Author Maher was contacted and confirmed "A single nucleotide insertion (T) was detected at position 375 (375insT)” from 2000 lab report - June 1, 2021 - therefore assume p. transcribed incorrectly.
1 France c.275A>G p.Asp92Gly
GroupID: 8
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: p.D92G (c.275A>G)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: N/A
CAID: CA351750765 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.275A%3EG
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: D92G (c.275A>G)
MultipleGeneVariants: N/A
2 UK c.332G>A p.Ser111Asn
GroupID: 11
DiseaseAssertion: VHL
GroupSize: 2
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: UK (country)
GroupAgeRange: N/A
GroupInfo: 2 registrants from the UK were grouped in this study via the mutation of c.332G>A
GroupPresentingHPOs: HP:0030393 (Endolymphatic sac tumor)
GroupHPOFreeText: N/A
GroupNotHPOs: N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.S111N (c.332G>A)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 223186 https://www.ncbi.nlm.nih.gov/clinvar/variation/223186/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: S111N (c.332G>A)
MultipleGeneVariants: N/A
1 Italy c.256C>G p.Pro86Ala
Patients with ELSTs were identified and included in the International Endolymphatic Sac Tumor Registry. The registry contained 93 patients as of July 2014, and of those, 25 were sporadic, and 68 associated with VHL. Patients with ELSTs and clinically confirmed diagnoses of VHL were included in this study. Statistics of this VHL subgroup are as follows: mean age 30, 62% female, 91% symptomatic, 54% with retinal angioma, 72% with CNS hemangioblastoma, 46% with renal cell carcinoma, 19% with pheochromocytoma, and 12% with pancreatic neuroendocrine tumour. In the data from this study, only endolymphatic sac tumours can be confirmed as a phenotype for this mutation (c.256C>G), which was found in 1 individual from Italy.
1 Italy c.470C>T p.Thr157Ile
GroupID: 22
Case: Sex unknown, Age unknown, Italian
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: p.T157I (c.470C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 223223 https://www.ncbi.nlm.nih.gov/clinvar/variation/223223/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: T157I (c.470C>T)
MultipleGeneVariants: N/A
nt 437 Del.TCT* 76 Del.Phe 437del3 In-frame del 2
A cohort of 141 patients with hemangioblastomas of the central nervous system was analyzed. 81 patients had germline mutations in the VHL gene, analyzed through peripheral blood by Southern blotting and SSCP analysis. This inframe mutation (c.224_226delTCT) was recorded in the paper as c.437delTCT due to a difference in transcript sequence. It was found in 2 patients with hemangioblastomas of the central nervous system. Any relation between patients is unknown. No other phenotypes described.
nt 407 C/G 65 Ser→Trp S65W Missense 2
A cohort of 141 patients with hemangioblastomas of the central nervous system was analyzed. 81 patients had germline mutations in the VHL gene, analyzed through peripheral blood by Southern blotting and SSCP analysis. This missense mutation (c.194C>G) was recorded in the paper as c.407C>G due to a difference in transcript sequence. It was found in 2 patients with hemangioblastomas of the central nervous system. Any relation is unknown. No other phenotype described.
726Fnt 393 del G, codon 137 exon 1, stopR, 12656
PatientID: 7
KindredID: 2656
Case: F, 26Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: Another member of her family (patient 8) also presented with pancreatic endocrine tumour.
CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumour)
CaseHPOFreeText: She presented with one pathologic pancreatic neuroendocrine tumors.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.V62Cfs*5 (c.180delG)
LegacyVariant: p.V62Cfs*5 (c.393delG)
CaseProblemVariantFreeText: N/A
ClinVar: 182986 https://www.ncbi.nlm.nih.gov/clinvar/variation/182986/
CAID: CA020069 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.180delG
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_1_frameshift_variant
CivicName: V62Cfs*5 (c.180delG)
MultipleGeneVariants: N/A
nt 713 G to A, Arg to Gln
Fourty-four of 389 patients with VHL (between 1988-1999) screened positive for pancreatic neuroendocrine tumours (PNETs) either by pathologic analysis of tissue specimens or by characteristic radiographic appearance on CT and MRI. VHL gene germline mutations were determined by quantitative Southern blotting to detect deletions of the gene and gene rearrangements as well as complete gene sequencing. Five patients presented with the c.500G>A VHL gene mutation (stated as 713 G to A in the paper which used the Latif sequence as reference) causing a change of Arg to Gln at protein position 167. From family 5960, patient 38 (41-year-old male) presented with a single radiologic PNET and patient 39 (39-year-old female) presented with a single pathologic PNET. From family 5069, patient 41 (48-year-old male) presented with five pathologic PNETs, and patient 42 (16-year-old male) presented with a three pathologic PNETs. Unrelated patient 40 (31-year-old female) presented with a single pathologic PNET. No ACMG code.
GroupID: 3770
DiseaseAssertion: assumed VHL
GroupSize: 6
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: Familial VHL stated; 6 family members recorded with this mutation.
GroupPresentingHPOs: HP:0009711; HP:0010797; HP:0005584 (retinal capillary hemangioma, hemangioblastoma, renal cell carcinoma)
GroupHPOFreeText: all members had CNS hemangioblastomas, 5 have RCC and 4 members had retinal angioma (hemangioma)
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: 8956040
SupplementalData: N/A
Variant: p.E186* (c.556G>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: p.E257* (c.769G>T)
ClinVarID: 381602 https://www.ncbi.nlm.nih.gov/clinvar/variation/381602/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: stop_gained
CivicName: E186* (c.556G>T)
MultipleGeneVariants: N/A
PatientID: None
KindredID: 4398
Case: Sex, Age, Ethnicity Unknown
DiseaseAssertion: assumed VHL
FamilyInfo: Familial VHL stated; although only 1 family member recorded.
CasePresentingHPOs: HP:0010797; HP:0009711; HP:0005584 (hemangioblastoma; retinal capillary hemangioma, renal cell carcinoma)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0002666 (Pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.N78H (c.232A>C)
CaseProblemVariantFreeText: N/A
LegacyVariant: p.N149H (c.445A>C)
ClinVarID: 625225 https://www.ncbi.nlm.nih.gov/clinvar/variation/625225/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: N78H (c.232A>C)
MultipleGeneVariants: N/A
In a study of 114 unrelated VHL families, 85 germline mutations were found. VHL mutations were detected in affected family members, but not in unaffected family members or 96 normal individuals. This missense mutation was detected in a VHL type 2B patient (family ID 4422), using PCR and SSCP sequencing. The mutation of c.482G>A was referred to in the paper by c.695G>A due to a difference in transcript sequence. The patient had retinal hemangioblastoma, renal cell carcinoma, and pheochromocytoma. Only supporting evidence for pathogenicity because patient's phenotyoe is highly specific for a disease with a single genetic etiology (ACMG code: PP4).
In a study of 114 unrelated VHL families, 85 germline mutations were found. VHL mutations were detected in affected family members, but not in unaffected family members or 96 normal individuals. This missense mutation was found in 4 VHL type 2 families of 51 individuals altogether (family IDs 2338, 3490, 4477, 4405). 36 of 51 individuals had retinal hemangioblastomas, 17 had CNS hemangioblastomas, 16 with renal cell carcinoma, and 36 with pheochromocytomas. This mutation was also detected in an additional family with 1 single member, with retinal angiomas (family ID 3699). Supporting evidence of pathogenicity because cosegregation with disease in multiple affected family members in a gene definitively known to cause the disease (ACMG code: PP1).
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
GroupID/ KindredID: 21CA, 56CE
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: This germline familial VHL mutation was taken from two databases: the Cambridge, Department of Pathology database and the Munich, university of Freiburg and Institute of Pathology database. There was an unknown number of members belonging to Family IDs: 21CA and 56CE. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without pheochromocytoma.
GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)
GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Q195* (c.583C>T)
LegacyVariant: p.Q195* (c.796C>T)
CaseProblemVariantFreeText: N/A
ClinVarID: 428794 https://www.ncbi.nlm.nih.gov/clinvar/variation/428794/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: stop_gained
CivicName: Q195* (c.583C>T)
MultipleGeneVariants: N/A
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
Germline mutational data on VHL was gathered from various countries to assess variation in germline mutations that produce disease within different populations. Families were grouped according to three possible outcomes of disease: renal cell carcinoma without pheochromocytoma, renal cell carcinoma with pheochromocytoma, or pheochromocytoma alone. SSCP and denaturing gradient gel electrophoresis identified mutations in 300/469 (63%) of families affected with VHL. This germline familial VHL mutation (G57fs (c.167_168insA)) was taken from the Cambridge, Department of Pathology database, with an unknown number of members belonging to Family ID 110CA. It was reported in the paper as c.380insA due to a difference in transcript reference. As reported in Table 3, this mutation is found in VHL family without pheochromocytoma, and with renal cell carcinoma.
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
GroupID/ KindredID: 3710NCI
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: This germline familial VHL mutation was taken from the National Cancer Institute database, with an unknown number of members belonging to Family ID 3710NCI. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without pheochromocytoma.
GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)
GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.L135* (c.404T>A)
LegacyVariant: p.L135* (c.617T>A)
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA351754021 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.404T>A
gnomAD: N/A
VariantEvidence: This paper declares this variant is predicted to compromise the Elongin-binding site by truncating the protein.
MutationType: stop_gained
CivicName: L135* (c.404T>A)
MultipleGeneVariants: N/A
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
GroupID/ KindredID: 8CE, 59CA, 21CE
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: This germline familial VHL mutation was taken from the Cambridge, Department of Pathology database and the Munich, university of Freiburg and Institute of Pathology database, with an unknown number of members belonging to Family IDs 8CE, 59CA, 21CE. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without pheochromocytoma.
GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)
GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.L89P (c.266T>C)
LegacyVariant: p.L89P (c.479T>C)
CaseProblemVariantFreeText: N/A
ClinVarID: 182979 https://www.ncbi.nlm.nih.gov/clinvar/variation/182979/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: L89P (c.266T>C)
MultipleGeneVariants: N/A
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
GroupID/ KindredID: 91CA
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: This germline familial VHL mutation was taken from the Cambridge, Department of Pathology database, with an unknown number of members belonging to Family ID 91CA. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without pheochromocytoma.
GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)
GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.L158V (c.472C>G)
LegacyVariant: p.L158V (c.685C>G)
CaseProblemVariantFreeText: N/A
ClinVarID: 567944 https://www.ncbi.nlm.nih.gov/clinvar/variation/567944/
CAID: N/A
gnomAD: N/A
VariantEvidence: This paper declares this variant is predicted to compromise the Elongin-binding site by location between codons 157 and 189.
MutationType: missense_variant; transversion
CivicName: L158V (c.472C>G)
MultipleGeneVariants: N/A
Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.
Germline mutational data on VHL was gathered from various countries to assess variation in germline mutations that produce disease within different populations. Families were grouped according to three possible outcomes of disease: renal cell carcinoma without pheochromocytoma, renal cell carcinoma with pheochromocytoma, or pheochromocytoma alone. SSCP and denaturing gradient gel electrophoresis identified mutations in 300/469 (63%) of families affected with VHL. This germline familial VHL mutation (S111fs (c.331delA)) was taken from the National Cancer Institute database, with an unknown number of members belonging to Family ID 3669NCI. It was reported in the paper as c.544delA due to a difference in transcript reference. As reported in Table 3, this mutation is found in VHL families without pheochromocytoma, and with renal cell carcinoma.
Interventional case report of a 28-year-old patient with multiple and large retinal capillary hemangiomas underwent PPV combined with relaxing retinectomy.
PatientID: 1 (case)
KindredID: 1
Case: F, 30Y0M, Vietnamese
DiseaseAssertion: VHL
FamilyInfo: None - The diagnosis of VHL had not been established in her parents or her relatives, who lived in Vietnam without further evaluation.
CasePresentingHPOs: HP:0009711; HP:0001737 (retinal capillary hemangioma; pancreatic cysts)
CaseHPOFreeText: At 28Y presented with multiple retinal capillary hemangioma (complicated tractional retinal detachment and multiple large angiomas) and multiple pancreatic cysts. Underwent PPV combined with relaxing retinectomy.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
The patient's father, now 51 years old, was found to have an angioma of the glans penis and had had surgery for a mandibular cyst and epididymal cystadenomas at age 43 years. Hence, we suspected that the father had an attenuated form of VHL. Indeed, abdominal ultrasonography and total-body magnetic resonance imaging (MRI) revealed a 2.3-cm cyst in his right kidney. His blood pressure and levels of plasma free metanephrines, fractionated urinary metanephrines, chromogranin A were normal. The other three first-degree relatives were normal both clinically and biochemically.
PatientID: DHPLC 1
KindredID: 1
Case: M, 51Y0M, Unknown Ethnicity
DiseaseAssertion: Assumed VHL
FamilyInfo: The patient’s daughter (DHPLC 1) had a pheochromocytoma at 11Y. At 18Y, she had a pheochromocytoma in the contralateral adrenal gland and two concurrent paragangliomas of the abdominal aorta and urinary bladder. At 25Y, she was found to have a right frontal meningioma. A family history obtained from his daughter’s other parent, one son and one other daughter (not DHPLC 1) was uninformative. The patient’s relatives (except for his daughter) were normal both clinically and biochemically.
CasePresentingHPOs: HP:0001028; HP:0000277; HP:0009715; HP:0000107 (Angioma, abnormality of the mandible, papillary cystadenoma of the epididymis, renal cyst)
CaseHPOFreeText: The patient had an attenuated VHL phenotype caused by mosaicism which led to what initially appeared to be a de novo mutation in his daughter (DHPLC 3). The patient was found to have an angioma of the glans penis and had had surgery for a mandibular cyst and epididymal cystadenomas at age 43Y. Abdominal ultrasonography and total-body magnetic resonance imaging (MRI) conducted at the time of the study (51Y) revealed a 2.3-cm cyst in his right kidney. His blood pressure and levels of plasma free metanephrines, fractionated urinary metanephrines, chromogranin A were normal.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R161Q (c.482G>A)
LegacyVariant: p.R161Q (c.695G>A)
ClinVarID: 182983, https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R161Q(c.482G>A)
MultipleGeneVariants: N/A
PatientID: V209
KindredID: V209
Case: Sex Unknown, Age Unknown, French
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: N/A
CaseHPOFreeText: Diagnosed with VHL Type 1.
CaseNotHPOs: HP:0002666 (Pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.S65L (c.194C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 182975, https://www.ncbi.nlm.nih.gov/clinvar/variation/182975/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: S65L (c.194C>T)
MultipleGeneVariants: N/A
Screening of 92 unrelated patients with VHL disease revealed 61 DNA variants. No variants were found in 96 control cases. Direct sequencing on peripheral blood was systematically performed on exon 1 PCR products. Southern blotting was used to search for larger alterations to the gene. The E46* (c.136G>T) missense mutation was found in a VHL type 1 (no pheochromocytoma) patient (patient no. V65).
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
245G→C Tv Exon 1 82 CGC R R82P
A study of 103 patients with VHL retinal manifestations and 108 patients without VHL retinal manifestations extracted from the French VHL database revealed that the number of hemangioblastomas appeared higher in patients who had a substitution when compared with patients with a truncated protein. Detected by PCR and SSCP, this mutation p.R82P (c.245G>C) was found in 3 VHL patients. 1 member was said to have retinal hemangioblastomas, while the other 2 were said not to have this phenotype. Other manifestations are not clearly stated. No family information or relation was provided. This is possibly previously published in PMID: 15300849
468T→G Ts Exon 3 156 TAT Y Y156X
A study of 103 patients with VHL retinal manifestations and 108 patients without VHL retinal manifestations extracted from the French VHL database revealed that the number of hemangioblastomas appeared higher in patients who had a substitution when compared with patients with a truncated protein. Detected by PCR and SSCP, this mutation p.Y156* (c.468T>G) was found in 3 VHL patients. All 3 were said not to have retinal hemangioblastomas, while other manifestations are not clearly stated. No family information or relation was provided. This is possibly previously published in PMID: 15300849
217C→T Ts Exon 1 73 CAG Q Q73X
A study of 103 patients with VHL retinal manifestations and 108 patients without VHL retinal manifestations extracted from the French VHL database revealed that the number of hemangioblastomas appeared higher in patients who had a substitution when compared with patients with a truncated protein. Detected by PCR and SSCP, this mutation (p.Q73* (c.217C>T)) was found in 5 VHL patients. 4 members were said to have retinal hemangioblastomas, while the other was said not to have this phenotype. Other manifestations are not clearly stated. No family information or relation was provided. This is possibly previously published in PMID: 15300849
351G→T Tv Exon 2 117 TGG W W117C
A study of 103 patients with VHL retinal manifestations and 108 patients without VHL retinal manifestations extracted from the French VHL database revealed that the number of hemangioblastomas appeared higher in patients who had a substitution when compared with patients with a truncated protein. Detected by PCR and SSCP, this mutation p.W117C (c.351G>T) was found in 5 VHL patients. 4 members were said to have retinal hemangioblastomas, while the other member was said not to have this phenotype. Other manifestations are not clearly stated. No family information or relation was provided. This is possibly previously published in PMID: 15300849
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
PatientID: 118
KindredID: 42
Case: F, Age unknown, Chinese
DiseaseAssertion: Asymptomatic
FamilyInfo: The proband (patient 42) had four family members confirmed with the mutation: his son (CNS hemangioblastoma at 12, retinal angioma at 11); his sister 1 (patient 116) presented with multiple pancreatic cysts/tumors at 53; his niece (daughter of sister 2) was asymptomatic at the time of assessment, and his nephew (son of brother 2) presented with a CNS hemangioblastoma at 12, and pheochromocytoma and multiple pancreatic cysts/tumors at 18. The proband also had three family members who passed away before diagnosis/ before they could be confirmed with the mutation: his sister 2 (patient 117) had multiple pancreatic cysts/tumors at 46, his brother 1 presented with a CNS hemangioblastoma at 47, renal cell carcinoma at 59, and multiple pancreatic cysts/tumors at 59; and his brother 2 presented with a retinal capillary hemangioma at 43, and CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors at 44.
CasePresentingHPOs: N/A
CaseHPOFreeText: The proband's niece (daughter of sister 2) was genetically confirmed with the mutation but was asymptomatic at the time of assessment.
CaseNotHPOs: HP:0002666; HP:0005584; HP:0010797; HP:0009711; HP:0001732; HP:0001737 (Pheochromocytoma, Renal cell carcinoma, Hemangioblastoma, Retinal capillary hemangioma, Abnormality of the pancreas, Pancreatic cysts)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: This cohort was also published in a paper by Wang et al., 2018 (PMID: 24581539) and Wang et al., 2014 (PMID: 29330336).
SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.
Variant: p.W117G (c.349T>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 862346; https://www.ncbi.nlm.nih.gov/clinvar/variation/862346/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: W117G (c.349T>G)
MultipleGeneVariants: N/A
A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. This familial mutation was confirmed in family #42. A male proband (patient 114) was diagnosed with CNS hemangioblastoma at 36Y, retinal angioma at 44Y, RCC at 44Y, and multiple pancreatic lesions at 44Y. His son (patient 115) was diagnosed with CNS hemangioblastoma at 12Y and retinal angioma at 11Y. His first sister (patient 116) was diagnosed with multiple pancreatic lesions at 53Y. His second sister (patient 117), who was not genetically confirmed for the mutation, was diagnosed with multiple pancreatic lesions at 46Y. His niece (daughter of second sister) (patient 118) was asymptomatic. His first brother (patient 119), who was not genetically confirmed for the mutation, was diagnosed with CNS hemangioblastoma at 47Y, RCC at 59Y, and multiple pancreatic lesions at 59Y. His second brother (patient 120), who was not genetically confirmed for the mutation, was diagnosed with CNS hemangioblastoma at 44Y, retinal angioma at 43Y, RCC at 44Y, and multiple pancreatic lesions at 44Y. His nephew (son of second brother) (patient 121) was diagnosed with CNS haemangioblastoma at 12Y, multiple pancreatic lesions at 18Y, pheochromocytoma at 18Y. This cohort was also published in a paper by Wang et al., 2018 (PMID: 24581539) and Wang et al., 2014 (PMID: 29330336). Wang et al., 2018 reported 8 patients from 1 family who were genetically confirmed with this germline mutation. Wang et al., 2014 reported 4 patients from 1 family who were genetically confirmed with the mutation. It is likely that all three papers published the same family.
A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. This frameshift mutation was found in the VHL gene of family #15. The proband (patient 42) has four family members confirmed with the mutation, and two family members who passed away before diagnosis/ genetic confirmation of the mutation. Family members confirmed with the mutation include: the proband's daughter (patient 43) who had retinal angioma (age 17), renal cell carcinoma (21), multiple pancreatic cysts/tumors (18), and a pheochromocytoma (19). His son (patient 44) who was asymptomatic at the time of assessment. His niece 1 (patient 47) who had a retinal angioma and renal cell carcinoma (22). And his niece 2 (patient 28) who had a CNS hemangioblastoma (19) and a retinal angioma (18). Family members who passed away before diagnosis and were not genetically confirmed include: his sister (patient 45) who had a CNS hemangioblastoma (22), and his brother (patient 46) who had a retinal angioma and renal cell carcinoma at 52. This cohort was also published in a paper by Wang et al., 2018 (PMID: 29330336). It is likely that the same family was published in both papers, with two additional members added in the 2018 paper.
PatientID: 132
KindredID: 50
Case: F, 45Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: The proband (patient 132) had multiple family members who were unconfirmed with the mutation. Her brother 1 (patient 133) had a CNS hemangioblastoma at 29, and renal cell carcinoma and multiple pancreatic cysts/tumors at 48; however no DNA sample was available for testing. Her brother 2 (patient 134) had a CNS hemangioblastoma at 27, but passed away before he could be genetically confirmed with the mutation. Similarly, her father (patient 135) had a CNS hemangioblastoma at 25, but passed away before he could be genetically confirmed.
CasePresentingHPOs: HP:0010797, HP:0001737, HP:0001732, HP:0005584 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)
CaseHPOFreeText: The proband's nephew (son of brother 2) (patient 233) had a renal cell carcinoma at age 30.
CaseNotHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, Retinal capillary hemangioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: This patient 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: p.Q145Yfs*27 (c.433_437del)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA2573131796, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573131796
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_2_frameshift_variant
CivicName: Q145fs (c.433_437delCAGCC)
MultipleGeneVariants: N/A
PatientID: 109
KindredID: 37
Case: M, 20Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0001732 (Hemangioblastoma, Renal cell carcinoma, Pancreatic cysts, Abnormality of the pancreas)
CaseHPOFreeText: The proband presented with a CNS hemangioblastoma at 19, renal cell carcinoma and multiple pancreatic cysts/tumors at 20.
CaseNotHPOs: HP:0009711; HP:0002666 (Retinal capillary hemangioma, Pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: This patient was also published in an earlier paper by Wang et al., 2014 (PMID 24581539) as well as a later paper by Wang et al., 2018 (PMID: 29330336).
SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.
Variant: p.S111Tfs*48 (c.332delG)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA913189247; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.332delG
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_1_frameshift_variant
CivicName: S111fs (c.332del)
MultipleGeneVariants: N/A
A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. A female proband, patient 111 from kindred 39, was found with this germline splice site mutation (c.340+5G>C). She was diagnosed with a CNS hemangioblastoma at 35Y. This kindred was likely published in a later paper by Wang et al., 2018 (PMID: 29330336).
PatientID: 107
KindredID: 36
Case: M, 18Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: The proband's mother presented with a CNS hemangioblastoma and retinal angioma at age 29, but passed away before the mutation could be confirmed.
CasePresentingHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)
CaseHPOFreeText: The proband presented with a CNS hemangioblastoma and retinal angioma at age 18.
CaseNotHPOs: HP:0005584; HP:0001737; HP:0001732; HP:0002666 (Renal cell carcinoma, Pancreatic cysts, Abnormality of the pancreas, 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: p.H110Pfs*49 (c.329delA)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 560741, https://www.ncbi.nlm.nih.gov/clinvar/variation/560741/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_1_frameshift_variant
CivicName: H110PFS*49 (c.329delA)
MultipleGeneVariants: N/A
PatientID: 37
KindredID: 12
Case: F, 27Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: The patient had the same germline mutation as her brother (the proband) and father. Her brother presented with CNS Hemangioblastoma, Renal cell carcinoma, and multiple pancreatic cysts/tumors at the age of 34. Her father presented with renal cell carcinoma at 55. The patient's uncle passed away before diagnosis and presented with a CNS hemangioblastoma at age 19, but could not be genetically confirmed for the mutation.
CasePresentingHPOs: HP:0001737; HP:0001732 (Pancreatic cysts, Abnormality of the pancreas)
CaseHPOFreeText: The patient presented with multiple pancreatic cysts/tumors at the age of 27.
CaseNotHPOs: HP:0010797; HP:0009711; HP:0002666; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, 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: p.N78S (c.233A>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 93326, https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: N78S (c.233A>G)
MultipleGeneVariants: N/A
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
A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. A male patient was confirmed for nonsense mutation in the VHL gene (c.217C>T; p.Gln73*). He was diagnosed with CNS haemangioblastoma at 66Y, retinal angioma at 66Y, renal cell carcinoma at 37Y, and multiple pancreatic cysts or tumours at 54Y. This cohort was also published in a paper by Wang et al., 2018 (PMID: 24581539) and Wang et al., 2014 (PMID: 29330336). It is likely that all three papers reported on the same individual.
PatientID: 141
KindredID: 52
Case: F, 69Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: The proband (patient 138) had multiple family members affected with the mutation. Their daughter (pt 139) was asymptomatic at the time of assessment; their son (pt 140) was also asymptomatic at the time of assessment; their mother (pt 141) presented with a CNS hemangioblastoma at 66, renal cell carcinoma at 69, and multiple pancreatic cysts/tumors at 66; their sister 1 (pt 142) presented with a CNS hemangioblastoma at 32, renal cell carcinoma at 36, and multiple pancreatic cysts/tumors at 36; the son of sister 1 was asymptomatic at the time of analysis; the daughter of sister 1 was asymptomatic at the time of analysis; the proband's sister 2 presented at age 39 with CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors; and the son of sister 2 was asymptomatic at the time of analysis. All members of this family were genetically confirmed to have this mutation.
CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0001732 (Hemangioblastoma, Renal cell carcinoma, Pancreatic cysts, Abnormality of the pancreas)
CaseHPOFreeText: The proband's mother (patient 141) had a CNS hemangioblastoma and multiple pancreatic cysts/tumors at 66, and renal cell carcinoma at 69.
CaseNotHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, Retinal capillary hemangioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: This patient 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: c.464-1G>C
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223220; https://www.ncbi.nlm.nih.gov/clinvar/variation/223220/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: splice_site_variant
CivicName: Splice Site (c.464-1G>C)
MultipleGeneVariants: N/A
35 (45%) had missense variants
PatientID: 10
KindredID: 10
Case: Age, Sex, Ethnicity unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0010797; HP:0100634; HP:0009711 (hemangioblastoma, neuroendocrine neoplasm, retinal capillary hemangioma)
CaseHPOFreeText: patient was recorded with a CNS hemangioblastoma, a pheochromocytoma and/or paraganglioma (neuroendocrine neoplasm), and a retinal hemangioblastoma.
CaseNotHPOs: HP:0030421; HP:0006770; HP:0030405 (epididymal tumour, clear cell renal cell carcinoma, pancreatic endocrine tumour)
CaseNotHPOFreeText: Patient was recorded without the manifestations of: an epididymal tumor, CCRCC, and a pancreatic endocrine tumour (pancreatic neuroendocrine neoplasm)
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.
Variant: p.R167Q (c.500G>A)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: R167Q (c.500G>A)
MultipleGeneVariants: N/A
35 (45%) had missense variants
A cohort of VHL patients from the Greater Toronto Area in Canada were retrospectively reviewed. Patients ID 3 and 25 had this germline mutation (p.D92V). Patient 3 had: CNS hemangioblastoma. Patient 25 pheochromocytoma/paraganglioma (recorded here as a neuroendocrine neoplasm). Whether patients were related, age, and sex data was not reported. ACMG PP4
missense variants
PatientID: 63
KindredID: 63
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0030405; HP:0100634 (pancreatic neuroendocrine neoplasm, Neuroendocrine neoplasm)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0010797; HP:0009711; HP:0030421; HP:0006770 (hemangioblastoma; retinal capillary hemangioma; Epididymal neoplasm, clear cell renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 29437867 (Family 7 - see here for more info)
SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.
Variant: p.R107G (c.319C>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 43599 https://www.ncbi.nlm.nih.gov/clinvar/variation/43599
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: R107G (c.319C>G)
MultipleGeneVariants: N/A
VHL{"type":"entrez-nucleotide","attrs":{"text":"NM_000551.4","term_id":"1779521775"}}NM_000551.4:c.202T>Cp.(Ser68Pro)CM073416
75 individuals pre-diagnosed with pheochromocytoma and/or paraganglioma were referred for molecular genetic testing. Genomic DNA of each participant was isolated from peripheral blood samples to look for germline mutations in pheochromocytoma and paraganglioma targeted susceptibility genes. 6 targeted genes (IF1B, RET, SDHB, SDHD, TMEM127, and VHL) were sequenced and identified variants were confirmed by sanger sequencing. Sequencing identified a germline S68P(c.202T>C) missense variant in the VHL gene of 3 patients: 4, 5 and 6. Patient 4 (29, M) was pre-diagnosed with pheochromocytoma (bilateral renal and eyes, pancreatic cysts) and had two affected family members, his mother (without any described phenotype or genotype) and his brother (patient 5). Patient 5 (32Y, M) was pre-diagnosed with pheochromocytoma (right kidney-clear cell carcinoma). Lastly, patient 6 was a 33Y male pre-diagnosed with paraganglioma and liver cysts. This patient's cousin was an affected family member described (without genotype or phenotypes details).
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
PatientID: 8
KindredID: 8
Case: Sex Unknown, 23Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0010797; HP:0009711; HP:0002666 (Hemangioblastoma, Retinal capillary hemangioma, Pheochromocytoma)
CaseHPOFreeText: CNS hemangioblastoma, retinal hemangioblastoma and pheochromocytoma.
CaseNotHPOs: HP:0001732; HP:0006770; HP:0000107 (Abnormality of the pancreas, Clear cell renal cell carcinoma, Renal cyst)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Table S1, S2 and S3
Variant: p.T157I (c.470C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223223, https://www.ncbi.nlm.nih.gov/clinvar/variation/223223/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: T157I (c.470C>T)
MultipleGeneVariants: N/A
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
PatientID: 44
KindredID: 44
Case: Sex Unknown, 33Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0009711; HP:0000107 (Retinal capillary hemangioma, Renal cyst)
CaseHPOFreeText: Retinal hemangioblastoma and renal cystic lesion.
CaseNotHPOs: HP:0002666; HP:0010797; HP:0006770; HP:0001732 (Pheochromocytoma, Hemangioblastoma, Clear cell renal cell carcinoma, Abnormality of the pancreas)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Table S1, S2 and S3
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
2 43 c.464T>G p.Val155Gly x x De novo Parents, sibling, and nephew -
PatientID: 2
KindredID: 2
Case: Sex Unknown, 43Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: Parents, siblings and nephew were negative for the mutation confirming that this variant was de novo in the proband. No phenotype details are noted for these family members.
CasePresentingHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, Retinal capillary hemangioma)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0000107; HP:0006770; HP:0010797; HP:0001732 (Renal cyst, Clear cell renal cell carcinoma, Hemangioblastoma, Abnormality of the pancreas)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Table S1, S2 and S3
Variant: p.V155G (c.464T>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA16621938, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.464T%3EG
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: V155G (c.464T>G)
MultipleGeneVariants: N/A
PatientID: 214
KindredID: 214
Case: Sex Unknown, 33Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: None
CasePresentingHPOs: HP:0001737, HP:0010797, HP:0000107 (pancreatic cyst, hemangioblastoma, renal cyst)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0002666, HP:0006770, HP:0009711 (pheochromocytoma, clear cell renal cell carcinoma, retinal capillary hemangioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Table S1, S2, S3.
Variant: p.S65W(c.194C>G)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID:43597 https://www.ncbi.nlm.nih.gov/clinvar/variation/43597/
CAID: CA020099 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.194C%3EG
gnomAD: N/A
VariantEvidence: N/A
MutationType:missense_variant;transversion
CivicName: S65W(c.194C>G)
MultipleGeneVariants: N/A
F6, II.1c.492G>T/c.340+574A>T*VHL p.Gln164His/SA2014/6 moM15.6496.91167Splenomegaly—
atientID: II.1
KindredID: F6
Case: M, 0Y6M, Ethnicity Unknown
DiseaseAssertion: Splenomegaly
FamilyInfo: N/A
CasePresentingHPOs: HP:0001744 (Splenomegaly)
CaseHPOFreeText: Diagnosed with splenomegaly at age 6 months (DOB: 2014).
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: c.340+574A>T
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 1040488, https://www.ncbi.nlm.nih.gov/clinvar/variation/1040488/
CAID: N/A
gnomAD: N/A
VariantEvidence: Variants are heterozygous.
MutationType: missense_variant;transversion; splice_site_variant
CivicName: Q164H (c.492G>T) and c.340+574A>T
MultipleGeneVariants: Germline, VHL, c.492G>T (p.Gln164His)
PatientID: 84
KindredID: 84
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: Assumed VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0002666 (Pheochromocytoma)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Patient information pulled from Supplemental Table 1b.
Variant: p.R107H (c.320G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223184, https://www.ncbi.nlm.nih.gov/clinvar/variation/223184/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R107H (c.320G>A)
MultipleGeneVariants: N/A
A study investigated paraganglioma/pheochromocytoma tumors in a retrospective cohort and a prospective cohort. Tumour tissue samples were sequenced by next-generation sequencing using a custom gene panel. In some cases, Sanger sequencing was used to detect germline mutations. Some of these tumors were found with germline VHL mutations. Patient ID 100, from the prospective cohort, presented with multiple paragangliomas and a germline mutation in the VHL gene c.191G>C. Other phenotypic and demographic information was not available. The paper performed carbonic anhydrase IX immunohistochemistry and immunostaining with CA9 was observed in patient 100.
In addition, her younger brother underwent brain surgery in his teens due to brain hemangioblastoma. He had not been diagnosed with diabetes mellitus.
PatientID: III-3
KindredID: 1
Case: M, Age Unknown, Korean
DiseaseAssertion: hemangioblastoma
FamilyInfo: His family members had features apparently related to VHL disease. His grandmother was troubled with severe headache during her lifetime, though the cause of death was unclear. His father was diagnosed with brain hemangioblastoma, which was his cause of death. In addition, his sister had various VHL phenotypes. His sister was tested with the same mutation, while whereas his other, clinically unaffected sister did not.
CasePresentingHPOs: HP:0010797 (hemangioblastoma)
CaseHPOFreeText: underwent brain surgery in his teens due to brain hemangioblastoma
CaseNotHPOs: N/A
CaseNotHPOFreeText: Not diagnosed with diabetes mellitus
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Y98Tfs*61 (c.291delC)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA432420512 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.291delC
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_1_frameshift_variant
CivicName: Y98fs (c.291delC)
MultipleGeneVariants: N/A
3-year-old white male child presented with hematuria of two days and a CT scan showed a right renal mass determined to be renal cell carcinoma. A nephrectomy was done and the tumour tissue was sent for karyotyping. Peripheral blood samples were also taken and sent for sequence analysis of the VHL gene. Genetic testing confirmed 2 mutations: a translocation between chromosome X and 1 t(X;1)(p11.2; p34.3) and a germline missense mutation, c.562C>G (p.Leu188Val) in the VHL gene. Family history was remarkable for a renal tumour in the paternal grandmother at age 65, treated by nephrectomy in 1998. Furthermore, a maternal uncle had a history of thyroid cancer, and a maternal cousin had a history of breast cancer. The patient’s parents and a 13-year-old half-brother were healthy.
PatientID: 13 (tumour 21)
KindredID: 14
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0002666 (pheochromocytoma)
CaseHPOFreeText: Patient had one benign pheochromocytoma.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: RET
PreviouslyPublished: 7759077, 9681856
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
LegacyVariant: p.Y98H (c.505T>C)
CaseProblemVariantFreeText: N/A
ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: CA020246 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.292T%3EC
gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: Refer to Table 1 for LOH information.
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
The N131S Mutation in the von Hippel-Lindau Gene in a Japanese Family with Pheochromocytoma and Hemangioblastomas
PMID: 17001110
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
c 244 C>G (p. Arg 82 Gly)
A case report reveals a 3Y girl with right adrenal malignant pheochromocytoma, with the mother diagnosed with von Hippel-Lindau syndrome. The mother was 38Y when diagnosed with bilateral pheochromocytoma that was resected when she was 18Y. She presented several relapses, the most recent one at 32Y when she was also diagnosed with cerebral angioma. Genetic tests revealed the presence of the VHL c 244 C>G (p. Arg 82 Gly) heterozygote mutation in the mother, as well as in the child. Genetic tests for mutations in RET, SDHB, SDHC and SDHD in the mother were negative. After 6 months from the complete resection of the tumor, the daughter is without any clinical symptoms, with normal blood pressure, normal ophthalmoscopy, no tumor markers and no evidence of tumor on cerebral or abdominal MRI.
PatientID: None
KindredID: 50
Case: F, 16Y0M, 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: Patient information was extracted from Table 1 of Supplementary.
Variant: p.R167Q (c.500G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVar: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence:N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500 G >A)
MultipleGeneVariants: N/A
GroupID: 47
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: VHL family found to have the c.712C>T (R167W) germline variant of the VHL gene. The number of family members included in this study is not specified.
GroupPresentingHPOs: HP:0002666 (Pheochromocytoma)
GroupHPOFreeText: Number of family affected members is not specified.
GroupNotHPOs: N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: 7728151 and/or 8956040
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: c.712C>T
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
GroupID: 20
DiseaseAssertion: VHL
GroupSize: N/A
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: N/A
GroupAgeRange: N/A
GroupInfo: VHL family found to have a germline rearrangement of the VHL gene. The number of family members included in this study is not specified.
GroupPresentingHPOs: N/A
GroupHPOFreeText: Patients within this family were found to have a clinical diagnosis of VHL disease, however, the presenting phenotypes were not specified.
GroupNotHPOs: HP:0002666 (Pheochromocytoma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: Stated as being previously reported in PMID 7728151 and/or 8956040. Both these reports include a family presenting with this variant and it is unclear if one or both coincide with the current family.
SupplementalData: N/A
Variant: p.Q73* (c.217C>T)
LegacyVariant: c.430C>T
CaseProblemVariantFreeText: N/A
ClinVarID: 223164, https://www.ncbi.nlm.nih.gov/clinvar/variation/223164/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition; stop_gained
CivicName: Q73* (c.217C>T)
MultipleGeneVariants: N/A
93 families examined at the Clinical Center of the National Institutes of Health (Bethesda, MD) underwent genetic testing for germline mutations of the VHL gene. Whole blood was extracted and genomic DNA was amplified by PCR and products were sequences using a cycle sequencing kit with dye-labeled terminators and automatically sequenced. This missense mutation was found in a VHL type 1 family (lineage 132). The variant was reported as c.440T>C (AF010238.1) and was mapped to F76S (c.227T>C) (NM_000551.3).
GroupID: 88
DiseaseAssertion: VHL
GroupSize: Unknown
GroupNumberMales: Unknown
GroupNumberFemales: Unknown
GroupEthnicity: Unknown
GroupAgeRange: Unknown
GroupInfo: This family group had a history of clinically confirmed VHL disease. Members of this family were found to harbour the c.500G>A variant causing a Arg167Gln missense mutation (noted in the paper as c.713G>A due to Latif reference transcript being used). It was noted that this family had patients with pheochromocytoma's.
GroupPresentingHPOs: HP:0002666 (pheochromocytoma)
GroupHPOFreeText: Patients within this family were found to have a clinical diagnosis of VHL disease, however, the presenting phenotypes were not specified. It was noted that this family had patients with pheochromocytoma's.
GroupNotHPOs: N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167Q (c.500G>A)
LegacyVariant: p.R167Q (c.713G>A)
ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500G>A)
MultipleGeneVariants: N/A
The selected tissue blocks were cut in 3-μm sections and were immunolabeled with antibodies directed against chromogranine A (Dako, clone DAK-A3), HIF-1α (BD Biosciences, clone 54), HIF-2α (Abcam, clone ep190b), cyclin D1 (Dako, clone DCF-6), and CA9 (Novus Biological, polyclonal). Non-neoplastic pancreatic tissue was also immunolabeled with antibodies against insulin (Dako, polyclonal) and glucagon (Sigma, clone K79bB10) to differentiate endocrine microadenomas from normal islets. In addition, 5 different blocks with microadenomas obtained from 5 patients who presented at least 5 microadenomas were selected for an additional immunostaining with VEGF (Santa-Cruz Biotechnologies, polyclonal) and CD34 (Immunotech, QBEND10) for evaluation of microvessel surface.
Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).
Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients. All patients had VHL germline mutations. Age is at the time of surgery. Patients #15 (male) was found with this germline VHL mutation (p.R82P (c.245G>C)) and pancreatic endocrine tumours. The last known age of the patient was 48Y. Other phenotypes and demographics were unknown. ACMG PP4
15 Dutch VHL patients from 5 families were taken to measure the expression of vascular endothelial growth factor (VEGF). Nine patients were found to harbour the VHL germline mutation V170D, referred to in the paper by V241D due to a difference in transcript sequence. Patient 1, a 57 year old female, presented with pancreatic cysts. Patient 4, a 31 year old male, presented with a kidney cyst and a brain hemangioblastoma and no signs of eye lesions. Patient 5, a 28 year old female, presented with a kidney cyst, brain hemangioblastoma, renal cell carcinoma and a left eye angioma. Patient 7, a 28 year old female, presented with a kidney cyst and a right eye angioma. Patient 8, a 28 year old female, presented with pancreatic cysts and a right eye angioma. Patient 9, a 61 year old male, presented with pancreatic and liver cysts, a brain hemangioblastoma and a left eye angioma. Patient 11, a 38 year old male, presented with pancreatic, liver and kidney cysts, brain and spinal cord hemangioblastomas and a right eye angioma. Patient 12, a 50 year old male, presented with kidney & pancreatic cysts, a pheochromocytoma and a brain hemangioblastoma as well as no sign of eye lesions. Patient 13, a 34 year old male, presented with pancreatic cysts, brain and spinal cord hemangioblastomas and right and left eye angiomas. ACMG: 'PP1' since we have cosegregation with the disease in multiple affected family members, 'PP4' since the patient presents phenotypes highly specific for a disease with a single genetic etiology.
ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3
GenotypingMethod: N/A
SamplingMethod: N/A
10bF““““Pheo, PPGL, HBA Ret, PanNET
PatientID: 10b
KindredID: 8
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: Family history was positive with 3 other members of unknown relation (10a, 10c, 10d) presenting with the mutation, with various phenotypes, however one member being asymptomatic as of age 3Y.
CasePresentingHPOs: HP:0002666; HP:0002668; HP:0009711; HP:0030405 (Pheochromocytoma; Paraganglioma; Retinal capillary hemangioma; Pancreatic endocrine tumor)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: MEN1/ RET
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
5aPExon 1Missensec.332G>Ap. Ser111AsnHBA CNS, Pan/Kid-Cysts
PatientID: 5a
KindredID: 4
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: An unspecified relative (5b) has the same familial mutation with renal cell carcinoma, pancreatic, and renal cysts.
CasePresentingHPOs: HP:0010797; HP:0001737; HP:0000107 (Hemangioblastoma; pancreatic cyst; renal cyst)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: MEN1/ RET
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.S111N (c.332G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223186 https://www.ncbi.nlm.nih.gov/clinvar/variation/223186/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: S111N (c.332G>A)
MultipleGeneVariants: N/A
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
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
PatientID: 1 (Proband)
KindredID: 10
Case: M, 10Y0M, Ethnicity Unknown
DiseaseAssertion: Asymptomatic
FamilyInfo: 2 members of this family presented with the c.712C>T/c.499C>T germline variant of the VHL gene. ID 3 presente with CNS hemangioblastoma, retinal angioma and renal cell carcinoma.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0000077; HP:0002666; HP:0001732; HP:0010797; HP:0005584; HP:0009711 (Abnormality of the kidney, Pheochromocytoma, Abnormality of the pancreas, Hemangioblastoma, Renal cell carcinoma, Retinal capillary hemangioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Supplementary Table 1.
Variant: p.R167W (c.499C>T)
LegacyVariant: c.712C>T
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: A point mutation (c.712C>T) was found. Being that this 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: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
20 unrelated VHL families were retrospectively identified in SickKids Genetics and Cancer Genetics Program SHIRE genetics database, with data entered between 30 August 1984 and 8 August 2016. Family 9 had one patient with the missense mutation c.257C>T in the VHL gene (legacy notation c.470C>T). The proband (male) was diagnosed with CNS hemangioblastoma at 16Y and was 23Y at the end of the study. This patient was later published in 31368132- updated phenotypes available.
PatientID: A-V6
KindredID: A-V6
Case: M, 30Y0M, Korean
DiseaseAssertion: VHL
FamilyInfo: 2 affected individuals (twin brothers) in this family but no further details provided. Twin brother of proband died of VHL.
CasePresentingHPOs: HP:0002666; HP:0006880 (Pheochromocytoma, Cerebellar hemangioblastoma)
CaseHPOFreeText: Cerebellar hemangioblastomas and bilateral pheochromocytoma. Diagnosed with VHL type 2.
CaseNotHPOs: HP:0005584 (Renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 25078357
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T
VariantEvidence: Variant is reported in Table 1 as c.499G>T which was assumed to be a typo and was corrected to c.499C>T. This assumption was made due to later publications referencing this mutation and paper. Variant is reported in Table 1 as c.499G>T which was assumed to be a typo and was corrected due to future publications' reference to this paper regarding this patient and mutation as c.499C>T
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
c.208 G>Tap.E70X
53 patients with a molecularly confirmed VHL mutation (by PCR through EDTA-anticoagulated blood) and a pancreatic neuroendocrine tumor (ICT) were collected from the German NET-Registry and the German VHL-registry. An additional 296 patients were stated in this paper with a VHL associated germline mutation, but without pancreatic neuroendocrine tumors. 2 patients were found to have the above mutation (c.208G>T). 1 was a VHL patient with an ICT (pancreatic neuroendocrine tumor) taken from the VHL-registry. The other patient was stated to be in this study with the given mutation, however no ICT. Other clinical manifestations outside of a pancreatic neuroendocrine tumor are possible, but were not discussed. ACMG evidence codes: 'PVS1' because they observe a nonsense variant in a gene where loss of function is a known mechanism of disease.
c.472 C>Gap.L158V
53 patients with a molecularly confirmed VHL mutation (by PCR through EDTA-anticoagulated blood) and a pancreatic neuroendocrine tumor (ICT) were collected from the German NET-Registry and the German VHL-registry. An additional 296 patients were stated in this paper with a VHL associated germline mutation, but without pancreatic neuroendocrine tumors. 2 patients were found to have the above mutation (c.472C>G). 1 was a VHL patient with an ICT (pancreatic neuroendocrine tumor) taken from the VHL-registry. The other patient was stated to be in this study with the given mutation, however no ICT. Other clinical manifestations outside of a pancreatic neuroendocrine tumor are possible, but were not discussed. ACMG evidence codes: 'PP2' because they observe a missense variant in a gene where missense variants are a common mechanism of disease.
MSY98H1 (5.6)1 (3.8)
GroupID: 7
Case: Age, Sex, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: 1 individual belonging to 1 family was mentioned with this VHL mutation. No other family info was provided.
CasePresentingHPOs: HP:0002666 (pheochromocytoma)
CaseHPOFreeText: Other manifestations aside from pheochromocytoma are possible; but not specified.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: N/A
gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
P14F8M2433nyOU20/200nn20/20nnn
PatientID: 14
KindredID: 8
Case: M, 35Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: No details regarding family information is provided.
CasePresentingHPOs: N/A
CaseHPOFreeText: Patient has VHL disease characterized by tumours, but specific types of tumours were not indicated
CaseNotHPOs: HP:0010797; HP:0009711 (hemangioblastoma, Retinal capillary hemangioma)
CaseNotHPOFreeText: Patient did not have CNS hemangioblastoma or Retinal capillary hemangiomas.
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.E52* (c.154G>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 182982, https://www.ncbi.nlm.nih.gov/clinvar/variation/182982/
CAID: N/A
gnomAD: 0.00001795, https://gnomad.broadinstitute.org/variant/3-10183685-G-T
VariantEvidence: N/A
MutationType: stop_gained
CivicName: E52* (c.154G>T)
MultipleGeneVariants: N/A
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
1 (100)
GroupID: 25
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: HP:0009711 (retinal capillary hemangioma)
CaseHPOFreeText: This individual patient was the only one discussed with this mutation. They had retinal hemangiomas; Other VHL manifestations were discussed but not per- variant.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Yes - Supplementary Table S1
Variant: p.W88R (c.262T>A)
LegacyVariant: N/A
GroupProblemVariantFreeText: N/A
ClinVarID: 456577 https://www.ncbi.nlm.nih.gov/clinvar/variation/456577/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: W88R (c.262T>A)
MultipleGeneVariants: N/A
2 (50)
GroupID: 24b
DiseaseAssertion: VHL
GroupSize: 2
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: N/A
GroupHPOFreeText: These 2/4 patients with a P86H (c.257C>A) mutation did NOT have retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.
GroupNotHPOs: HP:0009711 (retinal capillary hemangioma)
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P86H (c.257C>A)
LegacyVariant: N/A
GroupProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA351750632 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.257C>A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: P86H (c.257C>A)
MultipleGeneVariants: N/A
c.266T > C p.Leu89Pro
216 patients with clinically expected VHL disease due to family history or presence of VHL typical tumours were routinely examined in an eye centre in Germany between January 2019 and January 2020, majority of which were of European descent (~95%). Since data on the genotype–phenotype correlation of the onset of Retinal Hemangioblastoma (RH) is scarce in relation to VHL disease, this study wanted to inversitage the relationship between VHL gene variants (truncating vs single amino acid substitutions) and the ocular phenotype of the disease. 42 different rare VHL gene variants in 148 patients were detected - some of whom had RH and some who did not. Although date of onset of RH, as well as data on central nervous system haemangioblastomas (CNSH), pheochromocytoma/paraganglioma (PPGL), clear cell renal cell carcinoma (ccRCC) and pancreatic neuroendocrine neoplasm (PNEN) were collected, it was not reported on a per patient basis and therefore could not be discussed per variant. Out of the 3 patients with a p.L89P (c.266T>C) mutation, 67% (2/3) of individuals had RH while the other 33% (1/3) did not. No family information was provided.
The authors described the growth kinetics of 96 renal tumours in 64 VHL patients (32 males, 32 females). All patients had VHL disease with renal involvement. 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 patients, at least one or more RCC was diagnosed. However, at the time of diagnosis, an indication for treatment was not yet present. For all patients, several CT/MRI scans existed for retrospective description of tumour growth kinetics. 10-ml EDTA anticoagulated blood samples were available from each patient for mutation screening of all exons of the VHL gene. Genomic DNA from blood samples was extracted using standard methods. Small deletions/insertions or point mutations were identified by DNA sequencing followed by complete mutation screening using PCR/single-strand conformation polymorphism and denaturing high-performance liquid chromatography. A germline missense variant p.H115R(c.344A>G) was identified in patient #12. This mutation was noted as c.557A>G in the paper due to a difference in reference transcript used (see Table S1). No family information is available for this patient.
PatientID: 10
KindredID: N/A
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CohortInfo: The authors evaluated 64 VHL patients (32 women and 32 men) with renal involvement of whom 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 VHL patients, at least one or more RCC were diagnosed, however at the time of diagnosis an indication for treatment was not yet present. For all patients several CT/MRI scans existed for retrospective description of tumour growth kinetics.
CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)
CaseHPOFreeText: This is a tumor resolution study (VHL patients were investigated based on the presence of renal tumors.) No other phenotypic information is available.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Supplementary Table S1 describes 19 patients with missense mutations, including this patient.
Variant: p.V130F(c.388G>T)
LegacyVariant: c.601G>T
CaseProblemVariantFreeText: N/A
ClinVarID: 496061, https://www.ncbi.nlm.nih.gov/clinvar/variation/496061/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: V130F(c.388G>T)
MultipleGeneVariants: N/A
missense mutations
PatientID: None
KindredID: 160
Case: Age, sex ethnicity unknown
DiseaseAssertion: unknown; paper focused only on pheochromocytoma
FamilyInfo: No specific family info was present; although this was recorded as a family germline mutation belonging to Family ID 160
CasePresentingHPOs: N/A
CaseHPOFreeText: Unknown or unstated.
CaseNotHPOs: N/A
CaseNotHPOFreeText: Unknown evidence for phenochromocytoma (neither yes nor no was stated) in this family
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.N78S (c.233A>G)
CaseProblemVariantFreeText: N/A
LegacyVariant: N78S (c.446A>G)
ClinVarID: 93326 https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: N78S (c.233A>G)
MultipleGeneVariants: N/A
The index case was a 14 year-old boy who presented to us in 1971 with severe hypertension. On evaluation he was found to have a right adrenal mass with elevated urinary VMA (normal <7 mg/24 hr), confirming the diagnosis of a right adrenal pheochromocytoma. He underwent right adrenalectomy and the post-operative period was uneventful. He was subsequently lost to follow. In 1979, he presented to us again with severe headache and recurrent seizures. On examination his pulse rate was 100/min, blood pressure was 160/130 mm of Hg. Cardiac auscultation revealed a loud 2nd heart sound and a 3rd heart sound. There were no murmurs. Examination of the abdomen revealed a palpable mass in the left hypochondrium. This mass was confirmed as a pheochromocytoma. After adequately controlling his blood pressure he underwent left cortical sparing adrenalectomy. The post-operative period was uneventful. He was on steroid replacement that was subsequently withdrawn after his serum cortisol levels had normalized. His 8 AM cortisol after withdrawal of steroids was 12 µg/dl.He subsequently got married and had two children as shown in Figure 1, who also eventually developed similar tumors.
PatientID: II-1
KindredID: 1
Case: M, 57Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: Family in India but Ethnicity not explicitly confirmed. Two children with the same mutation. Eldest son presented at age 10 with severe hypertension and bilateral pheochromocytoma. Daughter presented at age 17 with palpitation, blurred vision, blurring vision, bilateral papilledema and bilateral pheochromocytoma. Wife and brother were negative for the mutation.
CasePresentingHPOs: HP:0000822; HP:0002666; HP:0006748; HP:0002315; HP:0001250; HP:0031657 (Hypertension, Pheochromocytoma, Adrenal pheochromocytoma, Headache, Seizure, Abnormal heart sound)
CaseHPOFreeText: Presented at 14 years-old with severe hypertension. On evaluation he was found to have a right adrenal mass with elevated urinary VMA, confirming the diagnosis of a right adrenal pheochromocytoma. Presented at age 22 with severe headache and recurrent seizures. Cardiac auscultation revealed a loud 2nd heart sound and a 3rd heart sound. Examination of the abdomen revealed a palpable mass in the left hypochondrium. This mass was confirmed as a pheochromocytoma. Asymptomatic at age 57.
CaseNotHPOs: HP:0030148 (Heart murmur)
CaseNotHPOFreeText: There were no heart murmurs during evaluation at age 22.
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Figure 1
Variant: p.R82L (c.245G>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 526675, https://www.ncbi.nlm.nih.gov/clinvar/variation/526675/
CAID: N/A
gnomAD: N/A
VariantEvidence: Authors carried out analysis of VHL variant p.Arg82Leu with six different in silico tools namely SIFT, I-Mutant3, PhD-SNP, MutPred, PolyPhen2 and SNPs&GO in order to determine the pathogenic potential of the variant.
MutationType: missense_variant;transversion
CivicName: R82L (c.245G>T)
MultipleGeneVariants: N/A
c.319C > T and c.353 T > C (p.Arg107Cys) and (p.Leu118Pro)
37 Danish patients diagnosed with VHL before 18 years from a prospective cohort study from Denmark's National vHL Research Database (Binderup et al., 2013) were assessed. One family with 1 patient (Family ID8) were found with 2 germline missense mutations in the VHL gene: (L118P; c.353T>C) and (R107G; c.319C>G). Patient 1 was diagnosed at 15Y old and had 6 CNS hemangioblastomas at 15Y, and 2 retinal hemangioblastomas at 15Y. The patient was 35Y by the end of the study.
PatientID: II-13
KindredID: 1
Case: F, Age unknown (deceased), Ethnicity Unknown
DiseaseAssertion: assumed VHL
FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. Patient’s only child (son) appeared to have the VHL mutation too. See family pedigree (Fig. 1).
CasePresentingHPOs: HP:0002011; HP:0009711 (Morphological central nervous system abnormality, retinal capillary hemangioma)
CaseHPOFreeText: Patient mentioned to have CNS (including retinal) involvement without renal involvement.
CaseNotHPOs: HP:0000077 (Abnormality of the kidney)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.E160Sfs*10 (c.477delA)
LegacyVariant: c.688delA
CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10
ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: minus_1_frameshift_variant
CivicName: E160fs (c.477del)
MultipleGeneVariants: SCA2 (an abnormal increase in CAG repeats in one allele of her ataxin-2 gene. This abnormal trinucleotide expansion is consistent with the diagnosis of spinocerebellar ataxia type 2)
21 missense mutations
PatientID: 27
KindredID: 11
Case: Sex unknown, Age unknown, French
DiseaseAssertion: VHL
FamilyInfo: None
CasePresentingHPOs: HP:0030405; HP:0002666; HP:0005584 (pancreatic endocrine tumour, pheochromocytoma, renal cell carcinoma)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P86S (c.256C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 178692 https://www.ncbi.nlm.nih.gov/clinvar/variation/178692/
CAID: N/A
gnomAD: N/A
VariantEvidence:N/A
MutationType: missense_variant;transition
CivicName: P86S (c.256C>T)
MultipleGeneVariants: N/A
P127FEA PGLMalignantVHL (c.470C>T (p.Thr157Ile)NA13
PatientID: P1
KindredID: P1
Case: F, 27Y0M, Ethnicity Unknown
DiseaseAssertion: Paraganglioma
FamilyInfo: N/A
CohortInfo: Tumour samples and paired peripheral blood samples were obtained from 39 patients, consisting of 31 PCs, seven extra adrenal PGLs and one metastasis from a malignant PC previously presenting with a PC.
CasePresentingHPOs: HP:0002668 (paraganglioma)
CaseHPOFreeText: The patient had a malignant extraadrenal paraganglioma measuring 13 mm at age 27.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: RET/SDHB/SDHD
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.T157I (c.470C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 223223 https://www.ncbi.nlm.nih.gov/clinvar/variation/223223/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: T157I (c.470C>T)
MultipleGeneVariants: N/A
251826Y26Y35NNNYNc.499C>TExon 3p.Arg167TrpMissense
PatientID: 25
KindredID: 18
Case: Sex Unknown, 35Y0M, Brazilian (Latino/Admixed American)
DiseaseAssertion: VHL
FamilyInfo: None
CasePresentingHPOs: HP:0002668, HP:0002666; HP:0030405; HP:0010797 (Paraganglioma, pheochromocytoma, pancreatic endocrine tumor, hemangioblastoma)
CaseHPOFreeText: The patient developed PPGL at 26Y of age, and a PNET at 35Y. They also presented with a CNS HB
CaseNotHPOs: HP:0005584; HP:0001737; HP:0009711; HP:0000107 (renal cell carcinoma, pancreatic cyst, retinal capillary hemangioma, renal cyst)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2218 https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954 https://gnomad.broadinstitute.org/variant/3-10191506-C-T
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
261913Y13Y47NYNNYc.371C>TExon 2p.Thr124IleMissense
PatientID: 26
KindredID: 19
Case: M, 47Y0M, Brazilian (Latino/Admixed American)
DiseaseAssertion: VHL
FamilyInfo: They had a 14Y family member (ID:27), however their relation is unclear.
CasePresentingHPOs: HP:0002666; HP:0030405; HP:0009711; HP:0000107 (pheochromocytoma, pancreatic endocrine tumor, retinal capillary hemangioma, renal cyst)
CaseHPOFreeText: The patient at 13Y was confirmed with VHL. He developed bilateral pheo at 13Y, which had recurrence at 48M later. He later at 47Y he developed a PNET. He also had renal cysts and retinal HB
CaseNotHPOs: HP:0002668; HP:0001737; HP:0010797; HP:0005584 (paraganglioma, pancreatic cyst, hemangioblastoma, renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.T124I (c.371C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 36902 https://www.ncbi.nlm.nih.gov/clinvar/variation/36902/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: T124I (c.371C>T)
MultipleGeneVariants: N/A
PatientID: 1
KindredID: A (II-5)
Case: M, 64Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: The patient's mother (I:1) died of renal cell carcinoma at age 55. The patient had seven siblings. His brother (II:3) died of cerebellar hemangioblastoma at age 39 and another (II:11), also died of cerebellar hemangioblastoma at age 33. His sister (II:7) was found to carry the mutation and presented with renal cell carcinoma, hemangioblastoma, and pheochromocytoma. Another sister (II:13) who did not undergo genetic testing, presented with hemangioblastoma. Brother (II:1) died of unknown causes and another brother (II:9) was asymptomatic and did not undergo genetic testing. The patient had four children; one was asymptomatic (III:9), another (III:6), the third (III-7) had a retinal angioma had a hemangioblastoma, and a daughter (III-8) had pheochromocytoma. Patient III-8 is the only child from this family who underwent genetic testing and was found to carry the mutation. Some of his nieces and nephews presented with VHL related phenotypes and were found to harbour the mutation. Refer to Figure 1 for family pedigree and information regarding extended family members.
CohortInfo: 10 VHL patients with renal cell carcinoma and a definite VHL family history.
CasePresentingHPOs: HP:0010797, HP:0005584, HP:0009711, HP:0002666, HP:0000107 (hemangioblastoma, renal cell carcinoma, retinal capillary hemangioma, pheochromocytoma, renal cyst)
CaseHPOFreeText: Diagnosed with renal cell carcinoma at age 42. Underwent radical nephrectomy of both the right and left side. He had five renal cell carcinomas and 15 renal cysts. The patient was on dialysis. He had a satellite lesion.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.V170D (c.509T>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 625256 https://www.ncbi.nlm.nih.gov/clinvar/variation/625256/
CAID: N/A
gnomAD: N/A
VariantEvidence:N/A
MutationType: missense_variant;transversion
CivicName: V170D (c.509T>A)
MultipleGeneVariants: N/A
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
FIP––2727Horseshoe kidney 2B
PatientID: None
KindredID: F (proband)
Case: M, 27Y0M, Hungarian
DiseaseAssertion: VHL
FamilyInfo: His mother was also found to have this mutation and she had renal cell carcinoma at age 49.
CasePresentingHPOs: HP:0009711, HP:0002666, HP:0000085 (retinal capillary hemangioma, pheochromocytoma, Horseshoe kidney)
CaseHPOFreeText: Patient developed retinal hemangiomas and unilateral pheochromocytoma at the age of 27 years. Abdominal CT showed also horseshoe kidneys.
CaseNotHPOs: HP:0010797, HP:0005584 (hemangioblastoma, renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167Q (c.500G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVar: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence:N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500 G >A)
MultipleGeneVariants: N/A
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
Methods
ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3
GenotypingMethod: PCR and direct sequencing
SamplingMethod: peripheral white blood cells
Mutations in the VHL gene was determined by direct sequencing of all coding exons and flanking intronic sequences
ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3
GenotypingMethod: Direct sequencing of coding exons and flanking intronic sequences.
SamplingMethod: N/A
PMID: 19399650
PatientID: P34
KindredID: 1
Case: M, 20Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0002666 (pheochromocytoma)
CaseHPOFreeText: diagnosed at the age of 20 years with VHL and presented with severe hypertension and a 40 mm PC of the right adrenal gland (pheochromocytoma)
CaseNotHPOs: No positive family history
CaseNotHPOFreeText: N/A
CasePreviousTesting: SDHB/ SDHD/ RET/ MEN2
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.L188P (c.563T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 625266 https://www.ncbi.nlm.nih.gov/clinvar/variation/625266/
CAID: N/A
gnomAD: N/A
VariantEvidence: also the polymorphism S69S of the SDHD gene.
MutationType: missense_variant;transition
CivicName: L188P (c.563T>C)
MultipleGeneVariants: Germline, SDHD, (p.Ser69Ser)
Mutations and polymorphisms in the SDHB, SDHD, VHL, and RET genes in sporadic and familial pheochromocytomas
PMID: 19399650
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
Thirty-five unrelated patients suspected of having von Hippel-Lindau disease were analyzed and 32 VHL gene variants were found in 35 patients using PCR and SSCP by peripheral blood leukocytes. An association of clear cell renal carcinoma development with a relatively high loss of structural stability in VHL protein missense mutations was discovered. A mutation, P154= (c.462A>G) (noted as a splice-site mutation: g.8665A>G, in the paper originally) was found in a patient with retinal hemangioblastomas, cerebellar hemangioblastomas, and pancreatic cyst, the pateints age on onset was 13 years old. The family history also included incidences of clear cell renal cell carcinoma and renal cysts.
GroupID/ KindredID: F8
Case: Sex unknown, 35Y0M, Spanish
DiseaseAssertion: assumed VHL
FamilyInfo: familial antecedents found; unknown of any additional features to index case relatives
CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)
CaseHPOFreeText: Multiple lesions were found with the patient’s retinal hemangioma. Age of onset is 35Y0M.
CaseNotHPOs: HP:0006770; HP:0002666 (clear cell renal cell carcinoma, pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167Q (c.500G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVar: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence:N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500G>A)
MultipleGeneVariants: N/A
c.99_100InsA*
PatientID: None (IV)
KindredID: 7
Case: Sex and Ethnicity unknown; Age <18Y0M
DiseaseAssertion: Asymptomatic
FamilyInfo: Total of 13 family members belonging to Family 7 (see Table 2; or follow KindredID 7)
CasePresentingHPOs: HP:0010797 (hemangioblastoma)
CaseHPOFreeText: asymptomatic upon pre- and first screening, + 1 HB by final 5 year follow up
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 16572651
SupplementalData: N/A
Variant: p.G34Rfs*98 (c.99_100insA)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: N/A
CAID: CA2018007671 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2018007671
gnomAD: N/A
VariantEvidence: N/A
MutationType: plus_1_frameshift_variant
CivicName: G34Rfs (c.99_100insA)
MultipleGeneVariants: N/A
43p.P86S>18YAffected1 Hb+ 3 Hb, 2 RCC, PCA, 1 Pheo
PatientID: None
KindredID: 43
Case: Sex and Ethnicity unknown; Age >18Y0M
DiseaseAssertion: assumed VHL
FamilyInfo: None
CasePresentingHPOs: HP:0010797; HP:0005584; HP:0002894; HP:0002666 (hemangioblastoma, renal cell carcinoma, neoplasm of the pancreas, pheochromocytoma)
CaseHPOFreeText: 1 HB at initial screening, as well as an additional 3 HB, 2 RCC, 1 pheochromocytoma, and pancreatic cancer at final screening (5 year follow up).
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 16572651
SupplementalData: N/A
Variant: p.P86S (c.256C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 178692 https://www.ncbi.nlm.nih.gov/clinvar/variation/178692/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: P86S(c.256C>T)
MultipleGeneVariants: N/A
p.F76del
PatientID: None (III)
KindredID: 1
Case: Sex and Ethnicity unknown; Age >18Y0M
DiseaseAssertion: hemangioblastoma
FamilyInfo: Total of 4 family members belonging to Family 1 (see Table 2; or follow KindredID 1)
CasePresentingHPOs: HP:0010797 (hemangioblastoma)
CaseHPOFreeText: 4 HB at first screening, and same by final screening (5 year follow up).
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 16572651
SupplementalData: N/A
Variant: p.F76del (c.227_229del)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 223166 https://www.ncbi.nlm.nih.gov/clinvar/variation/223166/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: inframe_deletion
CivicName: p.F76del
MultipleGeneVariants: N/A
20p.C162F>18YAffected2 Hb, Unilat RA, KC, PC, 1 pheo+ 1 RCC, 1 pheo
PatientID: None
KindredID: 20
Case: Sex and Ethnicity unknown; Age >18Y0M
DiseaseAssertion: assumed VHL
FamilyInfo: None
CasePresentingHPOs: HP:0010797; HP:0009711; HP:0000107; HP:0001737; HP:0005584; HP:0002666 (hemangioblastoma, retinal capillary hemangioma, renal cyst, pancreatic cysts, renal cell carcinoma, pheochromocytoma)
CaseHPOFreeText: At initial screening, patient was found with 2 HB, unilateral retinal capillary hemangioma, 1 renal cyst, 1 pancreatic cyst, and 1 pheochromocytoma. By final screening, the 5 year follow up, there was an additional RCC and pheochromocytoma.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.C162F (c.485G>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 43604 https://www.ncbi.nlm.nih.gov/clinvar/variation/43604/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: C162F(c.485G>T)
MultipleGeneVariants: N/A
Molecular and clinical analysis of 126 French VHL families tested for renal involvement revealed 92 different mutations. 90 of these families had renal involvement. The p.P86S (c.256C>T) germline variant of the VHL gene was detected in a family (ID 11). Member 319 presented with moderate renal disease (RCC). Members 600, 327, 1066 and 601 presented with severe renal disease (RCC). Members 334 and 332 had unknown renal involvement. Member 286 had no renal involvement. The paper states that this family is previously reported in PMID 12202531 and/or 9829912. Another family (ID 503) was found with this variant. Member 10602 presented with moderate renal disease (RCC) and member 10603 presented with mild renal disease. This family was not previously reported.
PatientID: 1347
KindredID: 363
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: Moderate renal disease (less than five solid lesions requiring surgical treatment, either unilateral or bilateral). Individual RCC phenotype is noted as positive.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 12202531
SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.
Variant: p.N78S (c.233A>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 93326, https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: N78S (c.233A>G)
MultipleGeneVariants: N/A
Molecular and clinical analysis of 126 French VHL families tested for renal involvement revealed 92 different mutations. 90 of these families had renal involvement. The p.R82P (c.245G>C) germline variant of the VHL gene was detected in a family (ID 12). Members 697, 752 and 2682 presented with moderate renal disease (RCC). Member 4321 presented with severe renal disease (RCC). Members 2062, 606, 607, 609, 444, 3974 and 2523 presented with unknown renal involvement. Member 5357 had no renal involvement. Member 5037 had mild renal disease and member 605 had moderate renal disease (RCC). The paper states that this family is previously reported in PMID 12202531 and/or 9829912.
Horm Res Paediatr 2016;86(suppl 1):I-IV https://doi.org/10.1159/000449141
PatientID: 1 (son)
KindredID: 1
Case: M, 9Y0M, Ethnicity Unknown
DiseaseAssertion: pheochromocytoma
FamilyInfo: Familial isolated pheochromocytoma is described as the father is a carrier of the same mutation: R79G (c.235C>G).
CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)
CaseHPOFreeText: history of fever, profuse sweating, intense headache and 190/120 blood pressure. He was currently asymptomatic with normal hormonal controls after complete tumor resection of his right adrenals
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R79G (c.235C>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 411988 https://www.ncbi.nlm.nih.gov/clinvar/variation/411988/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: N/A
MultipleGeneVariants: N/A
in seven of the asymptomatic family members.
PatientID: II-9
KindredID: 1
Case: M, Age Unknown (deceased), Turkish
DiseaseAssertion: asymptomatic
FamilyInfo: 17 family members from three generations were examined with the c.445G>T mutation and diagnosed with VHL type 2B. 11 individuals had clinical manifestations and 6 were asymptomatic carriers. This patient’s one child, 4 siblings, and more, had the mutation. See Fig. 1 for full family pedigree.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.A149S (c.445G>T) [assumed]
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 127829 https://www.ncbi.nlm.nih.gov/clinvar/variation/127829/
CAID: N/A
gnomAD: N/A
VariantEvidence: This patient passed away before testing however due to siblings and children carrying the same VHL mutation, it can be deduced that he had this variant.
MutationType: missense_variant;transversion
CivicName: A149S (c.445G>T)
MultipleGeneVariants: N/A
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
c.350G > C, p.Trp117Ser
Using polymerase chain reaction (PCR)-direct sequencing and universal primer quantitative fluorescent multiplex–PCR, 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 were examined. One proband (family 8) was found to carry the mutation c.350G>C in exon 2 of the VHL gene. The proband presented with hemangioblastoma at age 18 and renal cell carcinoma and abnormality of the pancreas at age 24. The patient had negative VHL family history. This patient was previously published in 29330336.
c.191G > C (p.Arg64Pro) in exon 1 of the VHL gene on chromosome 3.
A 17-year-old girl was referred to the Department of Endocrinology at La Rabta University Hospital for the investigation of a newly diagnosed diabetes mellitus and a severe arterial hypertension. The patient is the first child of consanguineous parents and has a family history of type 2 diabetes and dyslipidemia, but no conditions that may suspect VHL disease. Blood tests disclosed hypercalcemia and abdominal computed tomography showed bilateral adrenal tumors. A clinical diagnosis of multiple endocrine neoplasia type 2a (MEN2A) was originally suspected but genetic analysis (not further detailed) revealed the missense mutation c.191G > C (p.Arg64Pro) in exon 1 of the VHL gene. The authors concluded that the presence of pheochromocytomas and the missense mutation in VHL gene suggests type 2 VHL disease. She was further diagnosed with dyslipidemia and primary hyperparathyroidism. The patient underwent a bilateral adrenalectomy marked by normalization of blood pressure, blood glucose, calcium, and PTH levels.
KindredID: 26
GroupID: 48
GroupSize: Unknown
GroupNumberMales: Unknown
GroupNumberFemales: Unknown
GroupEthnicity: Unknown
GroupAgeRange: Unknown
DiseaseAssertion: VHL
GroupInfo: Kindred no. 26 describes a family where at least one member (unspecified how many) had this mutation in the VHL gene. Pheochromocytoma was observed in this kindred indicating VHL disease type 2.
GroupPresentingHPOs: HP:0002666 (Pheochromocytoma)
GroupHPOFreeText: Pheochromocytoma was observed in this kindred indicating VHL disease type 2.
GroupNotHPOs: N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.V170F (c.508G>T)
LegacyVariant: p.V241F (c.721G>T)
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA351756193, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.508G%3ET
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: V170F (c.508G>T)
MultipleGeneVariants: N/A
5-generation Chinese family with VHL
PatientID: IV-25
KindredID: 1
Case: F, 31Y0M, Chinese
DiseaseAssertion: Asymptomatic
FamilyInfo: Eight affected individuals in the patient’s family were retrospectively identified by reviewing medical records and from the recall of relatives. Three had passed away before 40 years of age because of central nervous system hemangioblastoma. Among the 10 living family members that carried the same NM_000551.3:c.326_339dupTCCACAGCTACCGA the patient carried, 3 had renal cysts and 1 had developed renal cell carcinoma, 2 had central nervous system hemangioblastoma, 1 had retinal hemangioblastomas, 1 was diagnosed with glioblastoma, and 5 were asymptomatic.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Gly114Serfs*50(c.326_339dupTCCACAGCTACCGA)
LegacyVariant: N/A
ClinVarID: N/A
CAID: CA2573051018 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573051018
gnomAD: N/A
VariantEvidence: N/A
MutationType: duplication
CivicName: G114fs (c.326_339dupTCCACAGCTACCGA)
MultipleGeneVariants: N/A
Recurrent polytopic chromaffin paragangliomas in a 9-year-old boy resulting from a novel germline mutation in the von Hippel-Lindau gene
PMID: 11990703
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
P86R (25) 4
GroupID: None
DiseaseAssertion: VHL
GroupSize: 4
GroupNumberMales:N/A
GroupNumberFemales:N/A
GroupEthnicity: N/A
GroupAgeRange: ≥12
GroupInfo: The four patients were grouped by mutation.
GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)
GroupHPOFreeText: N/A
GroupNotHPOs:N/A
GroupNotHPOFreeText: N/A
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P86R(c.257C>G)
LegacyVariant:N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223170 https://www.ncbi.nlm.nih.gov/clinvar/variation/223170/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: P86R(c.257C>G)
MultipleGeneVariants: N/A
P86S (26)
301 were enrolled in a prospective clinical protocol to evaluate the natural history of vHL-associated pancreatic lesions (NCT00062166). Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study. Individual patient phenotype was not described, but overall of the 60 patients, 57 had RCC, 41 had CNS hemangioblastomas, 28 had retinal hemangioblastoma, 23 had pheochromocytoma. 36/69 patients were female and the mean age was 50.5 years old. Four patients were listed with this missense mutation, c.256C>T. All patients underwent genetic testing using Sanger sequencing and Southern Blotting.
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
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
PatientID: None (Son)
KindredID: 1
Case: M, Age Unknown, Ethnicity Unknown
DiseaseAssertion:Asymptomatic
FamilyInfo: The patient's mother had pancreatic islet cell adenoma, renal cell carcinoma, extraadrenal pheochromocytoma, and spinal cord lesion. His sister had the same VHL gene mutation.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P86L (c.257C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 182977, https://www.ncbi.nlm.nih.gov/clinvar/variation/182977/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: P86L (c.257C>T)
MultipleGeneVariants: N/A
Of 246 patients affected with von Hippel-Lindau disease, 64 patients (26%) from 38 families had pheochromocytoma, including 33 newly diagnosed during screening studies and 31 treated before screening at NIH. Germline mutations in the VHL gene was determined from peripheral blood. Family 4339 were found with p.Arg176fs mutation (legacy notation c.739delA converted to NM_000551.3) in the VHL gene. Family 4339: 1/4 had pheochromocytoma, 4/4 had renal cell carcinoma, 1/4 had CNS hemangioblastoma, 1/4 had retinal angiomas, 1/4 had cysts. Individual patient phenotype-genotype was not described in the paper.
Novel MicroRNA Binding Site SNPs and the Risk of Clear Cell Renal Cell Carcinoma (ccRCC): A Case-Control Study
PMID: 33222672
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
The aim was to assess the frequency of von Hippel-Lindau disease (VHL) and the long-term prognosis of VHL and non-VHL patients among 110 consecutive patients with haemangioblastoma (HB) of the CNS treated between 1953 and 1993 at one neurosurgical unit.
The study assessed the long-term prognosis of VHL and non-VHL patients among 110 consecutive patients with haemangioblastoma (HB) of the CNS treated between 1953 and 1993 at one neurosurgical unit. 14 patients had VHL disease, but only the genotype of the patients was only described for case 8 (NM_000551.3:c.278G>C) and 11 (NM_000551.3:c.293A>G). One of these two patients had pheochromocytoma in a family member, but it is unclear which patient. Case 8 had a germline p.Gly93Ala mutation. Genotyping methods included PCR and direct sequencing. Additional phenotypes and family history were not provided on an individual level for VHL patients.
6 21.5 Retinal angioma, cysts of pancreas and kidney Yes Germline C to G base change at nucleotide 363 of exon 1, and G to T base change at −1 position of splice acceptor sequence for exon 3
PatientID: 6
KindredID: 6
Case: F, 21Y6M, ethnicity unknown
DiseaseAssertion: Assumed VHL
FamilyInfo: Positive history, with symptomatic father (no mutation known)
CasePresentingHPOs: HP:0006880; HP:0009711; HP:0001737; HP:0000107 (cerebellar hemangioblastoma; retinal capillary hemangioma; pancreatic cysts; renal cyst)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: c.464-1G>T
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 223221 https://www.ncbi.nlm.nih.gov/clinvar/variation/223221/
CAID: N/A
gnomAD: N/A
VariantEvidence: Compound heterozygous: Germline C to G base change at nucleotide 150 of exon 1, and G to T base change at -1 position of splice acceptor sequence for exon 3
MutationType: splice_site_variant
CivicName: [A50= (c.150C>G) and] Splice Site (c.463-1G>T)
MultipleGeneVariants: Germline, VHL, c.150C>G (p.Ala50Ala)
Germline G to A base change at −1 position of splice acceptor sequence for exon 2
Tumor registries from four paediatric referral centers (Lucile Salter Packard Children’s Hospital, Childrens Hospital of Los Angeles, the Johns Hopkins Hospital, and Childrens Hospital of Buffalo) were screened for all patients < / = 21 years at diagnosis of a cerebellar hemangioblastoma. Peripheral blood leukocytes were sampled and partial or entire deletions of the VHL gene or gene rearrangements were detected by quantitative Southern blot analysis. Genomic DNA was amplified by PCR, and exons 1, 2, and 3 of the VHL gene directly sequenced using SSCP. One patient with no family history for VHL was found with this c.341-1G>A mutation. The patient was 16.1Y old at cerebellar hemangioblastoma diagnosis, and also presented with retinal angioma, cervical spinal hemangioblastoma, pancreatic cysts, and renal cysts.
Hemangioblastomas and Neurogenic Polyglobulia
PMID: 23407287
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
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
VHL Variants
This report studied the prevalence of germline variants in Japanese PPGL patients. Of the 370 PPGL original Japanese probands, this cohort consisted of 15 patients with pheochromocytoma and/or paragangliomas with germline VHL varaints. Blood samples were used to examine 7 genes: MAX, SDHB, SDHC, SDHD, TMEM127, VHL, and RET, using Sanger sequencing. Of these 15 VHL patients: 10 had bilateral PCC, 4 had PCC with abdominal/thoracic PGL, and one had metastatic PPGL. The variant R167W (c.499C>T) was one of the 15 found in a patient with PPGL. Their family history or further manifestations were not detailed.
3.4. Tubulogenesis and Angiogenesis Assays of VHL versus Control BOECsUpon isolation and expansion of BOECs, it was visually clear that BOECs derived from VHL patients appeared morphologically different from healthy controls (Figure 5A). While controls appear as elongated and in closer contact, VHL BOECs are less elongated, rather rounded, and sparsely distributed. Angiogenesis can be measured in vitro by two functional assays for ECs: tubulogenesis and wound healing. VHL patient-derived BOECs showed differences compared to the control group. In the tubulogenesis assay, VHL cells displayed a significantly reduced number of closed tubules (Figure 5B). On the other hand, they were slower on average when migrating to cover the discontinuity inflicted in the confluent monolayers or wound (Figure 5C).Open in a separate windowFigure 5Morphological and functional differences between ECs derived from either healthy subjects or VHL patients. (A) Control and VHL ECs photographed under the microscope once confluence levels were reached. (B) Tubulogenesis assay performed on ECs from control vs. VHL groups, photographed 3 h after cell seeding on Matrigel-matrix-coated wells. (C) Wound healing assay performed on ECs from control vs. VHL groups, photographed 6.5 h after wound infliction on confluent wells. Error bars denote ± SEM. Student’s t-test: ** p < 0.01; and *** p < 0.001.3.5. VEGF Signaling PathwayThe VEGF signaling pathway appeared upregulated in VHL BOECs, according to the GSEA analysis (Figure 6A). Western blotting was used to check the phosphorylation of regulatory kinases belonging to the VEGFA-VEGFR2 pathway (AKT and ERK1/2) (Figure 6B).Open in a separate windowFigure 6(A) VEGF signaling pathway appeared upregulated, according to the GSEA analysis. (B) ERK1/2 and AKT phosphorylation assessment by Western Blot. Densitometric quantification of phosphorylated/total protein ratios are shown for control subject (n = 2) or VHL patients (n = 2). Error bars denote ± SEM. Student’s t-test: * p < 0.05 and *** p < 0.001.3.6. VHL ECs Have Higher Expression of ROSFigure 7A shows a table collecting genes involved in the ROS metabolism, which are downregulated in VHL ECs. Accordingly, a measure of ROS was made from in vitro cultures of control and VHL-derived ECs. In Figure 7B, a representative histogram of the results is depicted. As expected, and supporting the RNAseq results, we found that VHL ECs have on average almost double the amount of ROS than their non-VHL counterpart.Open in a separate windowFigure 7(A) ROS metabolism modulation in RNAseq analysis in VHL ECs. (B) ROS levels in control and VHL cells, showing a significant increase in VHL samples. Error bars denote ± SEM. Student’s t-test: ** p < 0.01.3.7. VHL Gene Expression in VHL Patients’ ECsNo differences in VHL gene expression were found between the patients and the control group, despite the heterozygosis of the patients in the VHL gene. This result could be explained by the type of mutation these patients present: four out of five present missense mutations (Table 1, Figure 3). Only in sample 4, where the mutation affects the splicing site of the DNA, the RNA levels show a lower tendency, although not significant (Table S1). In order to visualize the translational effect of the patients’ mutations, we mapped them on the 3D structure of pVHL, highlighting the changes in amino acids (Figure 8A,B). The altered amino acids fall within areas of close contact between the different subunits, which could affect its proteolytic activity and the assembly of a functional proteasomal complex. Proper folding of the protein, an altered interaction with the substrates, or assembly of the E3 ligase complex, which most likely lead to its loss of function. Further computational analysis should be performed to elucidate the definite cause of how those mutations impair protein function.Open in a separate windowFigure 8(A) 3D complex structure (PDB ID: 4AJY) of the von Hippel–Lindau protein (yellow), Elongin B (green), and Elongin C (purple), bound to Hif1- alpha peptide (depicted in dark blue), highlighting the heterodimerization interface of this complex in a gray box and the position of the R64P mutation. (B) Inset of the VHL-ELOb/c interface with their respective involved amino acids are represented as sticks, while the relevant mutation positions are represented with spheres and labelled in bold. (C) Confocal staining of sample V1 (p.R167Q) shows the distribution of pVHL in the cell cytoplasm, distributed in the perinuclear region in VHL cells and throughout the cell in control ones.A misfolding of the protein could explain the differential distribution of pVHL in sample V1 (p.R167Q). Confocal staining of ECs shows that pVHL accumulates in the perinuclear region. This result suggests a likely aggregation of pVHL in endoplasmic reticulum cysts. Conversely, control ECs show a more heterogeneous distribution of pVHL throughout the cytoplasm (Figure 8C). We believe that these differences in cellular pVHL distribution are caused by the mutations in pVHL present in this patient.
missense
PatientID: 56
KindredID: None
Case: Age and Sex unknown, Chinese
DiseaseAssertion: VHL
FamilyInfo: None
CasePresentingHPOs: HP:0010797; HP:0001737; HP:0000107; HP:0009711; HP:0005584 (hemangioblastoma, pancreatic cysts, renal cyst, retinal capillary hemangioma, renal cell carcinoma)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0002666; HP:0030405; HP:0030393 (Pheochromocytoma, Pancreatic endocrine tumour, Endolymphatic sac tumour)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Yes; See Suppl 1 (Supporting table)
Variant: p.N131K (c.393C>G)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: N/A
CAID: CA351753948 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.393C%3EG
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: N131K (c.393C>G)
MultipleGeneVariants: N/A
14EP 1.0VVHLVHL({"type":"entrez-nucleotide","attrs":{"text":"NM_000551.4","term_id":"1779521775","term_text":"NM_000551.4"}}NM_000551.4):c.407T>G (p. Phe136Cys)
PatientID: 14
KindredID: 1
Case: Sex Unknown, Age Unknown, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: N/A
CaseHPOFreeText: Unclear the exact manifestations; only stated VHL
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: MAX, NF1, RET, SDHA, SDHB, SDHC, SDHD, TMEM127
PreviouslyPublished: N/A
SupplementalData: Yes
Variant: p.F136C (c.407T>G)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 496065 https://www.ncbi.nlm.nih.gov/clinvar/variation/496065/
CAID: N/A
gnomAD: N/A
VariantEvidence: Described by authors as likely pathogenic.
MutationType: missense_variant;transversion
CivicName: F136C (c.407T>G)
MultipleGeneVariants: N/A
The VHL mutation pattern includes point mutations, small deletions and large deletions.
This paper analyzed the VHL gene of 21 patients who had clinical a clinical diagnosis of VHL, familial pheochromocytoma, or sporadic pheochromocytoma. 7 patients were from 3 families, while the remaining 14 were unrelated. Mutations were detected by realtime quantitative PCR (RQ-PCR) assays using peripheral venous blood. The mutation (c.499C>T) was found in 1 individual (33Y, M), without family history, who presented with pheochromocytoma, hypertension and diabetes mellitus. This case was also later presented in PMID: 24735130 (Pai et al, 2014). ACMG evidence codes: 'PP2' because they observe a missense variant in a gene where missense variants are a common mechanism of disease.
PatientID: 1
KindredID: 1
Case: F, 16Y0M, Ethnicity Unknown
DiseaseAssertion: VHL
FamilyInfo: Proband's father (M) had an operation for spinal tumor 9 years before, and renal cell carcinoma was detected during the screening. Proband's uncle (M) had an operation for a benign cervical spinal mass 27 years before, and a chondrosarcoma of the right femur 10 years before. He also had renal cell carcinoma. Both died owing to the disease, and no genotyping information is available for either. Proband's sister (20, F) was healthy. See Figure 1 for pedigree, including extended family phenotypic information.
CasePresentingHPOs: HP:0006748, HP:0009711 (adrenal pheochromocytoma, retinal capillary hemangioma)
CaseHPOFreeText: The proband had bilateral adrenal pheochromocytoma and a hemangioblastoma in the right eye. She was diagnosed with VHL type 2B. Four years post surgery, the patient remained well with no clinical or radiological evidence of recurrent disease. At her last visit, abdominal ultrasonography showed an angiomyolipoma 8 mm in diameter in her left kidney.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167Q (c.500G>A)
LegacyVariant: p.R167Q (c.713G>A)
CaseProblemVariantFreeText: N/A
ClinVarID: 2216, https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977, https://gnomad.broadinstitute.org/variant/3-10191507-G-A?dataset=gnomad_r2_1
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500G>A)
MultipleGeneVariants: N/A
Toenail DNA was genotyped using the Sequenom MassARRAY platform.
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: Sequenom MassARRAY platform was used to genotype the DNA
SamplingMethod: Toenail clippings
T152I missense mutation
PatientID: None (sister)
KindredID: 2
Case: F, Age unknown, Ethnicity Unknown
DiseaseAssertion: asymptomatic
FamilyInfo: Her sister and mother were found to carry the same mutation. Her mother was asymptomatic too (aged 48Y), while her sister (aged 25Y) was operated on for a carotid body tumour.
CasePresentingHPOs: None
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: An extensive clinical/physical examination was conducted: laboratory tests (urinary metanephrine and normetanephrine, plasma chromogranin A), an ophthalmoscopic examination and radiological exams (NMR of the brain, CT scan of the thorax and the abdomen) - all tests were normal.
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.T152I (c.455C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: N/A
CAID: CA351754382 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.455C%3ET
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: T152I (c.455C>T)
MultipleGeneVariants: N/A
PatientID: IV-6
KindredID: 2
Case: M, Age Unknown, German
DiseaseAssertion: VHL
FamilyInfo: Family 2 is comprised of 131 individuals over six generations including 65 members (50% of those at risk) with VHL type 2A (72% clinically affected, 12% obligate carriers, and 15% positive genetic analysis alone) and nearly equal gender distribution for affected status (54% male). An additional six members (II-3, II-4, II -5, III-1, III-2, and III-3) are suspected to have VHL without confirmation. Of note, the nuclear family (branch IV-13) contains 13 siblings, of whom 12 have been diagnosed with pheo. The presenting tumor types in Family 2 were pheo (70%), HB (17%), and RA (13%). No Family 2 member had RCC as the initial manifestation. Distribution of HB and RA are not described except for patient IV-8.
CasePresentingHPOs: HP:0002666 (Pheochromocytoma)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0005584 (Renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 7759077
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2223, https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: N/A
gnomAD: 0.00001343, https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
PatientID: V-16
KindredID: 2
Case: F, Age Unknown, German
DiseaseAssertion: VHL
FamilyInfo: Family 2 is comprised of 131 individuals over six generations including 65 members (50% of those at risk) with VHL type 2A (72% clinically affected, 12% obligate carriers, and 15% positive genetic analysis alone) and nearly equal gender distribution for affected status (54% male). An additional six members (II-3, II-4, II -5, III-1, III-2, and III-3) are suspected to have VHL without confirmation. Of note, the nuclear family (branch IV-13) contains 13 siblings, of whom 12 have been diagnosed with pheo. The presenting tumor types in Family 2 were pheo (70%), HB (17%), and RA (13%). No Family 2 member had RCC as the initial manifestation. Distribution of HB and RA are not described except for patient IV-8.
CasePresentingHPOs: N/A
CaseHPOFreeText: Deceased.
CaseNotHPOs: HP:0005584; HP:0002666 (Renal cell carcinoma, Pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 7759077
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2223, https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: N/A
gnomAD: 0.00001343, https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
PatientID: IV-12
KindredID: 2
Case: M, Age Unknown, German
DiseaseAssertion: VHL (Asymptomatic)
FamilyInfo: Family 2 is comprised of 131 individuals over six generations including 65 members (50% of those at risk) with VHL type 2A (72% clinically affected, 12% obligate carriers, and 15% positive genetic analysis alone) and nearly equal gender distribution for affected status (54% male). An additional six members (II-3, II-4, II -5, III-1, III-2, and III-3) are suspected to have VHL without confirmation. Of note, the nuclear family (branch IV-13) contains 13 siblings, of whom 12 have been diagnosed with pheo. The presenting tumor types in Family 2 were pheo (70%), HB (17%), and RA (13%). No Family 2 member had RCC as the initial manifestation. Distribution of HB and RA are not described except for patient IV-8.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0005584; HP:0002666 (Renal cell carcinoma, Pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 7759077
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2223, https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: N/A
gnomAD: 0.00001343, https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
von Hippel-Lindau (VHL) disease is an autosomal dominant familial cancer syndrome predisposing to the development of retinal and central nervous system haemangioblastomas, pheochromocytomas, renal and pancreatic cancer. In the course of a molecular analysis conducted to detect germline mutations of this gene in von Hippel-Lindau patients and individuals affected by sporadic tumors, we have identified a case of somatic mosaicism in the asymptomatic mother of a VHL patient who was subsequently diagnosed with pheochromocytoma. This is the first report providing molecular evidence of somatic mosaicism in von Hippel-Lindau disease. Mosaicism could provide some genetic explanation for the clinical heterogeneity and variable severity of the VHL phenotype, and should be considered, as a possible event when evaluating sporadic cases of VHL or patients with isolated VHL-related tumors. Hum Mutat 15:114, 2000.
PatientID: mother
KindredID: 1
Case: F, 48Y0M, Ethnicity Unknown
DiseaseAssertion: assumed VHL
FamilyInfo: The 50 year-old husband and 22 year-old sister were asymptomatic. Her 26 year-old son displayed pheochromocytoma, renal cysts, cerebellar hemangioblastoma, and retinal capillary hemangioma. He presented with the c.481C>G mutation.
CasePresentingHPOs: HP:0000107; HP:0002666 (renal cyst; pheochromocytoma)
CaseHPOFreeText: Originally referred to as referred to as totally asymptomatic, until testing on her son. A renal ultrasound revealed the presence of bilateral micro-cysts; a CT scan detected a pheochromocytoma that was subsequently removed. Both were clinically silent.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R161G (c.481C>G)
LegacyVariant: p.R161G (c.694C>G)
CaseProblemVariantFreeText: N/A
ClinVarID: 618484 https://www.ncbi.nlm.nih.gov/clinvar/variation/618484
CAID: N/A
gnomAD: N/A
VariantEvidence: Despite the identical bandshifting to her son, there were differences in the intensity of the aberrant bands (Fig.1a), suggested that the mother could be a somatic mosaic. To test this hypothesis the molecular analysis was repeated on tissues of different embryonic origin. DNA extracted from the mother's buccal mucosa showed higher levels of intensity of the same altered bands (Fig. 1b). The amplification products of exon 3 of the two mutated individuals were subjected to Fok I digestions that further confirmed the presence of mosaicism in the mother, as evidenced by the lower intensity of the fragments generated by the newly created restriction site (Fig.2).
MutationType: missense_variant; transversion
CivicName: R161G (c.481C>G)
MultipleGeneVariants: N/A
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
Peripheral blood from unrelated patients with pheochromocytoma was tested for mutations of proto-oncogene RET, tumor suppressor gene VHL, succinate dehydrogenase subunit D (SDHD) gene, and the succinate dehydrogenase subunit B (SDHB) gene. Of 271 patients with nonsydromic pheochromocytoma and no family history of the disease, 30 mutations were found in VHL. Multiple pheochromocytomas were statistically more frequent among patients with mutations than among patients without mutations (21 of 66 vs. 5 of 205, P<0.001). The mutation R161P (c.482G>C) was detected in the patient, referred to in the paper by c.695G>C due to a difference in transcript sequence. This missense mutation was found in the VHL gene and one patient with pheochromocytoma.
Mutation analysis revealed positive mutation in exon 3 of VHL gene at 167th position of amino acid Arg (arginine) is replaced by Gln (glutamine) happens due to CGG-CAG a single nucleotide change.
The case report details a 26-year-old male (case 4) presenting with cerebellar hemangioblastoma. Four years later, he was diagnosed with pancreatic endocrine tumour, pheochromocytoma, and pancreatic cysts. Mutation analysis reveals a c.500G>A change. The patient had family history of VHL. ACMG code "PS1", as this is the same mutation as a previously described pathogenic variant.
c.482G>A (p.Arg161Gln)
The medical records of 78 Korean patients with pheochromocytoma (PCC) and paragangliomas (PGL) were examined, 61 patients were diagnosed with PCC and the other 17 patients with PGL. 57 patients were included in the study. After excluding patients, 57 patients underwent sequencing. 14 patients received Sanger sequencing in pre-NGS period, while the other 43 patients underwent genetic testing by either direct sequencing (n=2) or targeted NGS (n=41) in the post-NGS period. 28 patients were found to have germline mutations in 7 PPGL-related genes (SDHB, RET, VHL, NF1, MAX, SDHA, and SDHD). Out of the 28 patients, 6 patients had germline mutations in VHL (5 presented with Pheochromocytoma and 1 with Paraganglioma). This patient was diagnosed with PCC due to bilateral adrenal mass and was found to have a R161Q(c.482G>A) missense variant in the VHL gene, which was detected by targeted NGS.
8 F/49 PCC VHL 1 c.262T>C (p.Trp88Arg) Pre-NGS Sanger Bilateral adrenal Metastatic No RCC, hemangioblastoma of cerebellum Incidental Silent
PatientID: 8
KindredID: 8
Case: F, 49Y0M, Korean
DiseaseAssertion: Assumed VHL
FamilyInfo: No information provided.
CasePresentingHPOs: HP:0006748; HP:0005584; HP:0006880 (adrenal pheochromocytoma, renal cell carcinoma, cerebellar hemangioblastoma)
CaseHPOFreeText: The patient presented with adrenal pheochromocytoma. She also had other tumours, including renal cell carcinoma and cerebellar hemangioblastoma (see table 3).
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: RET, NF1, MAX, SDHA/SDHAF2/SDHB/SDHC/SDHD
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.W88R (c.262T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 496053, https://www.ncbi.nlm.nih.gov/clinvar/variation/496053/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: W88R (c.262T>C)
MultipleGeneVariants: N/A
c.337C > Tp.Arg113X
43 Italian patients were molecularly analyzed for Von Hippel-Lindau disease based on clinical suspicion. Peripheral blood samples were directly sequenced on an automatic sequencer (ABI 3100, Applied Biosystems, Foster City, CA) and real-time quantitative PCR (RQ-PCR) was used to detect partial or complete VHL gene deletions. One of the 43 patients (Patient ID 1) was found to have the mutation c.337C>T leading to an early stop codon. The patient had multiple hemangioblastomas and renal cell carcinoma. This patient had family history of the disease and was classified as A1 by the authors (families meeting current VHL diagnostic criteria with involvement of at least three VHL tumors in two distinct organs).
recognized in a large family that originated in Newfoundland but has some members who live in New Brunswick and Ontario. A collaborative investigation was begun in 1982 to document the number of affected members and the extent of their disease and to improve management of the disease. The condition has been documented in 38 members of the family, 28 living and 10 dead. The most common manifestations are retinal angioma (present in 60% of the gene carriers) and pheochromocytoma (present in 53%). Of the 28 living affected members 14 had been identified before the study began. Only 3 of the 14 patients in whom the disease was subsequently diagnosed presented with symptoms; in the remaining 11 the condition was detected by routine screening. Overall the mean age at the time of diagnosis was 23 years; in the 21 affected members of the fourth generation it was 18 years.
PatientID: IV-34
KindredID: 1
Case: F, Age Unknown, Ethnicity Unknown
DiseaseAssertion: Assumed VHL
FamilyInfo: 38 family members had been affected at the date of 1986, and 10 had passed away. Pheochromocytoma, cerebellar, spinal and retinal hemangioblastomas, and various cysts were clinical manifestations of VHL seen throughout the family. This patient (IV-34) appears to have inherited this disease from her mother, along with many of her siblings. See Fig. 1 for family pedigree.
CasePresentingHPOs: HP:0002666; HP:0009711 (pheochromocytoma, retinal capillary hemangioma)
CaseHPOFreeText: This member was examined in St. Johns at the Memorial University of Newfoundland. She had pheochromocytoma and retinal angiomas which were not further described.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167W (c.499C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: Although never given at the time of this publication, the germline mutation is confirmed in this family in later publications (PMID 7987306; 29437867) for this specific family. It is only here assumed this member had the VHL mutation.
ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/
CAID: N/A
gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167W (c.499C>T)
MultipleGeneVariants: N/A
The data of 18 patients with solid renal tumours associated with VHL disease were analyzed. All patients except for Patient 12 came from families with a definite VHL family history (the paper does not provide further details on this.) The patients came from 12 Chinese families and 5 were from the same family. Extrarenal manifestations of VHL disease were detected in 17 patients. Of 18 patients, 15 (including 6 asymptomatic) volunteered for DNA testing as previously described. Patients 6 and 7 had genetic testing and were found to have the same germline frameshift mutation c.447del (p.Asn150Ilefs*)(noted as c.661delA in the paper due to a difference in the VHL reference sequence notation used.). It is unclear if these patients are related. Patient 7 had family study DNA test as their reason for treatment. Patient 6 was a 50-year-old female with a medical history of synchronous bilateral solid renal tumors some which were further characterized as clear cell RCC, multiple renal cysts, pancreatic cyst. Patient 7 was a 48-year-old male with a medical history of solid renal tumours some which were further characterized as clear cell RCC, multiple renal cysts, CNS hemangioblastoma , pancreatic cyts. AMCG evidence codes: ’PP4’ because the patients phenotype is highly specific for a mutation in the VHL gene.
PatientID: 16
KindredID: 16
Case: F, 50Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0009726; HP:0010797 (Renal neoplasm, Hemangioblastoma)
CaseHPOFreeText: Patient 16 had genetic testing and was found to have a germline mutation c.286C>T (Gln96*).
CaseNotHPOs:None
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Q96* (c.286C>T)
LegacyVariant: c.499C>T
CaseProblemVariantFreeText: N/A
ClinVar: 428804, https://www.ncbi.nlm.nih.gov/clinvar/variation/428804/
CAID: CA351750811
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_transition
CivicName: Q96* (c.286C>T)
MultipleGeneVariants: N/A
PMID: 23143947
PatientID: CIV:7
KindredID: C
Case: F, 29Y0M, Chinese
DiseaseAssertion: assumed VHL
FamilyInfo: A 4-generation family is given with 3 confirmed members with this mutation. 3 additional members had VHL-presenations however had not been tested for the gene.
CasePresentingHPOs: HP:0002666; HP:0010797 (pheochromocytoma, hemangioblastoma)
CaseHPOFreeText: initially diagnosed by genetic analysis and further verified radiologically and surgically - found with CNS hemangioblastomas and pheochromocytoma at 29Y.
CaseNotHPOs: HP:0005584; HP:0001737; HP:0009711 (renal cell carcinoma, pancreatic cysts, retinal capillary hemangioma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.S80I (c.239G>T)
LegacyVariant: p.S80I (c.452G>T)
CaseProblemVariantFreeText: N/A
ClinVarID: 625229 https://www.ncbi.nlm.nih.gov/clinvar/variation/625229/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: S80I (c.239G>T)
MultipleGeneVariants: N/A
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
775 C>G (L188V)
Study of a German family of 16 family members with cosegregation of the pheochromocytoma-only phenotype with two concurrent germline mutations in the VHL protein alpha and beta domains. These mutations were c.562 C>T (stated as 775C>G in the paper which used the Latif sequence as reference) and c.241C>T (stated as 454C>T in the paper). Patient 1 was unaffected and had the wild-type allele. His spouse, patient 2, presented with pheochromocytoma and had both mutations. They had four children; one had a pheochromocytoma and died, two (patients 5 and 7) had both mutations and presented with pheochromocytomas, and one child (patient 6) was unaffected and carried neither mutation. Patient 7 had a child (patient 9) who also carried both mutations and presented with pheochromocytoma. In the other branch of the family, patient 3 who carried both mutations and presented with pheochromocytoma had a child with patient 4 who was unaffected. Their child (patient 8) carried both mutations and presented with pheochromocytoma. Patient 8 had two children; one who did not carry the mutation and was unaffected (patient 10) and another that carried both mutations but was disease-free (patient 11). DNA was isolated with whole blood and denaturing high-performance liquid chromatography (DHPLC) and dye terminator method on an ABI Prism 310 genetic analyzer (Applied Biosystems, Weiterstadt, Germany) were used for sequencing. Cosegregation with disease in multiple affected family members in a gene definitively known to cause the disease (ACMG code: PP1).
Germline mutations in the vhl gene in patients presenting with phaeochromocytomas
PMID: 9663592
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
Coexpression of Erythropoietin and Erythropoietin Receptor in Von Hippel-Lindau Disease–Associated Renal Cysts and Renal Cell Carcinoma
PMID: 15709172
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
Pedigree analysis, diagnosis and treatment in Von Hippel-Lindau syndrome: A report of three cases
PMID: 29616089
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
c.500G > A
74 patients (38 males, 36 females; 24 with prior sequencing data) with pheochromoctyoma were first analyzed by denaturing high performance liquid chromatography (dHPLC). PCR of all exons of VHL was performed on leukocyte DNA extracted from stored blood samples, and those showing variance were sequenced. In addition, 35 positive controls were used to confirm this method. This patient was a positive control who has been previously sequenced (not referenced). One patient was found with the R167Q (c.500G>A) VHL mutation. No family history was mentioned or clearly stated of their phenotypes.
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
Overexpression of EGFR and TGFα in von Hippel-Lindau-Related Central Nervous System Hemangioblastomas
PMID: 32432044
Gene: VHL
StandardizedReferenceSequence: NM_000551.3
16 patients
PatientID: 3
KindredID: 3
Case: Sex Unknown, 38Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: Patient had family history of VHL disease. The patient’s aunt and her son had the same mutation, but no clinical manifestations. The patient’s mother, another aunt and her son had hemangioblastomas at age 30, 33, and 32, respectively, but died prior to genetic testing could be performed.
CohortInfo: 16 Chinese patients clinically diagnosed with VHL disease.
CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001732 (hemangioblastoma; renal cell carcinoma; abnormality of the pancreas)
CaseHPOFreeText: The patient presented with a hemangioblastoma at age 28, as well as renal cell carcinoma at age and abnormality of the pancreas at age 38.
CaseNotHPOs: HP:0009711, HP:0002666, HP:0030393, (retinal capillary hemangioma, pheochromocytoma, endolymphatic sac tumor)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.N90I (c.269A>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 223172, https://www.ncbi.nlm.nih.gov/clinvar/variation/223172/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: N90I (c.269A>T)
MultipleGeneVariants: N/A
germline mutations
Mutational analysis for 16 patients with clinically diagnosed VHL disease, revealed 12 germline mutations. This nonsense mutation was found in 2 unrelated families. One family of 3 had a asymptomatic 27-year-old female, a 27-year-old male with epididymal cystadenoma, and a 55-year old with hemangioblastomas of the central nervous system, renal cell carcinoma, and pancreatic cysts (proband no. 10). The other VHL family had 2 individuals with hemangioblastomas of the central nervous system (proband no. 11).
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
his maternal grandmother (71 years)
PatientID: None
KindredID: 1
Case: F, 71Y0M, Danish
DiseaseAssertion: Asymptomatic
FamilyInfo: The patient's father died of acute myeloid leukaemia at age 63. The patient had four children one of whom had the same VHL mutation as her and presented with breast cancer. That child had three sons all of whom carried the VHL mutation. Two of the sons were asymptomatic and one had renal cell carcinoma. The affected son also had a P2P mutation. See Figure 1 for family pedigree.
CasePresentingHPOs: N/A
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P81S (c.241C>T)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2233 https://www.ncbi.nlm.nih.gov/clinvar/variation/2233/
CAID: N/A
gnomAD: 0.0002179 https://gnomad.broadinstitute.org/variant/3-10183772-C-T
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName:P81S (c.241C>T)
MultipleGeneVariants: N/A
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
24 c.227_229delTCT p.Phe76del p.F76del Sporadic VHL
Between 1994 and 2001, the Dutch VHL working group conducted DNA analysis on 146 probands with VHL-associated manifestations. DNA of probands was extracted from peripheral blood samples. Exons 1, 2 and 3 of the VHL gene and their flanking untranslated and intronic coding sequences were amplified by PCR and subjected to semi-automated sequence analysis. Screening for structural rearrangements, including deletions, involving the VHL gene was performed by Southern blot analysis and the multiplex ligation-dependent probe amplification (MLPA) assay. Deletions encompassing the entire VHL gene were confirmed by FISH analysis on lymphocytes from affected individuals. VHL mutations were identified in 43 families. This in-frame deletion variant (c.227_229delTCT) was detected in 2 VHL families: 24 and 25. Family no. 24 was a type 2 family with 1 patient with central nervous system hemangioblastoma, pheochromocytoma, renal cell carcinoma, and epididymal cysts. They were identified as sporadic with their parents being excluded from having a germline mutation, although they were not available for DNA analysis. Family no.25 had 2 members with retinal hemangioblastomas and renal cell carcinoma, as well as 1 member with CNS hemangioblastoma. This was published in a future publication: PMID: 32179488.
14 Missense p.(Arg64Pro) 0 2
GroupID: 14
DiseaseAssertion: VHL
Group size: 2
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, two individual was suspected of VHL disease, but neither developed RH.
GroupPresentingHPOs: N/A
GroupHPOFreeText: N/A
GroupNotHPOs: HP:0009711 (retinal capillary hemangioma)
GroupNotHPOFreeText: This VHL patients did not present with retinal capillary hemangioma.
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: Table S1
Variant: p.R64P (c.191G>C)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2226, https://www.ncbi.nlm.nih.gov/clinvar/variation/2226/
CAID: N/A
gnomAD: N/A
VariantEvidence: Chr3(GRCh37): g.10183722G>C
MutationType: missense_variant; transversion
CivicName: R64P (c.191G>C)
MultipleGeneVariants: N/A
c.407T>C1 (1)141HBc, HBsc, RCC, Cr, Cp
GroupID: None
Case: Sex Unknown, 41Y0M, Dutch
DiseaseAssertion: VHL
FamilyInfo: N/A
CasePresentingHPOs: HP:0006880; HP:0009713; HP:0005584; HP:0000107; HP:0001737 (Cerebellar hemangioblastoma, Spinal hemangioblastoma, Renal cell carcinoma, Renal cyst, Pancreatic cysts)
CaseHPOFreeText: Diagnosed with VHL Type 1.
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 31087189
SupplementalData: N/A
Variant: p.F136S (c.407T>C)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 496064, https://www.ncbi.nlm.nih.gov/clinvar/variation/496064/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: F136S (c.407T>C)
MultipleGeneVariants: N/A
c.340+1G>A
Data was collected from 82 VHL mutation carriers in the Dutch VHL surveillance program. One patient was found with this splice varaint in the VHL gene. The patient was 32Y at the last follow-up and presented with: retinal hemangioblastoma, cerebellar hemangioblastoma, spinal cord hemangioblastoma, renal cell carcinoma, renal cysts and pancreatic cysts. Family history was not described. This cohort was published later in PMID 31087189.
c.533T>G p.Leu178Arg
PatientID: None (proband 10’s son)
KindredID: 10
Case: M, 30Y0M, Chinese
DiseaseAssertion: VHL
FamilyInfo: Patient’s father was found with hemangioblastoma diagnosed at 39Y, as well as retinal capillary hemangioma, renal cell carcinoma and pancreatic cysts diagnose at 57Y
CasePresentingHPOs: HP:0005584 (renal cell carcinoma)
CaseHPOFreeText: patient had RCC diagnosed at 30Y
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.L178R (c.533T>G)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 625261 https://www.ncbi.nlm.nih.gov/clinvar/variation/625261/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transversion
CivicName: L178R (c.533T>G)
MultipleGeneVariants: N/A
223_224insT
PatientID: 4
KindredID: 4
Case: F, 24Y0M, Korean
DiseaseAssertion: VHL
FamilyInfo: Family history involved.
CasePresentingHPOs: HP:0010797; HP:0009711 (hemangioblastoma, retinal capillary hemangioma)
CaseHPOFreeText: N/A
CaseNotHPOs: N/A
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.F75Yfs*57 (c.222_223insT)
CaseProblemVariantFreeText: paper states 2 mismatched protein changes vs cDNA changes: c.223_224insT matches with p.F76Lfs*56. To get the given protein sequence they use: p.I75fs, the mutation should be c.222_223insT.
LegacyVariant: N/A
ClinVar: N/A
CAID: CA2499306953 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499306953
gnomAD: N/A
VariantEvidence: N/A
MutationType: plus_1_frameshift_variant
CivicName: F76Lfs*56 (c.224dup)
MultipleGeneVariants: N/A
709 G-->T transversion present in all affected subjects and in four presymptomatic children.
PatientID: II:10
KindredID: 1
Case: F, Age Unknown (deceased), Jewish
DiseaseAssertion: VHL
FamilyInfo: This kindred of Jewish-Kurdish origin consisted of 3 generations of 25 members. 7 were clinically affected subjects with pheochromocytoma (5 of which had the confirmed mutation - I:1, II:2, II:4, II:7 and II:9, as the other 2, II:5 and II:10 were said to have passed due to complications of the disease - prior to any genetic testing), and 4 others were carriers, or pre-symptomatic (III:1, III:3, III:7 and III:12). Subject 11:7 developed a cerebellar hemangioblastoma 25 yr after his initial diagnosis of pheochromocytoma, leading to the clinical diagnosis of VHL in the kindred.
CasePresentingHPOs: HP:0002666 (pheochromocytoma)
CaseHPOFreeText: patient had unilateral pheochromocytoma. She was said to have died of complications of the disease, and although genotype was not established prior, it is assumed that she carried the same VHL mutation
CaseNotHPOs: HP:0005584 (renal cell carcinoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: 33471715
SupplementalData: N/A
Variant: p.V166F (c.496G>T) [assumed]
LegacyVariant: p.V166F (c.709G>T)
CaseProblemVariantFreeText: N/A
ClinVarID: 2224, https://www.ncbi.nlm.nih.gov/clinvar/variation/2224/
CAID: N/A
VariantEvidence: N/A
VariantEvidence: N/A
MutationType: missense_variant;transversion
CivicName: V166F (c.496G>T)
MultipleGeneVariants: N/A
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
407 C/T (F136S)
This paper presents the first case of VHL associated with acute myeloid leukemia. The patient is reported to have the 407 C/T (F136S) mutation of the VHL gene. He was admitted at the time of the study (38Y) with significant anemia, increased number of leukocytes and pneumonia. He had a history of renal cell carcinoma and a hemangioblastoma in his brainstem (medulla oblongata). Three years later he had recurrent renal cell carcinoma followed by a massive hematuria, dilated cardiomyopathy, complex valves defect, severe central sleep apnea, anemia, leukocytosis, moderate thrombocytopenia and erosive gastritis. Physical examination revealed a heart murmur and splenomegaly (confirmed by ultrasound). Prolonged bone marrow aplasia resulted in severe interstitial pneumonia and septicemia. The patient died from respiratory failure. The autopsy revealed a pulmonary edema, massive hyperemia of the left lower lobe with pneumonia confluens.
Paired whole-exome sequencing (WES), Sanger sequencing and immunohistochemistry (IHC)
ArticleReferenceSequence: NM_000551.3
GenotypingMethod: Paired whole-exome sequencing (WES), Sanger sequencing, and immunohistochemistry (IHC)
SamplingMethod: peripheral blood
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
A previous study of 26 Japanese, VHL families was extended to 41 additional families. Germline mutations were detected in 55 of 77 Japanese families using SSCP, direct sequencing, and Southern Blot analysis of peripheral blood samples. The L178P (c.533T>C) germline mutation was found in a VHL type 1 patient presenting with CNS hemangioblastoma, retinal angioma and renal cell carcinoma (family ID 34). This family was previously reported in PMID 8634692.
R238W
Screening of 3 patients affected with familial PC for mutations in the RET proto-oncogene (mutations related to MEN 2 syndrome) and the VHL tumor suppressor gene (mutations related to VHL disease) with the use of PCR, SSCP, heteroduplex analysis, and direct sequencing, revealed missense VHL gene mutations. Please note that there was no clinical diagnosis of VHL disease. This missense mutation c.499C>T was found in a Polish family with 3 siblings (two male siblings and their mother) with no evidence of RET; the older brother presented with unilateral pheochromocytoma at 15Y, the younger brother presented with bilateral pheochromocytoma at 11Y, and the mother presented with bilateral pheochromocytoma at 41Y. Additional phenotypic information was not provided. Please note that the paper states the mutation as c.712C>T because it uses a legacy reference sequence.
The genotype and phenotype in the large Chinese family with VHL disease. a The pedigree of the family 6 with 18 affected patients. b DNA sequence analysis showing a A–G transition at nucleotide 446. The change results in the mutation from Asn to Ser in codon78
PatientID: II-5
GroupID/ KindredID: 6
Case: Age unknown (deceased), M, Chinese
DiseaseAssertion: hemangioblastoma
FamilyInfo: Positive - 22 family members were recorded with the given mutation. 18 had VHL manifestations while 4 were asymptomatic carriers. See pedigree (Fig 3.), or follow GroupID/KindredID: 6
CasePresentingHPOs: HP:0010797 (hemangioblastoma)
CaseHPOFreeText: N/A
CaseNotHPOs: HP:0005584; HP:0009711; HP:0001732; HP:0002666 (Renal cell carcinoma, retinal capillary hemangioma, abnormality of the pancreas, pheochromocytoma)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.N78S (c.233A>G)
CaseProblemVariantFreeText: No VHL gene test was conducted but due to substantial family pedigree history, can assumed with confidence this mutation
LegacyVariant: p.N78S (c.446A>G)
ClinVarID: 93326 https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: N78S (c.233A>G)
MultipleGeneVariants: N/A
C>T substitution at nucleotide 470 (Pro86Leu)
GroupID/ KindredID: 10
DiseaseAssertion: assumed VHL
GroupSize: 4
GroupNumberMales: N/A
GroupNumberFemales: N/A
GroupEthnicity: Chinese
GroupAgeRange: N/A
GroupInfo: With a family history, 4 family members were recorded in this group with the given mutation.
GroupPresentingHPOs: HP:0005584; HP:0001732; HP:0010797; HP:0009711 (Renal cell carcinoma, abnormality of the pancreas, hemangioblastoma, retinal capillary hemangioma)
GroupHPOFreeText: 2 members had renal cell carcinoma, 1 had an abnormality of the pancreas, 1 had a CNS hemangioblastoma, and 1 had retinal capillary hemangioma
GroupNotHPOs: HP:0002666 (pheochromocytoma)
GroupNotHPOFreeText: No family members appeared to have the above manifestation.
GroupPreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.P86L (c.257C>T)
CaseProblemVariantFreeText: N/A
LegacyVariant: p.P86L (c.470C>T)
ClinVarID: 182977 https://www.ncbi.nlm.nih.gov/clinvar/variation/182977/
CAID: N/A
gnomAD: N/A
VariantEvidence: N/A
MutationType: missense_variant; transition
CivicName: P86L (c.257C>T)
MultipleGeneVariants: N/A
Missense mutation in codon 167, exon 3, arginine to glutamine substitution
Of 14 caucasian patients with retinal vascular proliferation and known family history of VHL disease, 12 patients were enrolled in an approved study protocol at the National Cancer Institute. 11 of these patients underwent genetic testing and were found to have mutations in the VHL gene. Patient 11, age 19, was diagnosed only with retinal vascular proliferation. She was found to carry the R167Q (c.500G>A) mutation. Presurgical and postsurgical optical coherence tomography in patient 11 demonstrated the fibrovascular complex as a hyperreflective layer that was limited to the vitreoretinal surface. There was traction on the underlying retinal tissue, resulting in thickening and obliteration of the foveal contour. Postsurgically, excision of the complex restored the overall shape of the foveal contour, leaving behind only a small disruption in the outer retinal lamination and a small residual macular epiretinal membrane. ACMG evidence codes: 'PP4' since the patient presents phenotypes highly specific for a disease with a single genetic etiology.
A 45-year-old man's vague symptoms and unusual medical history spurred an investigation that culminated with an examination of his genes. The patient presented to his primary care physician with a 2-week history of progressive fatigue and 2 episodes of intermittent left upper- and lower-extremity weakness. An extensive work-up for a cause was unrevealing. Magnetic resonance imaging (MRI) of the brain demonstrated bilateral chronic infarcts resulting from multiple cryptogenic strokes in his past medical history. Blood tests revealed unexplained lymphocytosis and thrombocytosis. An 18F-fluorodeoxyglucose-positron emission tomography-computed tomography scan was performed to further evaluate his signs and symptoms. Imaging disclosed abnormal uptake in the adrenal glands, which was concerning for malignancy. The patient was referred to the Mayo Clinic.
PatientID: None
KindredID: 1
Case: M, 45Y0M, Ethnicity Unknown
DiseaseAssertion: Assumed VHL
FamilyInfo: None.
CasePresentingHPOs: HP:0006748, HP:0100827, HP:0001894, HP:0009713, HP:0031496 (Adrenal pheochromocytoma, lymphocytosis, thrombocytosis, spinal hemangioblastoma, mucinous cystic neoplasm of the pancreas)
CaseHPOFreeText: At age 45 the patient was admitted for 2-week history of fatigue and muscle weekness. MRI showed bilateral chronic infarcts resulting from multiple cryptogenic strokes in his past medical history. Blood tests revealed unexplained lymphocytosis and thrombocytosis.The patient was found to have bilateral adrenal phoechromocytomas, hemangioblastomas in the spinal cord at T11 and in the cauda equina at L2, and multiple intraductal papillary mucinous neoplasms.
CaseNotHPOs: HP:0005584, HP:0030405 (renal cell carcinoma, pancreatic endocrine tumour)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.Y98H (c.292T>C)
CaseProblemVariantFreeText: N/A
LegacyVariant: N/A
ClinVarID: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/
CAID: N/A
gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: Y98H (c.292T>C)
MultipleGeneVariants: N/A
PatientID: 15
KindredID: 6
Case: F, 22Y0M, Indian
DiseaseAssertion: VHL
FamilyInfo: 1 other member of this family presented with the same variant. Patient 16 (Gen 2) presented with bilateral pheochromocytoma.
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:0002668 (Pheochromocytoma, Paraganglioma)
CaseHPOFreeText: Sympathetic paraganglioma and bilateral pheochromocytoma. Age of onset for pheochromocytoma and paragangliomas is stated as 11Y and 22Y but it is not clear which age pertains to which phenotype.
CaseNotHPOs: HP:0009711; HP:0010797; HP:0001737; HP:0005584; HP:0030405 (Retinal capillary hemangioma, Hemangioblastoma, Pancreatic cysts, Renal cell carcinoma, Pancreatic endocrine tumor)
CaseNotHPOFreeText: N/A
CasePreviousTesting: N/A
PreviouslyPublished: N/A
SupplementalData: N/A
Variant: p.R167Q (c.500G>A)
LegacyVariant: N/A
CaseProblemVariantFreeText: N/A
ClinVarID: 2216, https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/
CAID: N/A
gnomAD: 0.000003977, https://gnomad.broadinstitute.org/variant/3-10191507-G-A
VariantEvidence: N/A
MutationType: missense_variant;transition
CivicName: R167Q (c.500G>A)
MultipleGeneVariants: N/A