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Review coordinated by Life Science Editors Foundation Reviewed by: Dr. Angela Andersen, Life Science Editors Foundation & Life Science Editors Potential Conflicts of Interest: None

PUNCHLINE Prostate cancer–associated fibroblasts (CAFs) exhibit conserved and quantifiable differences in morphology and biomechanics compared to matched non-malignant fibroblasts (NPFs). These morphomechanical features—particularly increased stiffness, volume, and nuclear elongation—are correlated with transcriptional programs and clinical outcomes, positioning fibroblast biophysics as a potential biomarker and therapeutic target in prostate cancer.

BACKGROUND Tumor progression is tightly intertwined with the tumor microenvironment (TME), where CAFs play a key role by remodeling the extracellular matrix and altering tissue mechanics. While bulk tissue stiffness has been studied extensively in cancer, the mechanical properties of individual CAFs—and their consistency across patients and link to clinical outcomes—are not well defined. The study leverages a rare resource: 35 pairs of matched CAF and NPF primary cultures from radical prostatectomy specimens, enabling a systematic comparison of morphomechanical traits and their clinical relevance.

QUESTIONS ADDRESSED Do prostate CAFs exhibit consistent morphomechanical changes compared to matched NPFs?

Are these features linked to patient outcomes or tumor grade?

Can CAF biomechanics be modulated by signaling pathways or therapeutic agents?

Do these traits reflect distinct transcriptional signatures, particularly the myofibroblast-like (myCAF) phenotype?

SUMMARY Using real-time deformability cytometry (RT-DC), atomic force microscopy (AFM), and high-content imaging, the authors show that CAFs are consistently stiffer, larger, and more elongated than NPFs across patients. A principal component–derived morphomechanical score integrates five features (volume, Young’s modulus, nuclear area, nuclear circularity, and F-actin alignment) and stratifies patients by clinical outcome. Transcriptomic correlates reveal a link to microtubule dynamics and myCAF signatures. Notably, CAF stiffness can be altered by TGF-β signaling and anti-cancer agents, suggesting potential avenues for stromal reprogramming.

KEY RESULTS CAFs Exhibit Conserved Biophysical Phenotypes

Across 35 matched pairs, CAFs are consistently stiffer (RT-DC, AFM) and larger in both nuclear and cytoplasmic dimensions.

F-actin fibers in CAFs are more aligned, and nuclei more elongated, than in NPFs.

These features were independent of tumor grade but associated with clinical relapse.

A Composite Morphomechanical Score Correlates with Outcome

PCA of the five morphomechanical traits yields a score that stratifies patients.

Higher scores are associated with biochemical and clinical relapse.

Transcriptional Correlates of Biomechanical States

49 genes correlate with the morphomechanical score; top hits include NAV3, MYOCD, and ARHGAP28, implicating cytoskeletal remodeling.

Enrichment for microtubule and myCAF signatures supports a contractile phenotype underlying mechanical changes.

Biophysical Traits Are Pharmacologically Modifiable

TGF-β1 increases nuclear size and stiffness in CAFs, while TGF-β inhibition reduces stiffness.

Docetaxel and axitinib also modulate fibroblast biophysics, suggesting that approved cancer therapies may influence the stromal compartment.

STRENGTHS Large, well-annotated cohort with matched CAF/NPF pairs.

Rigorous integration of imaging, biophysical assays, and transcriptomics.

Clear demonstration of phenotypic consistency and clinical relevance.

Insight into mechanobiological regulation and therapeutic modulation of CAFs.

FUTURE WORK Can morphomechanical profiling be applied to in situ biopsies or circulating fibroblasts?

Is the morphomechanical phenotype of CAFs reversible, and does this influence tumor behavior?

How do CAF mechanics interface with epithelial cell signaling and immune exclusion?

Could targeted reprogramming of CAFs (e.g., via TGF-β blockade) improve therapeutic response?

FINAL TAKEAWAY This study establishes that prostate CAFs are not only functionally distinct but also physically distinct in measurable and clinically relevant ways. The morphomechanical phenotype of CAFs emerges as a novel dimension of tumor biology—potentially serving as both a biomarker and a therapeutic target. By placing CAF biomechanics in the context of differentiation state, gene expression, and treatment response, the work opens new avenues for integrating stromal biology into precision oncology.

for - Deep Humanity - Mortality Salience - Oliver Sacks - Announces his terminal cancer and says farewell - Source: NY Times - Opinion - My Own Life - Oliver Sacks - 2015, Feb 19

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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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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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

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

for - adjacency - food - angiogenesis - cancer

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

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.

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?

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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Fenbendazole cancer prophylaxis protocol.

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.

• 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

• comment

  • colon cancer starts in the mouth!

• references

  • 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.

  • 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.

• for: quote - Michael Levin, quote - MET of individuality, quote - memory wipe, quote - cancer therapy - MET of individuality

• 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

• comment

  • Michael refers to cancer as a "memory wipe" where they have forgotten the normative programmed narrative of bodily / collective / multicellular unity

• for: MET of individuality - examples of breakdown - cancer

• 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

• 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

• 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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成人癌症：上皮組織 兒童癌症：胚胎型癌、中胚層癌

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I always feel better during and after a forest walk.

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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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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

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.

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

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

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

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.

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).

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

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

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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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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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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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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https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

https://github.com/lmichan/BioDBS

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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/

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

Replicating scientific results is tough—But essential. (2021). Nature, 600(7889), 359–360. https://doi.org/10.1038/d41586-021-03736-4

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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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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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

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

Attitude doesn't have anything to do with healing Cancer.

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.