- Dec 2024
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www.youtube.com www.youtube.com
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Sommaire minuté des temps forts du webinaire "REPLAY 🦋 Webinaire HPV : enjeux et nouveaux outils sur les papillomavirus | Crips IDF"
Ce sommaire met en avant les points clés du webinaire sur les papillomavirus (HPV), en présentant les enjeux de santé publique liés à cette infection, les actions du Crips pour améliorer la couverture vaccinale et les outils de communication développés pour sensibiliser les jeunes et les parents.
La dernière partie consacrée aux échanges permet d'apporter des précisions sur des points importants comme l'autorisation parentale et le carnet de santé, et d'ouvrir la discussion sur la manière de motiver les parents à faire vacciner leurs enfants.
0:00 - 5:00 : Introduction et présentation du Crips Ile-de-France
- Fanny Forgestier et Léa, chargées de projets au Crips, présentent le thème du webinaire : les papillomavirus (HPV), les enjeux et les nouveaux outils de prévention.
- Le Crips, association loi 1901, intervient sur la promotion et la prévention en santé, notamment auprès des jeunes et des publics prioritaires.
- Le Crips propose des actions directes auprès des publics (stands, animations) et accompagne les professionnels (formations, projets de prévention).
5:00 - 9:00 : Les papillomavirus (HPV): définition, vaccination et dépistage
- Les HPV sont une infection sexuellement transmissible (IST) très fréquente, touchant 80% de la population sexuellement active.
- 90% des personnes infectées éliminent naturellement le virus, mais pour 10% il persiste et peut engendrer des problèmes de santé graves.
- Les HPV peuvent provoquer des cancers HPV-induits (col de l'utérus, vulve, pénis, anus, voies aérodigestives supérieures) et des condylomes (verrues génitales).
- La vaccination est recommandée dès 11 ans pour les filles et les garçons, avec un schéma vaccinal en 2 ou 3 injections.
- Le vaccin Gardasil 9 protège contre les 9 souches de HPV les plus dangereuses.
- La vaccination est efficace et sûre, avec peu d'effets secondaires.
9:00 - 16:00 : La couverture vaccinale en France : un enjeu de santé publique
- La couverture vaccinale HPV en France est faible, en dessous de 50% pour les filles et 6% pour les garçons, comparée à d'autres pays où elle atteint 80%.
- Des disparités territoriales existent, notamment en Seine-Saint-Denis (93) qui présente le taux de vaccination le plus faible de France métropolitaine.
- L'exemple d'autres pays comme la Suède et l'Australie montre que la vaccination est efficace pour réduire les lésions précancéreuses et les cancers.
- Une campagne nationale de vaccination dans les collèges a été lancée en 2023 pour les classes de 5ème, avec un objectif de 30% de couverture la première année.
- Le vaccin est gratuit dans le cadre de cette campagne.
- Le dépistage est complémentaire à la vaccination, avec un frottis tous les 3 ans à partir de 25 ans et un test HPV à partir de 30 ans.
16:00 - 36:00 : Présentation des projets du Crips pour améliorer la couverture vaccinale
- Présentation d'un état des lieux réalisé à Pantin (93) auprès des jeunes, des parents et des professionnels.
- Les résultats montrent un manque d'information sur les HPV et la vaccination, ainsi que des craintes liées aux effets secondaires.
- Le Crips a développé des actions pour renforcer l'information des publics et des professionnels, en insistant sur la fréquence de l'infection, la prévention des cancers et l'efficacité et la sécurité du vaccin.
- Présentation d'une expérimentation menée dans des collèges de Pantin et de Sarcelles (95) : formation des professionnels, animations en classe, actions sur les territoires.
- Création d'un jeu pédagogique "Puberté HPV" pour sensibiliser les jeunes de manière ludique.
36:00 - 58:00 : La campagne de communication "Les Papiomas je n'en veux pas"
- Présentation de la campagne de communication du Crips, avec une identité visuelle "fun" et ludique, axée sur les emojis.
- Création de kits d'information pour les jeunes et les parents, avec des brochures, des affiches et des jeux.
- Réalisation de vidéos de sensibilisation diffusées sur les réseaux sociaux et dans les cabinets de santé.
- La communication est axée sur la prévention des cancers, en désexualisant le message pour éviter les craintes des parents.
58:00 - fin : Conclusion, échanges et questions/réponses
- Les participants peuvent télécharger les outils du Crips sur le site internet ou demander des brochures par mail.
- Le Crips propose des formations pour les professionnels de santé, de l'éducation nationale et d'autres secteurs.
- Importance du tissu associatif local pour mobiliser les parents.
- Échanges sur les modalités de la vaccination en collège (autorisation parentale, carnet de santé).
- Réflexion sur l'importance de la prévention des cancers comme levier de motivation pour la vaccination.
- Clôture du webinaire et invitation à contacter le Crips pour toute question ou demande d'information.
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- Oct 2024
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www.youtube.com www.youtube.com
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Résumé de la vidéo [00:00:00][^1^][1] - [00:21:39][^2^][2]:
Cette vidéo traite de l'augmentation inquiétante des cancers du côlon chez les jeunes. Elle présente des témoignages de patients et des explications médicales sur les causes possibles et les efforts de recherche en cours.
Moments forts: + [00:00:45][^3^][3] Témoignage de Christina * Diagnostiquée à 31 ans avec un cancer du côlon stade 4 * Subit une opération majeure et une chimiothérapie * Rémission après 5 ans + [00:03:47][^4^][4] Augmentation des cas chez les jeunes * Augmentation des cancers du côlon chez les moins de 50 ans * 13% d'augmentation en 2022 en Europe * Nécessité d'une nouvelle approche médicale + [00:05:01][^5^][5] Symptômes et diagnostic * Symptômes courants : sang dans les selles, douleurs abdominales, perte de poids * Importance de consulter en cas de symptômes * Retard de diagnostic fréquent chez les jeunes + [00:09:01][^6^][6] Études et recherches * Études en cours pour comprendre les causes * Hypothèses sur l'inflammation et le microbiome * Différences immunitaires entre jeunes et âgés + [00:16:42][^7^][7] Facteurs de risque environnementaux * Pollution, pesticides, microplastiques * Études pour identifier les liens avec le cancer * Importance de la recherche pour des solutions préventives
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- Sep 2024
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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www.biorxiv.org www.biorxiv.org
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- Apr 2024
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- Feb 2024
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docdrop.org docdrop.org
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for - healthy eating - Dr. William Li - nutrition - healthy food - inflammation - angiogenesis
summary - A good interview about human health and healthy diet. William Li begins by talking about angiogenesis as a key aspect of human health - and how pathology of angiogenesis is at the root of many major diseases. - The interviewer then asks Dr. Li about the connection between another keystone disease, and angiogenesis. - Dr. Li then describes some healthy foods and good dietary practices including extra virgin olive oil.
adjacency - between - angiogenesis - inflammation - Micheal Levine's work - evolutionary biology - adjacency statement - they all seem related, as evolutionary biology has created legacy subsystems within the human body
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if a tumor is kind of like a wound it can hijack blood vessels and you got inflammation and now the cancer itself causes some inflammation you're just making it a hell of a lot 00:28:49 easier for that tumor to get a blood supply which means that the cancer is more likely to grow
for - adjacency - cancer - inflammation - angiogenesis
adjacency - between - cancer - angiogenesis - inflammation - adjacency statement - if a tumor is kind of like a wound - it can hijack blood vessels - if you have some form of chronic inflammation - and cancer causes inflammation - it makes it easier to access blood supply - making cancer growth more likely
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what foods are able to do foods that inhibit angiogenesis
for - adjacency - food - angiogenesis - cancer
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once an avascular or bloodless cancer 00:22:48 is able to get vessels to touch it that moment that touch is that the cancer can grow 16 000 times in two weeks
for - avascular (bloodless) cancer - angiogenesis creates malignancy - stats - angiogenesis and avascular cancer
stats - angiogenisis and avascular cancer - During research, the research lab that William Li worked in discovered that once blood vessesl touch a harmless avascular (bloodless) cancer - it transforms it into a deadly, malignant tumor that grows 16,000x in two weeks
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cancer without disease
for - cancer without disease - microscopic cancer
definition - cancer without disease
- biologically we are actually all forming cancers in our body all the time
- because all it takes for our 40 trillion cells to do is
- to make those little mistakes
- I told you 10 000 mistakes are fixed every day
- A few of those sneaking through
- will turn into a microscopic tumor microscopic cancer
- and this is called cancer without disease
- because as tiny little mutant cancer can grow up to the size of the tip of a ballpoint pen
- and then it's frozen like a pimple can't go any bigger
- because it doesn't have
- a blood supply
- no oxygen
- no food
- nothing to feed it and so
- those little microscopic cancers sit there
- until another one of our defense systems our immune system wings by like a cop on a beat and sees this abnormal cell sitting on that street corner in a good neighborhood and then says
- "get in the car we're taking you away"
- and so our immune system destroys these microscopic cancers
- but some microscopic cancers are able to hijack our body's regular angiogenesis defense system
- and selfishly grow blood vessels to feed themselves.
Tags
- adjacency - michael levine - evolutionary biology - angiogenesis
- adjacency - Michael Levine - angiogenesis - inflammation
- angiogenesis
- avascular cancer - angiogenesis creates malignancy
- inflammation
- angiogenesis - how blood vessels turns benign avascular cancer into malignant one
- adjacency - cancer - inflammation - angiogenesis
- microscopic cancer
- cancer without disease
- adjacency - food - angiogenesis - cancer
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Local file Local file
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Uncontrolledself-replication in these newer technologies runs a much greater risk: arisk of substantial damage in the physical world.
As a case in point, the self-replication of misinformation on social media networks has become a substantial physical risk in the early 21st century causing not only swings in elections, but riots, take overs, swings in the stock market (GameStop short squeeze January 2021), and mob killings. It is incredibly difficult to create risk assessments for these sorts of future harms.
In biology, we see major damage to a wide variety of species as the result of uncontrolled self-replication. We call it cancer.
We also see programmed processes in biological settings including apoptosis and necrosis as means of avoiding major harms. What might these look like with respect to artificial intelligence?
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- Dec 2023
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www.youtube.com www.youtube.com
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Will artificial intelligence create useless class of people? - Yuval Noah Harari
1:00 "bring the latest findings of science of the public", otherwise the public space "gets filled with conspiracy theories and fake news and whatever".<br /> he fails to mention that ALL his beautiful "scientists" are financially dependent on corporations, who dictate the expected results, and who sabotage "unwanted research".<br /> for example, the pharma industry will NEVER pay money for research of natural cancer cures, or "alternative" covid cures like ivermectin / zinc / vitamin C, because these cures have no patent, so there is no profit motive, and also because the "militant pacifists" want to fix overpopulation this way.<br /> a "scientist" should be someone, who has all freedom to propose hypotheses, which then are tested in experiments (peer review), and compared to real placebo control groups. because that is science, or "the scientific method". everything else is lobbying for "shekel shekel".
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- Nov 2023
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www.linkedin.com www.linkedin.com
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CANCER PREVENTION (prophylactic) – Those that have had genetic tests and know they’re really prone to getting cancer can take Fenbendazole prophylactically. Take one capsule (222 mg) 3 times a week, once a day after a fatty meal. Then no Fenbendazole for four days. Repeat for 10 weeks and then take 10 weeks off; Curcumin (600 mg) one capsule two times a day after breakfast and lunch; CBD oil (25mg) 1-2 drops under the tongue every day before sleep. Continue that regimen indefinitely.
Fenbendazole cancer prophylaxis protocol.
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Inhibition of Glucose uptake in cancer cells. Malignant cells are known to have an enormous glucose uptake. That’s why I tell everybody that has cancer to immediately (a) get on a ketogenic diet, and (b) take High Dose Vitamin C. Note: Cancer cells consume glucose 200 times faster than ordinary cells. If you study cancer you know of the Warburg Effect. This is the aerobic glycolysis effect and it can be seen on PET scans. It’s pretty obvious. Fenbendazole limits cancer cell fueling with sugar by limiting this glucose uptake, decreasing the amount of what are called “glute transporters” (canals that take the glucose into cancer cells from the blood). An enzyme called hexokinase 2 is inhibited as well. This is very important. It helps those tumors to not divide rapidly and prevent sugar from getting in there.
Sugar (glucose) is the primary fuel for cancer. Fenbendazole limits glucose uptake in cancer cells, limiting growth.
Also a reason for adopting a ketogenic diet with high dose vitamin c.
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docdrop.org docdrop.org
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there's a microbe in the mouth called fusobacterium nucleotide it over proliferates it's okay to have normally but it over proliferates when 01:28:39 you have bleeding gums gingivitis or periodontitis where it then enters the bloodstream this is called translocation and colonize the colon and the evidence is very good it is a principal cause of 01:28:52 colon cancer colon cancer starts in the mouth incredibly and doesn't get there by swallowing gets her through the bloodstream translocation
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for:holistic medicine - example - oral microbiome and colon cancer, oral microbiome - colon cancer, bleeding gums - colon cancer, gingivitus - colon cancer, periodontitis - colon cancer, bloodstream translocation, complexity - example - human body - colon cancer - oral microbiome
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comment
- colon cancer starts in the mouth!
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references
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Oral-Intestinal Microbiota in Colorectal Cancer: Inflammation and Immunosuppression (2022)
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8824753/
- Abstract
- It is widely recognized that microbial disorders are involved in the pathogenesis of many malignant tumors.
- The oral and intestinal tract are two of the overriding microbial habitats in the human body. Although they are anatomically and physiologically continuous, belonging to the openings at both ends of the digestive tract, the oral and intestinal microbiome do not cross talk with each other due to a variety of reasons, including
- intestinal microbial colonization resistance and
- chemical barriers in the upper digestive tract.
- However, this balance can be upset in certain circumstances, such as
- disruption of colonization resistance of gut microbes,
- intestinal inflammation, and
- disruption of the digestive tract chemical barrier.
- Evidence is now accruing to suggest that the oral microbiome can colonize the gut, leading to dysregulation of the gut microbes.
- Furthermore, the oral-gut microbes create an
- intestinal inflammatory and
- immunosuppressive microenvironment
- conducive to
- tumorigenesis and
- progression of colorectal cancer (CRC).
- Here, we review
- the oral to intestinal microbial transmission and
- the inflammatory and immunosuppressive microenvironment, induced by oral-gut axis microbes in the gut.
- A superior comprehension of the contribution of the oral-intestinal microbes to CRC provides new insights into the prevention and treatment of CRC in the future.
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Insights into oral microbiome and colorectal cancer – on the way of searching new perspectives (2023)
- https://www.frontiersin.org/articles/10.3389/fcimb.2023.1159822/full
- Abstract
- Microbiome is a keystone polymicrobial community that coexist with human body in a beneficial relationship.
- These microorganisms enable the human body to maintain homeostasis and take part in mechanisms of defense against infection and in the absorption of nutrients.
- Even though microbiome is involved in physiologic processes that are beneficial to host health, it may also cause serious detrimental issues.
- Additionally, it has been proven that bacteria can migrate to other human body compartments and colonize them even although significant structural differences with the area of origin exist.
- Such migrations have been clearly observed when the causes of genesis and progression of colorectal cancer (CRC) have been investigated.
- It has been demonstrated that the oral microbiome is capable of penetrating into the large intestine and cause impairments leading to dysbiosis and stimulation of cancerogenic processes.
- The main actors of such events seem to be oral pathogenic bacteria belonging to the red and orange complex (regarding classification of bacteria in the context of periodontal diseases), such as
- Porphyromonas gingivalis and
- Fusobacterium nucleatum respectively,
- which are characterized by significant amount of cancerogenic virulence factors.
- Further examination of oral microbiome and its impact on CRC may be crucial on early detection of this disease and would allow its use as a precise non-invasive biomarker.
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docdrop.org docdrop.org
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this is a cancer uh approach that we work on which is to not to kill those cells but to force them to re reconnect to their neighbors and when they reconnect to the 00:31:24 neighbors they once again become part of the collective that's working on making nice skin nice muscle they stop being metastatic and they they go back
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for: quote - Michael Levin, quote - MET of individuality, quote - memory wipe, quote - cancer therapy - MET of individuality
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quote: Michael Levin
- this is a cancer approach that we work on which is to not to kill those cells but to force them to re reconnect to their neighbors and when they reconnect to the neighbors they once again become part of the collective that's working on making nice skin nice muscle they stop being metastatic and they they go back
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comment
- Michael refers to cancer as a "memory wipe" where they have forgotten the normative programmed narrative of bodily / collective / multicellular unity
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when we work on cancer what you see is that when when 00:30:18 individual cells electrically disconnect from the rest of the body they their cognitive light cone shrinks they're back to their amoeba tiny little e gos and as far as they're concerned the rest of the body is just environment to them
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for: MET of individuality - examples of breakdown - cancer
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paraphrase
- cancer is an example of when some part of the evolutionary program that coheres multicellularity into a cohesive whole goes faulty
- then some subset of cells lose their coherence programming / story / narrative, the unity is lost and that cellular subset no longer identifies as part of the higher order collective individual, but return to a much more evolutionarily primitive state of pre-MET of individuality
- this means that the MET individuality coherence program has weaknesses that can cause groups of cells to lose sight of the unifying logic and return to the primitive state
- cancer demonstrates that these primitive programs still exist in all cells in our bodies and when the regulating coherence program is faulty, they can return to these more primitive states
- cancer is an example of when some part of the evolutionary program that coheres multicellularity into a cohesive whole goes faulty
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Tags
- quote - cancer therapy - MET of Individuality
- MET of Individuality - example of breakdown - cancer
- quote - MET of individuality
- quote - memory wipe - cancer
- MET of Individuality - cancer therapy
- memory wipe
- quote - Michael Levin
- MET of individuality - breakdown
- cancer therapy - evolutionary approach
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- Sep 2023
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Defections from large-scale anatomical goals, such as those that occur due to an inappropriate reduction of gap junctional connectivity [74], present as cancer, cause reversions of cell behavior to ancient unicellular concerns which lead to metastasis and over-proliferation as the cells treat the rest of the body as external environment.
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fresh perspective
- cancer can be interpreted as a breakdown in the bodies multiscale competency architecture causing cancerous cells to lose their higher level synchronizing signals and revert to their more evolutionarily primitive forms as individuals that see the body as simply an external environment
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adjacency between
- gap junction coupling
- cancer
- healthy tissue coherence
- multiscale competency architecture
- adjacency statement
- gap junction coupling appears to be an evolutionary means of cohering individuals together to form a larger group
- hence, they seem to play a critical role in the continued evolution of more complex multicellular organisms
- their pathologies within multicellular beings destroy multicellular structures and create disease, reverting the organism, or competent multicellular structures of the organism such as tissues and organs back to individualistic behavior, as in cancers
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- Aug 2023
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- Jun 2023
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- May 2023
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- Apr 2023
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research.sinica.edu.tw research.sinica.edu.tw
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成人癌症通常是大腸癌、肝癌、肺癌等，這些發生在上皮組織的癌症（carcinoma），通常是經過長時間累積基因變異與細胞損壞才會發生；至於兒童癌症，主要是中胚層癌或胚胎型癌，例如腦瘤、軟組織瘤及骨癌等，不是經由體細胞基因變異累積，通常很早就發病。
成人癌症：上皮組織 兒童癌症：胚胎型癌、中胚層癌
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- Mar 2023
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- Feb 2023
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- Jan 2023
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- Nov 2022
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nautil.us nautil.us
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phytoncides, antibacterial and antimicrobial substances that trees and other plants release into the air to help them fight diseases and harmful organisms. When humans breathe in these substances—typically by spending time in nature—their health can improve. Across several studies, phytoncides have been shown to boost immune function, increase anticancer protein production, reduce stress hormones, improve mood, and help people relax.
I always feel better during and after a forest walk.
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- Aug 2022
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twitter.com twitter.com
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ReconfigBehSci on Twitter: “RT @acweyand: Kids account for <0.2% of cancer deaths in US Kids account for <0.2% of heart disease deaths in US Kids account for <0.3% of…” / Twitter. (n.d.). Retrieved January 21, 2022, from https://twitter.com/SciBeh/status/1483869918332432388
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- Jun 2022
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- May 2022
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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DICER1 syndrome encompasses a variety of benign and malignant manifestations including multinodular goitre
Gene: DICER1 PMCID: PMC8451242 PMID: 34552563 Pathogenic Inheritance Pattern: Autosomal Dominant MultipleDiseaseEntities Disease Entity: DICER1 syndrome, multinodular goitre, cystic nephroma, anaplastic renal sarcoma, Wilms tumour, differentiated thyroid carcinoma, gynandroblastoma, ciliary body medulloepithelioma, embryonal rhabdomyosarcoma, pineoblastoma, pituitary blastoma, kidney cyst, pulmonary cyst, Sertoli-Leydig Cell Tumor. Mutation: Germline MultipleGeneVariants Variant & Clinvar IDs: c.3452_3453del (485534), c.316del (no ClinVar ID), c.171_172insAC (no ClinVar ID), c.3434del (no ClinVar ID), c.988C>T (933007), c.5388dup (no ClinVar ID) Zygosity: None provided. Case: At time of operation, the goitre patients living in Denmark were ages 21, 12, 21, 8, 14, and 16. Four underwent total thyroidectomies, and two underwent partial thyroidectomies. The patient originally aged 21 previously had a kidney cyst at age 14 and a pulmonary cyst at an unknown age. The patient aged 14 at time of partial thyroidectomy later manifested a Sertoli-Leydig Cell Tumor at age 15. All six patients were female. CasePresentingHPO: None provided. CasePreviousTesting: thyroidectomy gnomAD: ENSG00000100697.10, https://gnomad.broadinstitute.org/gene/ENSG00000100697 Mutation Type: Frameshift, Nonsense
Tags
- goitre
- Mutation:Frameshift
- Germline
- DICER1
- c.316del
- thyroidectomy
- c.3452_3453del
- gnomAD:ENSG00000100697.10
- ClinvarID:485534
- Nonsense
- female
- c.5388dup
- Age:8
- Pathogenic
- Mutation:Nonsense
- c.988C>T
- PMCID:PMC8451242
- PMID:34552563
- ClinvarID:933007
- Cohort
- MultipleGeneVariants
- goiter
- Age:12
- cancer
- AutosomalDominant
- MultipleDiseaseEntities
- c.3434del
- Gene:DICER1
- ClinvarID:NotProvided
- Age:14
- Age:21
- Frameshift
- c.171_172insAC
Annotators
URL
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pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
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DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types.
GeneName: DICER1 PMID: 29762508 HGNCID: N/A Inheritance Pattern: Autosomal dominant Disease Entity: Cancer Mutation: Germline Zygosity: Heterozygosity Variant: Unregistered Family Information: 12% of children with pleuropulmonary blastomas have cystic nephromas Case: 11 year old patient with Hodgkin lymphoma with DICER1 mutation in 2016.
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GeneName: DICER1 syndrome (pleuropulmonary blastoma familial tumor susceptibility syndrome), PMID (PubMed ID): 29762508, HGNCID: 17098, Inheritance pattern: autosomal-dominant disease, Disease entity: Plueropulomary Blastoma, Mutation: Somatic, Zygosity: heterozygous, Variant: multiple variants, Family information: NA, Case: young children, CasePresentingHPO: N/A, CasePreviousTesting: N/A, Gnomade #: N/A , Mutation type: deletion
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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DICER1 syndrome is a rare genetic condition predisposing to hereditary cancer and caused by variants in the DICER1 gene.
GeneName: DICER1 PMID: 33552988 HGNCID: Unavailable Inheritance Pattern: Autosomal Dominant with reduced penetrance Disease Entity: Cystic nephroma, familial pleuropulmonary blastoma (PPB), ovarian Sertoli-Leydig cell tumor (SLCT), cervix embryonal rhabdomyosarcoma, multinodular goiter, Wilms' Tumor, Ciliary body medulloepithelioma, nasal chondromesenchymal hamartoma, differentiated thyroid carcinoma, pituitary blastoma, pineoblastoma, sarcomas of different sites. Mutation: germline mutation Zygosity: heterozygous Variant: ClinVar ID not listed Family Information: No family cases listed Case: No specific case mentioned gnomAD: N/A Mutation Type: Frameshift, Nonsense mutation
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- Apr 2022
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pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
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DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer
GeneName: DICER1 PMID: 29762508 HGNCID: Can't find Inheritance: Autosomal Dominant Disease Entities: Endocrine and Reproductive Tumors Mutation: Somatic and germline Zygosity: Heterozygous Mutant: Can't find Family: Can't find
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The DICER1 gene, located on chromosome 14, position q32.13, encodes the endoribonuclease Dicer protein of the ribonuclease III family
GeneName: Dicer1 PMID (PubMedID): 29782508 HGNCID= Unavailable Inheritance Pattern: Autosomal Dominant Disease Entity: cancer, multinodular goiter, pleuropulmonary blastoma, cystic nephroma, and ovarian Sertoli-Leydig Cell Tumor Mutation: germline or somatic Zygosity: causes loss of heterozygosity Variant: unregistered Family: those that have the mutation almost always pass it on.
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DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types
GeneName: DICER1 PMID (PubMed ID): 29762508 HGNCID: Unavailable Inheritance Pattern: Autosomal Dominant Disease Entity: cancer, rare genetic disorder, pleuroplumonary blastomas, cystic nephroma, rhabdomyosarcoma, multinodular goiter, thyroid cancer, overian Sertoli-Leydig cell tumors, and other meoplasias Mutations: Germline mutations or Somatic mutations Zygosity: Heterozygosity Variant: unregistered Family Information: Cystic nephromas has been reported in approximately 12% of children with pleuripulmonary blastomas or those with a family member with cystic nephroma. Patient with two DICER1 mutations and several of his family members shared these mutations. All members developed a least one type of tumor with differing origins. The patient was an 11-year old boy with a rare Hodgkin lymphoma with DICER1 in 2016. (c.5299delC and c.4616C>T).
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DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types.
GeneName = DICER1 PMID = 29762508 HGNCID = Can't find Inheritance pattern = Autosomal dominant Disease entity = cancer, multinodular goiter, pleuropulmonary blastoma, cystic nephroma, ovarian Sertoli-Leydig cell tumor Mutation = germline OR somatic Zygosity = causes loss of heterozygosity Variant = unregistered Family = those with the mutation almost always passed it on
Tags
- somatic
- Autosomal Dominant
- DICER1 Cancer Autosomaldominant blastoma pleuropulmonary neohroma cystic goiter multinodular raregeneticdisorder
- nephroma
- Heterozygosity
- HGNCID:Unavailable
- DICER1
- endocrine tumor
- PMID:29762508
- cystic nephroma
- goiter
- tumor
- cancer
- reproductive tumor
- Variant
- autosomal
- blastoma
- HGNCID: Unavailable
- miRNA
- Gene:DICER1
- dominant
- rare genetic disorder
- PMID: 29762508
- Gene name
- DICER1 Syndrome
- Inheritance:Autosomal Dominant
Annotators
URL
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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The DICER1 syndrome is an autosomal dominant tumor‐predisposi-tion disorder associated with pleuropulmonary blastoma, a rare pediatric lung cancer
GeneName:DICER1 PMID (PubMed ID): PMCID: PMC6418698 PMID: 30672147 HGNCID: NOT LISTED<br /> Inheritance Pattern: Autosomal Dominant Disease Entity: Cancer; benign and malignant tumors including pleuropulmonary blastoma, cystic nephroma, Sertoli-Leydig cell tumors, multinodular goiter, Thryoid cancer, rhabdomyosarcoma, and pineoblastoma. Mutation: Somatic missense variation Mutation type: missense Zygosity: None stated Variant: unregistered…. Family Information: Characterize germline variants in familial early-onset clorectal cancer patients; The observation of germline DICER1 variation with uterine corpus endometrial carcinoma merits additional investigation. CasePresentingHPOs: uterine and rectal cancers in germline mutation
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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DICER1 syndrome is a cancer-predisposing disorder caused by pathogenic variants in the DICER1 gene
Gene: DICER1 PMCID: PMC7859642 PMID: 33552988 HGNCID: Unavailable Inheritance Pattern: Autosomal Dominant Disease Entity: familial pleuropulmonary blastoma (PPB),cystic nephroma, ovarian Sertoli-Leydig cell tumor (SLCT), multinodular goiter, cervix embryonal rhabdomyosarcoma, Wilms’ tumor, nasal chondromesenchymal hamartoma, ciliary body medulloepithelioma, differentiated thyroid carcinoma, pituitary blastoma, pineoblastoma, and sarcomas of different sites. Mutation: Germline Zygosity: Heterozygosity most common Variant: ClinVarID not available Family Information: No mention of disease within family Case: No case specified GnomAD: N/A Mutation Type: Nonsense or Frameshift
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twitter.com twitter.com
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ReconfigBehSci on Twitter: "RT @tylerblack32: Ghouls BEFORE COVID: 🤮🤮🤮🤮🤮🤮 ‘Only 0.2% of cancer deaths occur in children! <0.003% will die of cancer! Only about 0.16%…’ / Twitter. (n.d.). Retrieved 7 February 2022, from https://twitter.com/SciBeh/status/1490254426719899655
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- Mar 2022
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blog.lolofit.com blog.lolofit.com
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Valter Longo, PhD has been studying an aspect of fasting and autophagy that is fascinating enough, I wanted to include it in it’s own section. One area of his research focuses on how fasting induces differential stress resistance to make chemotherapy far more effective. In a food scarce environment, normal cells become more resistant to oxidative stress, but cancer cells don’t. Remember, cancer cells are broken cells. Something went wrong with them and they are replicating out of control. Being broken means they don’t retain all the typical functions and protective mechanisms of normal cells, like antioxidant generation. That’s one of the reasons cancer cells switch their metabolism from oxidative phosphorylation to glycolysis even in the presence of oxygen. It’s known as the Warburg effect. There are many theories on why this happens, but one is because cancer cells are more sensitive to the reactive oxygen species created during normal metabolism. Eating creates an environment where cancer cells thrive and normal cells are stressed. Cancer cells need an environment rich with sugar, growth factors (like IGF-1) and amino acids like glutamine. For normal cells, metabolism creates reactive oxygen species and triggers an immune response to deal with all the pathogens riding along on top of your meals. However, when you fast, normal cells become 1000 times more resistant to reactive oxygen species, but cancer cells do not. This same starvation-protection also makes normal cells far more resistant to chemotherapy drugs.
So fasting helps protect healthy cells and weakens cancerous ones. That's cool. But then it says cacer clles need sugar, growth factors like [[IGF-1]] and amino acids like glutamine. The [[Carnivore Diet]] is going to increse IGF-1 and amino acid levels but should starve the cancer cells of sugar. Given Dr Clemens' success treating cancer with the [[PKD]] protocol I'm inferring that it's the triad that needs to be inn place and if sugar is missing then the other factors being elevated eoesn't matter that much.
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- Feb 2022
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news.vcu.edu news.vcu.edu
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McNeill, B. (n.d.). Patients undergoing treatment for cancer more susceptible to COVID-19 misinformation, study finds. VCU News. Retrieved February 14, 2022, from https://news.vcu.edu/article/2022/02/patients-undergoing-treatment-for-cancer-more-susceptible-to-covid-19-misinformation
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everything2.com everything2.com
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People like to say to and about cancer patients: "How brave." And "What a brave fight." And he/she "fought cancer valiantly." Holy mother of god. There is no bravery. There is only fear. There is only pain. If we could escape this by retreating - all of us would. Seriously, show me a coward's way out, and I will take it. We are not brave. We are struggling to survive.
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www.biobdlab.cn:8000 www.biobdlab.cn:8000
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crdd.osdd.net crdd.osdd.net
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www.cogvic.vip www.cogvic.vipHomepage1
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cnvintegrate.cgm.ntu.edu.tw cnvintegrate.cgm.ntu.edu.twCNV-home1
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silver.sejong.ac.kr silver.sejong.ac.kr
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lncexplore.bmi.nycu.edu.tw lncexplore.bmi.nycu.edu.tw
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cancer.sanger.ac.uk cancer.sanger.ac.uk
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- Jan 2022
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www.nbcnewyork.com www.nbcnewyork.com
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•. (n.d.). Even Mild COVID Infections Can Have Lasting Impacts Like ‘Chemo Brain,’ Study Finds. NBC New York. Retrieved 12 January 2022, from https://www.nbcnewyork.com/news/coronavirus/even-mild-covid-infections-can-have-lasting-impacts-like-chemo-brain-study-finds/3489958/
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www.biorxiv.org www.biorxiv.org
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Fernandez-Castaneda, A., Lu, P., Geraghty, A. C., Song, E., Lee, M.-H., Wood, J., Yalcin, B., Taylor, K. R., Dutton, S., Acosta-Alvarez, L., Ni, L., Contreras-Esquivel, D., Gehlhausen, J. R., Klein, J., Lucas, C., Mao, T., Silva, J., Pena-Hernandez, M., Tabachnikova, A., … Monje, M. (2022). Mild respiratory SARS-CoV-2 infection can cause multi-lineage cellular dysregulation and myelin loss in the brain (p. 2022.01.07.475453). https://doi.org/10.1101/2022.01.07.475453
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- Dec 2021
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www.nature.com www.nature.com
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Replicating scientific results is tough—But essential. (2021). Nature, 600(7889), 359–360. https://doi.org/10.1038/d41586-021-03736-4
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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US28-mediated activation of MAPKs and of PLCβ was also shown to mediate activation of the cAMP response element binding protein (CREB) in HEK-293 cells and COS-7 cells transiently transfected with US28 [31,38], a transcription factor linked to a broad range of cellular processes, such as cell proliferation, differentiation, survival, angiogenesis, immune response, migration and invasion [83] (Figure 2). Although this has not been proven in the context of HCMV infection, in HEK-293 cells transiently transfected with US28, this activation of CREB by US28 has also been reported to stimulate the major immediate early gene promoter/enhancer (MIE) [84], thus playing a key role in the activation and replication of HCMV, but also in HCMV reactivation from latency
CREB stimulates the major immediate early gene promoter/enhancer, and it plays a key role in the activation and replication of HCMV.
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- Nov 2021
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www.biorxiv.org www.biorxiv.org
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- Oct 2021
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www.bmj.com www.bmj.com
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Mahase, E. (2021). Covid-19: Just a third of blood cancer patients had antibodies against delta variant after two vaccine doses, study finds. BMJ, 375, n2623. https://doi.org/10.1136/bmj.n2623
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www.euro.who.int www.euro.who.int
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Denmark campaign rebuilds confidence in HPV vaccination. (n.d.). Retrieved October 6, 2021, from https://www.euro.who.int/en/health-topics/disease-prevention/vaccines-and-immunization/news/news/2018/3/denmark-campaign-rebuilds-confidence-in-hpv-vaccination
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www.thelancet.com www.thelancet.com
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Simms, K. T., Hanley, S. J. B., Smith, M. A., Keane, A., & Canfell, K. (2020). Impact of HPV vaccine hesitancy on cervical cancer in Japan: A modelling study. The Lancet Public Health, 5(4), e223–e234. https://doi.org/10.1016/S2468-2667(20)30010-4
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- Aug 2021
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www.theatlantic.com www.theatlantic.com
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When I began to understand that attitude doesn’t have anything to do with survival, I felt myself coming up out of deep water. I didn’t cause my cancer by having a bad attitude, and I wasn’t going to cure it by having a good one.And then Coscarelli told me the whole truth about cancer. If you’re ready, I will tell it to you.Cancer occurs when a group of cells divide in rapid and abnormal ways. Treatments are successful if they interfere with that process.That’s it, that’s the whole equation.Everyone with cancer has a different experience, and different beliefs about what will help. I feel strongly that these beliefs should be respected—including the feelings of those who decide not to have any treatment at all. It’s sadism to learn that someone is dangerously ill and to impose upon her your own set of unproven assumptions, especially ones that blame the patient for getting sick in the first place.
Attitude doesn't have anything to do with healing Cancer.
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nooshu.com nooshu.com
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https://nooshu.com/blog/2021/05/12/weve-spotted-something-on-your-scan/
The waiting and not knowing is one of the worst parts. Even reading updates into August is difficult. I was hoping that the surgery would have taken place already.
Hoping the best for you and your family Matt.
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- Jul 2021
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- Jun 2021
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www.migrationencounters.org www.migrationencounters.org
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Luisa: I wanted Northwestern. I had my eye set on Northwestern. I don't know what it was about Northwestern that called to me, but I wanted Northwestern. That's what I wanted, and it wasn't unachievable. One of my friends got into Brown University and she had worse grades than I did, so I was like, "Northwestern's going to be easy. I got this." I wanted to be an oncologist—yes, an oncologist, cancer. I don't know why [Chuckles]. I don't know. Human tragedy, I wanted to save people. That's been my thing. I want to save people. I want to make people better. So [Pause] I killed myself in school. 4.6 GPA. I had all these extracurriculars.
Time in the US, Higher Education, Dreaming About
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Thank God for Cook County Hospital [Chuckles]. They don't charge you a thing, but she got the medical treatment that she needed. She had brain surgery. They removed the tumor and she had to be in therapy for a few years in order to gain … she couldn't talk. She didn't have movement in half of her face, so she couldn't speak because her tongue was numb on one side, so she had to have physical therapy. I went with her a couple times because I had to translate. Sometimes they didn't have people who would translate for my mother. At this point, I had already learned English, but she had to practice every single day. Still to this day, there are a few words that she cannot say.
Time in the US, Illness
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since my mom … my mom at the time, we did not know she had a tumor in the back of her brain. Right where her brain stem is, she had a huge tumor there and we had no idea. Nobody knew. She doesn't remember a lot of this. I don't know if it's because of the emotional trauma or because of the tumor, but once we got to Chicago, it was evident that something was wrong with my mother and she started going to the doctor.
Time in the US, Illness
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- May 2021
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crookedtimber.org crookedtimber.org
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I worked on a recent project to sketch out for a centre-right German think-tank how a European data commons might work. I tried to steer it away from property rights and towards what you’d get if you started with the commons and then worked back to what data could be harnessed, and to which collective purposes. This is eminently do-able, and pushes you towards two distinct areas; groups of people who are served poorly or not at all by current data regimes, and existing cooperatives, unions and mutual societies who could collect and process their members’ data to improve collective bargaining, or licence access to it to generate revenue and boost affiliate membership. Viewing personal data as a collective asset points towards all sorts of currently under-provided public goods (I briefly describe several, on p. 74 here – yes, oddly enough, this stuff got shoved into an annex).
Apparently lots of reading to catch up on here.
I definitely like the idea of starting with the commons and working backwards, not only with respect to data, but with respect to most natural resources. This should be the primary goal of governments and the goal should be to prevent private individuals and corporations from privatizing profits and socializing the losses.
Think of an individual organism in analogy to a country or even personkind. What do we call a group of cells that grows without check and consumes all the resources? (A cancer). The organism needs each cell and group of cells to work together for the common good. We can't have a group of cis-gender white men aggregating all the power and resources for themselves at the cost of the rest otherwise they're just a cancer on humanity.
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- Apr 2021
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- Mar 2021
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link.springer.com link.springer.com
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Brewer, N. T., Cuite, C. L., Herrington, J. E., & Weinstein, N. D. (2007). Risk compensation and vaccination: Can getting vaccinated cause people to engage in risky behaviors? Annals of Behavioral Medicine, 34(1), 95. https://doi.org/10.1007/BF02879925
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www.iomcworld.org www.iomcworld.org
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Jenkins, P., Sikora, K., & Dolan, P. (2021). Life-Years and Lockdowns: Estimating the Effects on Covid-19 and Cancer Outcomes from the UK’s Response to the Pandemic. 1, 3.
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- cancer
- mental health
- social service
- lang:en
- lockdown
- mortality
- economy
- pandemic
- UK
- is:article
- health
- policy
- COVID-19
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www.google.co.uk www.google.co.uk
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Greene, G. (1999). The Woman who Knew Too Much: Alice Stewart and the Secrets of Radiation. University of Michigan Press.
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twitter.com twitter.com
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ReconfigBehSci on Twitter: ‘RT @AdamJKucharski: Alice Stewart on epidemiology (from: Https://t.co/mt3pAwCLXP) https://t.co/P5oI6k4HjG’ / Twitter. (n.d.). Retrieved 2 March 2021, from https://twitter.com/SciBeh/status/1341017627746050049
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- Feb 2021
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twitter.com twitter.com
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Dr. Tara C. Smith. (2021, January 23). A reminder: Especially among the elderly, some individuals will die shortly after receipt of the vaccine. What we need to understand is the background rate of such deaths. Are they higher then in the vaccinated population? We didn’t see that in the trials. Some data from @RtAVM. https://t.co/LJe9k1WJQC [Tweet]. @aetiology. https://twitter.com/aetiology/status/1352810672359428097
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www.dailymail.co.uk www.dailymail.co.uk
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Humphrys, J. (2021, January 22). JOHN HUMPHRYS: Let’s not kid ourselves - NHS puts price on ALL lives. Mail Online. https://www.dailymail.co.uk/debate/article-9178171/JOHN-HUMPHRYS-Lets-not-kid-NHS-puts-price-lives.html
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www.scientificamerican.com www.scientificamerican.com
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Stix, Y. Z., Gary. (n.d.). COVID Is on Track to Become the U.S.’s Leading Cause of Death—Yet Again. Scientific American. Retrieved 22 February 2021, from https://www.scientificamerican.com/article/covid-is-on-track-to-become-the-u-s-s-leading-cause-of-death-yet-again1/
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- Nov 2020
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www.plymouth.edu www.plymouth.edu
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Tumor suppressor genes
These are genes that slow down cell division, repair DNA errors, and/or tell cells to terminate. If these Tumor Suppressor Genes fail to function properly, they go rouge and become cancer cells.
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- Oct 2020
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parenting.nytimes.com parenting.nytimes.com
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How this phenomenon translates into absolute, rather than relative, risk, however, is a bit thorny. A large study published in 2018, for instance, found that among women who had children between 34 and 47, 2.2 percent developed breast cancer within three to seven years after they gave birth (among women who never had children, the rate was 1.9 percent). Over all, according to the American Cancer Society, women between 40 and 49 have a 1.5 percent chance of developing breast cancer.
The rates here are so low as to be nearly negligible on their face. Why bother reporting it?
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www.biorxiv.org www.biorxiv.org
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- Aug 2020
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bjgp.org bjgp.org
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Smith, C. F., Drew, S., Ziebland, S., & Nicholson, B. D. (2020). Understanding the role of GPs’ gut feelings in diagnosing cancer in primary care: A systematic review and meta-analysis of existing evidence. British Journal of General Practice, 70(698), e612–e621. https://doi.org/10.3399/bjgp20X712301
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- Jul 2020
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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Su, Q., Hu, J., Lin, H., Zhang, Z., Zhu, E. C., Zhang, C., Wang, D., Gao, Z., & Cao, B. (2020). Prevalence and risks of severe events for cancer patients with COVID-19 infection: A systematic review and meta-analysis. MedRxiv, 2020.06.23.20136200. https://doi.org/10.1101/2020.06.23.20136200
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- Jun 2020
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.thelancet.com www.thelancet.com
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Oncology, T. L. (2020). COVID-19 and the US health insurance conundrum. The Lancet Oncology, 21(6), 733. https://doi.org/10.1016/S1470-2045(20)30286-2
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- May 2020
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www.bbc.com www.bbc.com
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“Thousands missing out on cancer diagnosis.” (2020, April 22). BBC News. https://www.bbc.com/news/health-52382303
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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Scherer, L. D., Valentine, K. D., Patel, N., Baker, S. G., & Fagerlin, A. (2019). A bias for action in cancer screening? Journal of Experimental Psychology. Applied, 25(2), 149–161. https://doi.org/10.1037/xap0000177
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www.theguardian.com www.theguardian.com
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Correspondent, H. D. S. (2020, May 27). Cancer undiagnosed “for nearly 2,000 people in UK every week.” The Guardian. https://www.theguardian.com/society/2020/may/28/cancer-undiagnosed-for-nearly-2000-people-in-uk-every-week
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psyarxiv.com psyarxiv.com
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Kosir, U., Loades, M. E., Wild, J., Wiedemann, M., Krajnc, A., Roškar, S., & Bowes, L. (2020, May 18). What was the impact of COVID-19 on Adolescent and Young Adult cancer care and their wellbeing? Results from a cross-sectional online survey conducted in the early stages of the pandemic. https://doi.org/10.31234/osf.io/kb6t5
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www.nature.com www.nature.com
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Desai, A., Warner, J., Kuderer, N., Thompson, M., Painter, C., Lyman, G., & Lopes, G. (2020). Crowdsourcing a crisis response for COVID-19 in oncology. Nature Cancer, 1–4. https://doi.org/10.1038/s43018-020-0065-z
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- Mar 2020
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www.goodtherapy.com.au www.goodtherapy.com.au
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Cancer - a symbolic drama between mother and child Bahne-Bahnson (1982) notes that people suffering from cancer experience in a psychosomatic way old emotional deficits that have never been consciously addressed. He suggests that cancer patients have been deprived of being innocent children, and that many of them had to look after and emotionally support their parents. These people missed out on much of the essential emotional nurturing that would have allowed them to develop a strong sense of self.
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www.nature.com www.nature.com
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The Power of Spheres
This "article" is in fact an advertorial, i.e. paid for content. It looks like a scientific article but is not peer reviewed. And it does not include declarations of conflict of interest even though the first author is a founder of a company that develop therapies based on the technology advertised in this feature.
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- Dec 2019
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adaa.org adaa.org
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After diagnosis, 40 percent of cancer patients report developing significant distress that can include serious worry, panic attacks, depression, and PTSD, or posttraumatic stress disorder
I feel like not these should be a more serious concern
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- Sep 2019
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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www.biorxiv.org www.biorxiv.org
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- Jun 2019
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elemental.medium.com elemental.medium.com
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five percent of new cancer cases (roughly 80,000 people a year) are caused by poor nutrition
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- May 2019
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www.proteinatlas.org www.proteinatlas.org
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For cancer tissues, two cores are sampled from each individual and protein expression is annotated in tumor cells.
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www.proteinatlas.org www.proteinatlas.org
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(Uhlén M et al, 2015). The cell lines have been harvested during log phase of growth and extracted high quality mRNA was used as input material for library construction and subsequent sequencing. The expression level of gene-specific transcripts is given as Transcript Per Million (TPM) values. Genes with a TPM value ≥1 are considered as detected. Altogether the transcriptome of 64 cell lines have been analyzed to form a basis of different expression categories.
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- Feb 2019
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Some of those mutations could lead to cancer.
This is interesting.
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www.smithsonianmag.com www.smithsonianmag.com
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A new study suggests not only that prehistoric creatures got cancer, but also that the disease looked similar to cancers in modern humans
I'm not surprised.
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- Jan 2019
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murtagh.mhmedical.com murtagh.mhmedical.com
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Nodular melanoma ++ Nodular melanomas account for 20% of melanomas, are aggressive and invasive, and have no radial growth phase. They are typically found on the trunk and limbs of young to middle-aged individuals (see FIG. 125.8). It may have a ‘blueberry’-like nodule. Prognosis is determined by thickness at the time of excision. Dermatoscopy is usually less useful. ++ FIGURE 125.8 Nodular melanoma on the back. It has no radial growth phase and because it grows vertically can be readily misdiagnosed. The ABCD rule often does not apply but this lesion shows variable colours and an irregular border. Photo courtesy Robin Marks Graphic Jump LocationView Full Size| Favorite Figure|Download Slide (.ppt) ++ The early nodular melanoma problem4,5 ++ Nodular melanoma can present a diagnostic dilemma since the ABCD rule (see later in this chapter) often does not apply. The mnemonic EFG, standing for ‘Elevated’, ‘Firm’ and ‘Growing for more than 1 month’, is more appropriate. Early melanomas tend to be symmetrical, non-pigmented, even in colour, of small diameter and to grow vertically. ++ They are often mistaken for a haemangioma or a pyogenic granuloma. If one is suspicious, refer early to a specialist/specialist clinic. ++ Acral lentiginous melanoma ++ These typically occur on palms, soles and distal phalanges (see FIG. 125.9). They have a poorer prognosis than other types. They occur mainly in people with dark skin. ++ FIGURE 125.9 Acral lentiginous melanoma. A 30-year-old man presented with a ‘mole’ on his toe that had become ‘lumpier’. This type of melanoma, which occurs on the distal areas of the limbs, begins as a spreading pigmented, macule before developing into a nodule surrounded by a pigmented halo (as shown). Photo courtesy Robin Marks Graphic Jump LocationView Full Size| Favorite Figure|Download Slide (.ppt) ++ Desmoplastic melanoma4 ++ This is a rare and aggressive subtype of melanoma. They are often subtle
nicely reviewed article.
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- Dec 2018
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www.headsuphealth.com www.headsuphealth.com
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Zhou, W., Mukherjee, P., Kiebish, M. A., Markis, W. T., Mantis, J. G., & Seyfried, T. N. (2007). The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutrition & metabolism, 4(1), 5.
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- Oct 2018
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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Large-scale analysis of genome and transcriptome alterations in multiple tumors unveils novel cancer-relevant splicing networks
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- May 2018
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pubs.acs.org pubs.acs.org
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Green-Synthesis-Derived CdS Quantum Dots Using Tea Leaf Extract: Antimicrobial, Bioimaging, and Therapeutic Applications in Lung Cancer Cells
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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SRSF1-Regulated Alternative Splicing in Breast Cancer
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www.cell.com www.cell.com
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Somatic Mutational Landscape of Splicing Factor Genes and Their Functional Consequences across 33 Cancer Types
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- Jan 2018
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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Combination therapy strategies for improving PD-1 blockade efficacy
Methods of augmenting PD-1 blockade against cancer involve concomitant CTLA-4 inhibition among others. Here is a visual representation of common biological pathways and cell types between these genes.
https://www.biovista.com/vizit-research/#!bv_gid=1357fa5ee3b610d1918476e21c7be00c
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- Dec 2017
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jcb.rupress.org jcb.rupress.org
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Page note
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- Nov 2017
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blog.bulletproof.com blog.bulletproof.com
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There are some other doctors that have looked at depriving cancer patients of all vitamin C for periods of time and then hitting them really hard with high doses of vitamin C as a possible way of inducing apoptosis in cancer cells. There’s a lot of research in this area and it’s not like it’s all worked out now. It’s more like we are in the early stages of flight and we need research is what we really need and unfortunately, it’s hard to come by at the funding for this particular area.
Vitamin C Cancer
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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In silico modeling predicts drug sensitivity of patient-derived cancer cells
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www.lrjournal.com www.lrjournal.com
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Computational drug treatment simulations on projections of dysregulated protein networks derived from the myelodysplastic mutanome match clinical response in patients
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www.sciencedirect.com www.sciencedirect.com
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pairwise overlaps using Fisher’s test and mutual exclusion (Leiserson et al., 2016xA weighted exact test for mutually exclusive mutations in cancer. Leiserson, M.D.M., Reyna, M.A., and Raphael, B.J. Bioinformatics. 2016; 32: i736–i745Crossref | PubMed | Scopus (4)See all ReferencesLeiserson et al., 2016)
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www.nature.com www.nature.com
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CIBERSORT, a computational approach for inferring leukocyte representation in bulk tumor transcriptomes
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gmt.genome.wustl.edu gmt.genome.wustl.edu
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SomaticSniper
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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tier 1 contains all changes in the amino acid coding regions of annotated exons, consensus splice-site regions, and RNA genes (including microRNA genes). Tier 2 contains changes in highly conserved regions of the genome or regions that have regulatory potential. Tier 3 contains mutations in the nonrepetitive part of the genome that does not meet tier 2 criteria, and tier 4 contains mutations in the remainder of the genome
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- Sep 2017
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www.scientificamerican.com www.scientificamerican.com
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One Test May Spot Cancer, Infections, Diabetes and More
based on cell free DNA fragments in blood; DNA methylation patterns and fragment length distributions can inform on organ of origin.
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- Jul 2017
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Local file Local file
- Apr 2017
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science.sciencemag.org science.sciencemag.org
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The Administration could also exercise its regulatory authority—most potently, to direct the Centers for Medicare and Medicaid Services (CMS) to allow reimbursement for molecular profiling of cancers
Perhaps the most important measure to keep precision medicine initiate alive. Surge in risk and treatment response prediction in genomic assays is of little value without practical means of affordable molecular profiling of a patient's tumor or more importantly, pre-diagnosis genomic screen.
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www.the-scientist.com www.the-scientist.com
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While it seems like such multiple mutations should be unlikely, computational biologist Niko Beerenwinkel of ETH Zurich in Basel, Switzerland, recently posted a preprint to bioRxiv suggesting that recurrent mutations can and do occur, and not infrequently (bioRxiv, doi:10.1101/094722, 2016).
Fig 1 of preprint: mutated allele may get lost due to LOH event or less likely due to recurrent mutation, and thus reverting to the original base.
In the former event, SNV could be a preceding dominant negative loss-of-function event which may follow LOH event to remove the beneficial trait (SNV itself). This makes sense for a haploinsufficient gene. However, that's not a strictly speaking a recurrent mutation event as the latter is a copy number level and not mutation change.
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- Mar 2017
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www.buzzfeed.com www.buzzfeed.com
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9. And regular orgasms can reduce the risk of prostate cancer.
The study that is hyperlinked in this article takes you to a blog post on the Harvard Medical School Prostate Knowlegde blog. They didn't do the study, but they wrote a post about two studies that were conducted on the topic and gave references, which made it nice to follow. After reading the two studies, i found that this title tends to be misleading in its statement. Both studies conducted found that men who ejaculate more than either 7 times per week or more than 21 times a month have a decreased risk of prostate cancer. To me, this is not regular orgasms, that amount seems to be on the higher end for most people and hard to continue through out your life. In conclusion, yes, more ejaculations can reduce your risk of prostate cancer, but the amount needed is high and must be started at a young age to fully reap the benefits.
APA References:
Giles, G.G., Severi, G., English, D.R., McCredie, M.R.E., Borland, R., Boyle, P., & Hopper, J.L. (2003). Sexual factors and prostate cancer. BJU International, 92(3), 211-216.
Leitzmann, M.F., Platz, E.A., Stampfer, M.J., Willett, W.C., Giovannucci, E. (2004). Ejaculation frequency and subsequent risk of prostate cancer. JAMA: Journal of the American Medical Association, 291(13), 1578-1586.
Links: http://jamanetwork.com/journals/jama/fullarticle/198487?=quot;,gt;
http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410X.2003.04319.x/full
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www.healthy-holistic-living.com www.healthy-holistic-living.com
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Research proving cannabis kills cancer cells has been suppressed since 1974.
Like so many other kids I was told that marihuana kills brain cells and to stay away from it. When I saw this article it peeked my interest. I was skeptical of its truthfulness Then, I looked up the 1974 National Institute of Health referenced in the article. In the article I found evidence that an adenocarcinoma (cancer) tumor tested on mice resulted in inhibited and or reduced size when using delta-8-tetrahydrocannabinol (THC) and cannabinol (CBN). According to the study supported by the Public Health Service grant, the National Institute on Drug Abuse, Health Services & Mental Health Administration and by other grants. “Lewis lung adenocarcinoma growth was retarded by the oral administration of delta-9-tetrahydrocannabinol”. (A.E. Munson, L.S. Harris, M.A. Friedman, W.L Dewey, and R.A Carchman) National Cancer Institute, Vol. 55, No. 3, September 1975 and also I found a Canadian review article published in Current Oncology, “a large body of evidence shows that these molecules can decrease tumour growth in animal models of cancer.” The results of these studies leave me surprised. I found references that were opposite from what I have taught. Although, I would not advise the recreational use of smoking cannabis. I can see its usefulness in inhibiting and or reducing the size of cancerous tumors. I did not, however, find evidence to support the statement that cannabis kills cancer cells. In any case this subject is definitely warrants further study.
References A.E. Munsion, L.S. Harris, M.A. Friedman, W. Dewey, and R.A. Carchman, Jornal of the National Cancer Institute, Vol. 55, No. 3, September 1975 Research Providing Cannabis Kills Cancer Cells Safely has been Suppressed since 1974 (2016, December 24). Retrieced March 9, 2017, from http://www.realfarmacy.com/research-proving-cannabis-kills-cancer-cells-safely-suppressed-since 1974 Ware, M. (n.d.). Cannabis and cancer: towards a new understanding. Retrieved March 29, 2017,
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www.chronicle.com www.chronicle.com
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A UConn engineering professor has uncovered new information about how particles behave in our bloodstream, an important advancement that could help pharmaceutical scientists develop more effective cancer drugs.
What a great development!
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- Feb 2017
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en.wikipedia.org en.wikipedia.org
- Sep 2016
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www.davidwolfe.com www.davidwolfe.com
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Credibull score = 0.76 / 10
What is Credibull? getcredibull.com
To provide feedback on the score fill in the form available here
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- Mar 2016
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www.cancer.org www.cancer.org
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Does fluoride cause cancer?
This is one of my questions.
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- Feb 2015
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www.mayoclinic.org www.mayoclinic.org
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The survival rate for people with your particular cancer might be based on thousands of people.
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- Dec 2014
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www.canceractive.com www.canceractive.com
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Hi
In my opinion this site supports the use of unproven (experimental) therapies and disproven (proven to be not effective) therapies. This Cancer Society site presents a balanced aprroache which will help you to evaluate for yourself the use of alternative therapies. Using alternative therapies in cancer care
Bridge
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- Nov 2014
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blog.sfgate.com blog.sfgate.com
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Marijuana kills cancer cells in proportion to its dose and duration of treatment, researchers found, and whole plant cannabis rich in THC was more efficacious than pure, lab-grade THC alone.
We clearly have a lot to learn about cannabinoids and terpenes. There are maybe medical breakthroughs to be made here, breakthroughs that have been delayed for decades by reactionary, draconian drug laws.
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- May 2014