Podcasts about Carcinogenesis

If you've spent any time on TikTok or Instagram, there is no doubt you've heard about the “dangers of glyphosate”. This message has only increased since the introduction of MAHA and RFK Jr. A group of people who continuously spread misleading and false claims about nutrition, food science, vaccines, COVID-19, climate change, pharmaceutical industry, gun violence, and more. The MAHA group is convinced that glyphosate in our food is one of the leading causes of poor health outcomes in America. Meanwhile, there is a large body of research, including both human and animal subjects, showing no evidence of this risk. This group also forgets to address and acknowledge the social determinants of health and how oppressive systems impact a person's overall health, but that's for another post. Let's talk about the facts. Sources: Williams, G. M.; Kroes, R.; Munro, I. C. Safety evaluation and risk assessment of the herbicide Roundup and its active ingredient, glyphosate, for humans. Regul. Toxicol. Pharmacol. 2000, 31, 117-165. Stout, L.; Ruecker, F. Chronic study of glyphosate administered in feed to albino rats. Unpublished Report no. MSL-10495 R.D. 1014, 1990, submitted to U.S. Environmental Protection Agency by Monsanto Agricultural Company. Reregistration Eligibility Decision (RED) Glyphosate; EPA-738-F-93-011; U. S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1993. Atkinson, C.; Strutt, A.V.; Henderson, W.; Finch, J.; Hudson, P. Glyphosate: 104 week combined chronic feeding/oncogenicity study in rats with 52 week interim kill (results after 104 weeks). Unpublished report No. 7867, IRI project no. 438623, 1993, submitted to World Health Organization by Cheminova A/S, Lemvig, Denmark, prepared by Inveresk Research International, Tranent, Scotland. Pesticide Residues in Food - 2004: Toxicological evaluations; International Programme on Chemical Safety, World Health Organization: Geneva, Switzerland, 2004. Roberts, T. R. Metabolic Pathways of Agrochemicals-Part 1: Herbicides and Plant Growth Regulators; The Royal Society of Chemistry: Cambridge, UK, 1998; pp 396-399. Davoren M.J., Schiestl R.H. Glyphosate-based herbicides and cancer risk: A post-IARC decision review of potential mechanisms, policy and avenues of research. Carcinogenesis. 2018;39:1207–1215. Williams G.M., Kroes R., Munro I.C. Safety Evaluation and Risk Assessment of the Herbicide Roundup and Its Active Ingredient, Glyphosate, for Humans. Regul. Toxicol. Pharmacol. 2000;31:117–165. Benbrook C.M. Trends in glyphosate herbicide use in the United States and globally. Environ. Sci. Eur. 2016;28:1–15. Bai S.H., Ogbourne S.M. Glyphosate: Environmental contamination, toxicity and potential risks to human health via food contamination. Environ. Sci. Pollut. Res. 2016;23:18988–19001.

Folge ansehen auf YouTubeDanke an die WerbepartnerDiese Folge wird durch foryouehealth unterstützt. Selbsttests für zu Hause. foryou Selbsttests ermöglichen es Dir, Deine Biomarker aus Blut, Speichel, Atem oder Stuhl einfach und bequem zu messen. Einfach und bequem den Test zu Hause durchführen? Das geht mit den Tests von for you eHealth. Die Ergebnisse Deiner Darm- und Blutanalyse kannst du dann online abrufen. https://www.foryouehealth.de Mit dem Gutscheincode: Julia10 sparst du 10% auf die Produkte!Kapitel00:00:00 Intro und Einleitung zur Folge 00:02:30 ForYou Heimtest für zu Hause - Sponsor 00:03:38 Begrüßung und Vorstellung von Dr. Henning Saupe 00:05:34 Steigenden Krebsdiagnosen und die Notwendigkeit, das Risiko zu senken. 00:11:15 Die Notwendigkeit, die Schulmedizin durch ganzheitliche Ansätze zu ergänzen 00:14:55 Einführung in die zwölf Vitalfelder 00:22:31 Chronische Entzündungen und Krankheiten 00:26:56 Unterstützung der Entgiftung 00:33:33 Nahrungsmangel und Nährstoffe 00:36:33 Einfluss von Stress auf das Nervensystem und die Gesundheit 00:47:36 Bedeutung von Sauerstoff für die Krebszellen und Strategien zur Verbesserung der Sauerstoffversorgung im Körper. 00:58:48 Insulin-potenzierte Therapie 01:07:53 Hyperthermie als Therapie 01:09:54 Forschung zu kostengünstigen TherapienWir sprechen überKrebs ist eine zunehmend häufige Erkrankung.Die moderne Medizin hat einen engen Fokus auf Symptome.Holistische Ansätze können die Schulmedizin ergänzen.Entzündungen sind ein zentraler Faktor für viele Krankheiten.Entgiftung ist entscheidend für die Gesundheit.Die Ernährung spielt eine wichtige Rolle bei der Prävention von Krebs.Stress hat negative Auswirkungen auf das Immunsystem.Die Darmgesundheit ist entscheidend für das allgemeine Wohlbefinden.Veränderung von Glaubenssätzen ist notwendig für eine gesunde Lebensweise. Motivation ist entscheidend, um ungesundes Verhalten zu überwinden.Insulin kann die Wirkung von Chemotherapie verstärken.Hyperthermie kann die Effektivität von Therapien erhöhen.Mitochondrien sind entscheidend für die Energieproduktion in Zellen.Gesunder Zellstoffwechsel ist entscheidend für die Krebsbekämpfung.Alles über Dr. Henning SaupeDr. med. Henning Saupe, geboren 1964 in Laupheim, Deutschland, ist ein international anerkannter Experte auf dem Gebiet der ganzheitlichen Krebstherapie. Sein Medizinstudium absolvierte er von 1986 bis 1992 an der Universität Ulm, wo er 1992 seine Approbation als Arzt erhielt. Im Jahr 1995 erlangte er nach seiner Promotion in Psychotherapie den Titel Dr. med.Dr. Saupe erhielt 1996 auch die schwedische Approbation und arbeitete zehn Jahre lang in Stockholm als Allgemeinmediziner mit Schwerpunkten in Naturheilkunde, anthroposophischer Medizin und ganzheitlicher Krebstherapie. Von 1997 bis 2006 war er Vorstandsmitglied des Schwedischen Verbandes anthroposophischer Ärzte. 2005 gründete er die erste Hyperthermie-Klinik Schwedens, die sich auf onkologische Hyperthermie spezialisierte. Im Jahr 2006 verlegte er die Klinik nach Kassel und eröffnete 2014 die Arcadia-Praxisklinik in Bad Emstal, wo er als ärztlicher Leiter mit einem Team von 25 Mitarbeitern tätig ist.Dr. Saupe ist ein gefragter Vortragsredner in Skandinavien und den USA, wo er regelmäßig zum Thema ganzheitliche Krebsbehandlung spricht. Im Jahr 2007 wurde ihm im Stockholmer Parlamentsgebäude der Professor Olof Lindals Preis für Komplementärmedizin verliehen. Er ist Mitglied der International Clinical Hyperthermia Society (ICHS) und der Deutschen Gesellschaft für Onkologie (DGO).Sein Buch "Krebs verstehen und ganzheitlich behandeln" erschien 2021 auf Deutsch und 2022 auf Englisch unter dem Titel "Holistic Cancer Medicine". Weitere Übersetzungen, unter anderem ins Niederländische, Portugiesische und Koreanische, sind bereits erschienen oder in Planung.Seit 2023 ist Dr. Saupe Mitglied des "Holistic Leadership Council" in den USA, wo er seine Expertise weiter einbringt und internationale Anerkennung für seine Arbeit erfährt.BuchKrebs verstehen und ganzheitlich behandeln: Integrative Strategien für einen neuen Umgang mit Krebshttps://amzn.to/4ffCDN6Websitehttp://www.arcadia-praxisklinik.dehttps://www.facebook.com/henning.hahn.90/Relevante ArtikelQin, Junhong, et al. "Ketogenic diet reshapes cancer metabolism through lysine β-hydroxybutyrylation." Nature Metabolism (2024): 1-24.https://www.nature.com/articles/s42255-024-01093-wSeyfried, Thomas N., et al. "Cancer as a metabolic disease: implications for novel therapeutics." Carcinogenesis 35.3 (2014): 515-527.https://academic.oup.com/carcin/article/35/3/515/2463440Seyfried, Thomas N., et al. "Consideration of ketogenic metabolic therapy as a complementary or alternative approach for managing breast cancer." Frontiers in Nutrition 7 (2020): 21.https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2020.00021/fullLe Guevelou, Jennifer, et al. "Combined hyperthermia and radiotherapy for prostate cancer: a systematic review." International Journal of Hyperthermia 39.1 (2022): 547-556.https://pubmed.ncbi.nlm.nih.gov/35313781/Damyanov, Chr, et al. "Low dose chemotherapy in combination with insulin for the treatment of advanced metastatic tumors. Preliminary experience." J BUON 14.4 (2009): 711-5.https://pubmed.ncbi.nlm.nih.gov/20148468/Damyanov, Christo, et al. "Low‐Dose Chemotherapy with Insulin (Insulin Potentiation Therapy) in Combination with Hormone Therapy for Treatment of Castration‐Resistant Prostate Cancer." International Scholarly Research Notices 2012.1 (2012): 140182.https://pmc.ncbi.nlm.nih.gov/articles/PMC3357525/#ref-list1Zeige deinen SupportDir gefällt die Show und die Inhalte? Der beste Weg, uns zu unterstützen, kostet dich nur ein paar Sekunden. Hinterlasse eine Bewertung und/ oder einen Kommentar auf YouTube, iTunes oder Spotify. https://www.youtube.com/@JuliaTulipanKeto?sub_confirmation=1 Bitte beachten Sie auch immer den aktuellen "Haftungsausschluss (Disclaimer) und allgemeiner Hinweis zu medizinischen Themen" auf https://juliatulipan.com/haftungsausschluss/

Kristina Marusic, author of 'A New War on Cancer,'  discusses her motivation and research into the chemicals contributing to rising cancer rates.  Tina and Leah cover a lot of ground in this interview. She discusses the pitfalls of individual responsibility. She talks about a system that permits the use of known carcinogens. She also covers what can be done to push the agenda toward a healthier place for all of us. Did you know that of the over 300,000 industrial chemicals invented in the last century, only five have ever been taken off the market in the USA?  Neither did we! Hit play and join us for an enlightening and hopeful discussion! More about Kristina MarusicBuy her book at Island Press, use the checkout code WAR for 20% off  Link to Cancer Moonshot Project (add your two cents!)Environmental Working Group (EWG) Skin Deep Project (find cleaner products)Anti-Cancer Lifestyle ProgramSupport the Show.Our website:https://www.thecancerpod.com Have an idea or question? Email us: thecancerpod@gmail.comJoin our growing community, we are @TheCancerPod on: Instagram Twitter Facebook LinkedIn THANK YOU for listening!

Dr. Goodson grew up in Missouri and graduated from the University of Missouri Columbia and Harvard Medical School. He trained as a general surgeon and specialized in breast surgery before it was a recognized field. He was a member of the research group that established breast conservation, i.e., lumpectomy, as the preferred treatment for early breast cancer. Recognizing that he was treating more young women with breast cancer, he joined with Dr. Shanaz Dairkee in 2005 to investigate how common environmental chemicals such as BPA, methylparaben, PFOA, etc. disrupt the normal biology of non-cancerous, human breasts. He has been a professor at the University of California San Francisco and a Senior Scientist at the California Pacific Medical Center Research Institute. He is a fellow of the American College of Surgeons, a member of the American Society for Clinical Oncology, and a spokesperson for The Halifax Project. In addition to research, he enjoys photography, writing, and creating hand-drawn animation as on his website, www.drwilliamgoodson.com A Ternary Mixture of Common Chemicals Perturbs Benign Human Breast Epithelial Cells More Than the Same Chemicals Do Individually. Dairkee SH, Luciani-Torres G, Moore DH, Jaffee IM, Goodson WH 3rd. Toxicol Sci. 2018 Sep 1;165(1):131-144. doi: 10.1093/toxsci/kfy126. PMID: 29846718 Free PMC article.   Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead. Goodson WH 3rd, Lowe L, Carpenter DO, Gilbertson M, Manaf Ali A, Lopez de Cerain Salsamendi A, Lasfar A, Carnero A, Azqueta A, Amedei A, Charles AK, Collins AR, Ward A, Salzberg AC, Colacci A, Olsen AK, Berg A, Barclay BJ, Zhou BP, Blanco-Aparicio C... See abstract for full author list ➔ Carcinogenesis. 2015 Jun;36 Suppl 1(Suppl 1):S254-96. doi: 10.1093/carcin/bgv039. PMID: 26106142 Free PMC article.   Consensus on the key characteristics of endocrine-disrupting chemicals as a basis for hazard identification. La Merrill MA, Vandenberg LN, Smith MT, Goodson W, Browne P, Patisaul HB, Guyton KZ, Kortenkamp A, Cogliano VJ, Woodruff TJ, Rieswijk L, Sone H, Korach KS, Gore AC, Zeise L, Zoeller RT. Nat Rev Endocrinol. 2020 Jan;16(1):45-57. doi: 10.1038/s41574-019-0273-8. Epub 2019 Nov 12. PMID: 31719706 Free PMC article.   Exposure to the polyester PET precursor--terephthalic acid induces and perpetuates DNA damage-harboring non-malignant human breast cells. Luciani-Torres MG, Moore DH, Goodson WH 3rd, Dairkee SH. Carcinogenesis. 2015 Jan;36(1):168-76. doi: 10.1093/carcin/bgu234. Epub 2014 Nov 19. PMID: 25411358 Free PMC article.   The Key Characteristics of Carcinogens: Relationship to the Hallmarks of Cancer, Relevant Biomarkers, and Assays to Measure Them. Smith MT, Guyton KZ, Kleinstreuer N, Borrel A, Cardenas A, Chiu WA, Felsher DW, Gibbons CF, Goodson WH 3rd, Houck KA, Kane AB, La Merrill MA, Lebrec H, Lowe L, McHale CM, Minocherhomji S, Rieswijk L, Sandy MS, Sone H, Wang A, Zhang L, Zeise L, Fielden M. Cancer Epidemiol Biomarkers Prev. 2020 Oct;29(10):1887-1903. doi: 10.1158/1055-9965.EPI-19-1346. Epub 2020 Mar 9. PMID: 32152214 Free PMC article.   Testing the low dose mixtures hypothesis from the Halifax project. Goodson WH, Lowe L, Gilbertson M, Carpenter DO. Rev Environ Health. 2020 Aug 24;35(4):333-357. doi: 10.1515/reveh-2020-0033. Print 2020 Nov 18. PMID: 32833669 Review.   Using the Key Characteristics of Carcinogens to Develop Research on Chemical Mixtures and Cancer. Rider CV, McHale CM, Webster TF, Lowe L, Goodson WH 3rd, La Merrill MA, Rice G, Zeise L, Zhang L, Smith MT. Environ Health Perspect. 2021 Mar;129(3):35003. doi: 10.1289/EHP8525. Epub 2021 Mar 30. PMID: 33784186 Free PMC article.   Bisphenol-A-induced inactivation of the p53 axis underlying deregulation of proliferation kinetics, and cell death in non-malignant human breast epithelial cells. Dairkee SH, Luciani-Torres MG, Moore DH, Goodson WH 3rd. Carcinogenesis. 2013 Mar;34(3):703-12. doi: 10.1093/carcin/bgs379. Epub 2012 Dec 7. PMID: 23222814 Free PMC article.   Activation of the mTOR pathway by low levels of xenoestrogens in breast epithelial cells from high-risk women. Goodson WH 3rd, Luciani MG, Sayeed SA, Jaffee IM, Moore DH 2nd, Dairkee SH. Carcinogenesis. 2011 Nov;32(11):1724-33. doi: 10.1093/carcin/bgr196. Epub 2011 Sep 1. PMID: 21890461 Free PMC article.  

Unlock the secrets of the ketogenic diet with Dr. Dominic D'Agostino as we navigate the nuances of ketogenic protocols, from their clinical roots in epilepsy treatment to their modern-day applications in enhancing athletic prowess and brain health. Whether you're a seasoned keto aficionado or simply curious about this high-fat lifestyle, you're in for a wealth of knowledge that could reshape your understanding of nutrition.Timeline (Episode 64)1:50 Dr. Dom has cows and gators in his backyard! His dogs have fought with gators. The mammals win! 3:45 Definition of Ketogenic Diet (KD)8:18 There are over 100 years of clinical use of the KD9:04 Fasting was a “cure” for seizures11:00 Effects on the brain – how does the KD affect normal healthy subjects15:10 Dom has been a KD for 15 years18:34 Dom used the old MET-Rx brand way back when!21:00 Exogenous ketone ester supplementation studies – where do we stand on this?21:58 Consume MCT oil (the poor man's ketone ester)26:30 Higher ketone levels is not better27:00 Ketone esters > Ketone salts in extreme environments28:00 Dosing of Ketone esters (higher is not better)29:22 Don't exceed 10 grams of Beta-hydroxybutyrate34:07 Advantage of being in ketosis vis a vis performance – under conditions of glycogen depletion esp. in the cognitive domain41:57 A good supplement to start with are MCT oils (since it will elevate your ketones)45:20 Perhaps use these esters as a training aid; given acute may enhance PVT49:30 Debunking the myth that high fat diets are always “bad.”About our guest: Dominic D'AgostinoPh.D., Physiology, Neuroscience, University of Medicine and Dentistry of New Jersey, 2004B.S., Biological Sciences, Nutrition Science, Rutgers University, 1998A researcher and professor with a diverse background in neuroscience, molecular pharmacology, nutrition, and physiology, Dominic D'Agostino, Ph.D., is a tenured Associate Professor in the Department of Molecular Pharmacology and Physiology at the University of South Florida (USF) Morsani College of Medicine. He is also a Research Scientist at the Institute for Human and Machine Cognition (IHMC). Dr. D'Agostino earned his Ph.D. in 2004 and subsequently entered into a postdoctoral fellowship in neuroscience at the Boonshoft School of Medicine at Wright State University in Ohio.He has been awarded numerous grants that have resulted in national and international research collaborations and publications in such peer-reviewed journals as the Journal of Applied Physiology, Cell Metabolism, Neuroscience, Carcinogenesis, Nature Medicine, Journal of Neurophysiology, and the Journal of Microscopy.About the ShowWe cover all things related to sports science, nutrition, and performance. The Sports Science Dudes represent the opinions of the hosts and guests and are not the official opinions of the International Society of Sports Nutrition (ISSN), the Society for Sports Neuroscience, or Nova Southeastern University. The advice provided on this show should not be construed as medical advice and is purely an educational forum.Hosted by Jose Antonio, PhDDr. Antonio is the co-founder and CEO of the International Society of Sports Nutrition and the co-founder of the Society for Sports Neuroscience, www.issn.net. Dr. Antonio has over 120 peer-reviewed publications and 16 books. He is a Professor at Nova Southeastern University, Davie, Florida in the Department of Health and Human Performance.Twitter: @JoseAntonioPhDInstagram: the_issn and supphdCo-host Anthony Ricci EdDDr Ricci is an expert on Fight Sports and is currently an Assistant Professor at Nova Southeastern University in Davie Florida in the Department of Health and Human Performance.Instagram: sportpsy_sci_d

BUFFALO, NY- December 18, 2023 – A new research #perspective was #published in Oncotarget's Volume 14 on December 12, 2023, entitled, “Melatonin and carcinogenesis in mice: the 50th anniversary of relationships.” Fifty years ago, in 1973, Vladimir N. Anisimov and coauthors demonstrated for the first time an inhibitory effect of the pineal gland hormone melatonin on cancer in vivo, namely on transplantable mammary tumors in mice. Subsequently, it was shown in a number of studies that melatonin administration with drinking water at night inhibits chemically induced mammary carcinogenesis in mice and rats. On the contrary, maintaining female mice and rats under round-the-clock lighting conditions, which suppresses the nighttime production of melatonin, stimulates spontaneous and chemical carcinogen-induced mammary tumor development. As of today, the query “cancer AND melatonin AND mice” in Pubmed returns about 550 entries. In this new research perspective, researchers Vladimir N. Anisimov and Alexey G. Golubev from N.N. Petrov National Medical Research Center of Oncology outline the history of studies of melatonin effects on cancer in mice, with the main lesson being that the systemic in vivo effects of melatonin on animals may overwhelm the in vitro effects found using tissue explants or cell cultures. “In particular, the timing of melatonin administration is of crucial importance for using the drug, which is freely available over [the] counter and thus needs no licensing for its applications in oncology.” DOI - https://doi.org/10.18632/oncotarget.28537 Correspondence to - Vladimir N. Anisimov - aging@mail.ru Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28537 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, melatonin, mice About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

In today's episode with Dr. Sonia Malani, you'll hear us take a deep dive on: 1. The impact of integrative oncology on cancer care; 2. Supplements in integrative oncology; 3. The role of integrative oncologists in addressing holistic health factors; 4. Reducing stress, detoxification, and improving outcomes in cancer care; 5. Strategic dietary choices for cancer prevention and supportive care; 6. Ketamine-assisted psychotherapy for cancer patients. Dr. Sonia Malani is a board-certified naturopathic oncologist with specialized expertise in pain management and palliative care. Passionate about cancer prevention, she delves deeply into precision oncology utilizing ctDNA technology and focuses on addressing metabolic comorbidities in patients with cancer. Beyond her medical honors, Dr. Malani is a published author and dedicated researcher. Moreover, she wears multiple hats as a certified yoga instructor, meditation teacher, and a provider of Ketamine-Assisted Psychotherapy. Dr. Malani also plays a vital role as a co-investigator in the AIMS Cancer Outcomes Study (ACOS). Order tests through Rupa Health, the BEST place to order functional medicine lab tests from 30+ labs - https://www.rupahealth.com/reference-guide

Dr Philip Smith, Digital and Education Editor of Gut and Honorary Consultant Gastroenterologist at the Royal Liverpool Hospital, Liverpool, UK interviews Professor Markus Gerhard from the Institute for Medical Microbiology, Immunology and Hygiene, School of Medicine, Technical University of Munich, Germany, on the paper "Helicobacter pylori promotes colorectal carcinogenesis by deregulating intestinal immunity and inducing a mucus-degrading microbiota signature" published in paper copy in Gut in July 2023 and available online: https://gut.bmj.com/content/72/7/1258   Please subscribe to the Gut Podcast via all podcast platforms, including Apple Podcasts, Google Podcasts, Stitcher and Spotify, to get the latest podcast every month. If you enjoy our podcast, please consider leaving us a review or a comment on the Gut Podcast iTunes page (https://podcasts.apple.com/gb/podcast/gut-podcast/id330976727).

This episode explores how social media and cognitive psychology can be used to optimise patient–doctor relationships, and enhance teaching and diagnosis in dermatology and dermatopathology. Christine Ko, Professor of Dermatology and Pathology, Yale University, New Haven, Connecticut, USA, joins Jonathan for a second podcast episode where they discuss Ko's publications, dive deeper into cognitive bias and visual perception in clinical practice, and consider the challenges in humanising medicine in dermatology and dermatopathology.   Use the following timestamps to navigate the topics discussed in this episode:  (00:00)-Introduction (00:30)-Using social media to learn about patient experience (04:12)-The role of visual perception in dermatology and dermatopathology (09:05)-Cognitive bias and its implications in dermatology (13:15)-Discussing Ko's book, ‘How to Improve Doctor-Patient Connection', and the importance of building good relationships  (19:37)-Challenges in humanising medicine in dermatology and dermatopathology (26:03)-Three wishes for the future of healthcare

Christine Ko, Professor of Dermatology and Pathology, Yale University, New Haven, Connecticut, USA, joins Jonathan to discuss her early career and the ever-increasing burden of skin cancer. Ko also introduces Jonathan to the field of transplant dermatology.   Use the following timestamps to navigate the topics discussed in this episode:  (00:00)-Introduction  (02:15)-Ko's journey into dermatology and dermatopathology  (04:31)-Squamous cell carcinogenesis  (08:45)-Why skin cancer is becoming more common  (11:11)-Transplant dermatology  (14.02)-Changes in education 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.28.517589v1?rss=1 Authors: Fuller, A. D., Karami, A. L., Kabir, M. F., Klochkova, A., Jackson, J. L., Mu, A., Tan, Y., Klein-Szanto, A., Whelan, K. A. Abstract: Under homeostatic conditions, esophageal epithelium displays a proliferation/differentiation gradient that is generated as proliferative basal cells give rise to suprabasal cells then terminally differentiated superficial cells. This proliferation/differentiation gradient is perturbed in esophageal pathologies both benign and malignant. Esophageal cancer is among the deadliest forms of human malignancy with 5-year survival rates of less than 20%. Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are the two most common subtypes of esophageal cancer. Gastroesophageal reflux disease (GERD) is a primary risk factor for EAC. Although GERD and the food allergy-mediated condition eosinophilic esophagitis (EoE) are both associated with chronic esophageal inflammation and epithelial remodeling, including basal cell hyperplasia, epidemiological evidence suggests that EoE patients do not develop esophageal malignancy. Here, we perform single cell RNA-sequencing in murine models of EoE and ESCC to delineate the effects that these two conditions have specifically upon the cellular landscape of esophageal epithelium. In mice with EoE or ESCC, we find expansion of cell populations as compared to normal esophageal epithelium. In mice with EoE, we detect expansion of 4 suprabasal populations coupled with depletion of 4 basal cell populations. By contrast, mice with ESCC display expansion of 4 basal populations as well as depletion of 3 superficial populations. We further evaluated modules of co-expressed genes in EoE- and ESCC-enriched epithelial cell clusters. Senescence, glucocorticoid receptor signaling, and granulocyte-macrophage colony-stimulating factor pathways were associated with EoE-enriched clusters while pathways associated with cell proliferation and metabolism were identified in ESCC-enriched clusters. Finally, by pairing murine models of EoE and ESCC, we demonstrate that exposure to EoE inflammation limits esophageal carcinogenesis. Our findings provide the first functional investigation of the relationship between EoE and esophageal cancer and suggest that esophageal epithelial remodeling events occurring in response to EoE inflammation may limit act to esophageal carcinogenesis which may have future implications for leveraging allergic inflammation-associated alterations in epithelial biology to prevent and/or treat esophageal cancer. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In questo audio il prezioso incontro con Vanni Cuoghi artista Adriana Albini biochimica.L'intervista con Vanni Cuoghi e Adriana Albini è in Contemporaneamente a cura di Mariantonietta Firmani il podcast pensato per Artribune.In Contemporaneamente podcast trovate incontri tematici con autorevoli interpreti del contemporaneo tra arte e scienza, letteratura, storia, filosofia, architettura, cinema e molto altro. Per approfondire questioni auliche ma anche cogenti e futuribili. Dialoghi straniati per accedere a nuove letture e possibili consapevolezze dei meccanismi correnti: tra locale e globale, tra individuo e società, tra pensiero maschile e pensiero femminile, per costruire una visione ampia, profonda ed oggettiva della realtà. Vanni Cuoghi e Adriana Albini ci raccontano di arte e scienza, dove l'essere e il fare coincidono. Di risultati eccellenti cui si arriva attraverso strade ampie e contorte, strettamente calato nel tempo in cui vive. Arte e scienza sono ambiti professionali altamente specializzati e rigorosi, fondati su intuito di ricerca. Ci raccontano di necessità delle relazioni, nutraceutica, nutrigenetica, nutrigenomica, tra bellezza e gioielli. E molto altro.ASCOLTA L'INTERVISTA!BREVI CENNI BIOGRAFICI DEGLI AUTORIVanni Cuoghi, artista dall'ottobre del 2015 è titolare della cattedra di Pittura presso l'Accademia Aldo Galli di Como.Ha partecipato a numerose biennali in Italia e all'estero, tra cui: Biennale di San Pietroburgo (2008), Biennale di Praga (2009). 54° Biennale di Venezia, Corderie dell'Arsenale, Padiglione Italia (2011), Biennale Italia-Cina (2012) e 56° Biennale di Venezia, Collateral Italia Docet (2015). Sue opere esposte in fiere internazionali come: Frieze (Londra), MiArt (Milano), Artefiera (Bologna), Scope (New York), Off (Bruxelles), Daegu Artfair (Corea), KIAF Seoul (Corea), Bank (Hong Kong). È presente in molte mostre collettive in prestigiose location pubbliche come: Palazzo Reale di Milano (2007 ), Haidian Exhibition Center di Pechino (2008). Liu Haisu Museum di Shangai (2008), Museo d'Arte Contemporanea di Permm, in Russia (2010), Castello Sforzesco di Milano (2012). Fabbrica del Vapore di Milano (2015), Vestfossen Kunstlaboratorium Museum in Norvegia (2018). Tra le mostre personali pubbliche si ricordano nel 2011 “Novus Malleus Maleficarum”, presso San Pietro in Atrio e Pinacoteca di Palazzo Volpi a Como.Nel 2013, “Aion" presso i Musei Civici Cremaschi a Crema, nel 2016 “Da Cielo a Terra” al Museo Ebraico di Bologna. Ed ancora nel 2017 “The Invisible Sun”, presso il Museo Francesco Messina a Milano. Nel 2012, su commissione di Costa Crociere, ha realizzato otto grandi dipinti per la nave Costa Fascinosa e nel 2014 sei per Costa Diadema. Le ultime mostre personali: nel maggio 2019 inaugura “The eye of the Storm”, una mostra personale presso la Rossi-Martino Gallery a Hong Kong. In ottobre inaugura la personale “Esuli pensieri” presso la Fondazione Balestra a Longiano (FC). A luglio del 2020 inaugura la mostra personale “Apnea”, a cura di Elisabetta Sgarbi presso le Argenterie nella Villa Reale di Monza. Nel 2021 inaugura la mostra personale “Submariner” al Civico Acquario di Milano, a cura di Nicoletta Castellaneta e Ivan Quaroni. Adriana Albini biochimica, docente e scrittrice italiana, unica donna italiana nella lista BBC 100 Women of 2020. Prima donna italiana eletta nel Board of Directors dell'American Association for Cancer Research.L'intensa attività scientifica è affiancata dalle passione per la scrittura che la porterà a pubblicare diversi romanzi. Appassionata di scherma è medaglia d'argento al campionato europeo del 2015 e bronzo ai Campionati del mondo per veterani 2018. Laurea in chimica organica nel 1979 all'università di Genova, dal 1988 è stata responsbabile di Laboratorio all'Istituto Scientifico Tumori di Genova, (ora San Martino) dove resterà fino al 2006 quando ne era vice-direttrice e direttrice di dipartimento. Specializzazione biochimica all'Istituto Max Plank, di Monaco di Baviera, e Scientist all'National Institute of Health a Bethesda USA fino al 1988, quando è rientrata in Italia. Nel 1985 mette a punto un modello di “metastasi in provetta” usato in tutto il mondo per facilità d'uso e basso costo, anche per lo studio dell'angiogenesi.Dal 2006 dirige laboratori di ricerca biomedica a Milano, Reggio Emilia e dal 2015 dirige un laboratorio di ricerca all'IRCCS MultiMedica ed è Direttore Scientifico di Fondazione MultiMedica Onlus di Milano. Inoltre insegna al Corso di Medicina in Englishall'Università Bicocca di Milano.. Ha diretto o coordinato laboratori di ricerca e gruppi di lavoro. È stata Presidente di società e Gruppi di studio: Comitato Tecnico Scientifico di O.N.Da (Osservatorio Nazionale sulla salute della Donna). Società Italiana di Cancerologia (SIC). Società Internazionale per lo Studio della Metastasi, Metastasis Research Society (MRS). Componente del Direttivo dell'American Association for Cancer Research. E molti altri. È titolare di 14 brevetti per nuove strategie terapeutiche contro il cancro.Conduce diversi studi sulla tossicità per il sistema cardiovascolare di farmaci antineoplastici e sul contributo alla progressione dei tumori, da parte delle cellule infiammatorie.Ha contribuito all'identificazione di un una nuova popolazione di cellule natural killer (NK), nei tumori solidi. Studia gli aspetti molecolari di componenti della dieta alimentare per la creazione di un programma di prevenzione delle neoplasie. Come immunologa ha lavorato su HIV e Covid-19. Svolge ricerca nell'ambito oncologico, in particolare sul microambiente tumorale e angiogenesi, sulla prevenzione farmacologica con derivati alimentari; le sue ricerche hanno evidenziato nelle acque di vegetazione dell'olio di oliva e nelle alghe principi attivi per la lotta contro il cancro; ha coordinato inoltre ricerche sui principi anticancerogeni del luppolo, nella ricerca “La birra e le sue proprietà nutraceutiche” su multimedica.it. e molti altri.Impegnata nella divulgazione Iscritta all'albo dei giornalisti è direttore editoriale della rivista online Cancerworld. Invitata in diversi programmi televisivi RAI tra cui Elisir e Geo. È componente delle redazioni di riviste scientifiche: Journal of the National Cancer Institute, Carcinogenesis, Molecular Cancer Therapeutics, Clinical & Experimental Metastasis, Pathology Oncology Research. Autrice di oltre 300 articoli scientifici, e diversi romanzi tra i cui La danza delle cellule immortali, 2008. In USA si sensibilizza al tema del gender gap e entra a far parte della associazione Women in Cancer Research curando corsi di formazione volti ad insegnare alle donne a farsi strada mettendo a frutto capacità e merito. Ha ideato e è presidente di TIWS (Top Italian Women Scientists), il club delle scienziate italiane più citate in campo biomedico. Tra i molti premi e riconoscimenti: Premio EUWIIN (Network Europeo Donne Inventrici ed Innovatrici nel 2015, Ambasciatrice di Genova nel mondo, BBC 100 women 2020.

Dr. Maricel V. Maffini is an Independent Consultant based in Maryland, US. She has more than 25 years of research experience in the fields of carcinogenesis and breast cancer in particular, reproductive biology and endocrine disruption. For the past 10 years, her work has focused on the safety and regulation of chemicals in food and the decision-making process behind them. Before becoming a consultant, she was senior scientist with the Natural Resources Defense Council; a senior science officer at The Pew Charitable Trust and a Research Assistant Professor at Tufts University School of Medicine. She has authored numerous peer-reviewed journal articles, blogs and book chapters.

ReferencesKoning, Ruud & Matheson, Victor & Nathan, Anil & Pantano, James. (2014). The Long-Term Game: An Analysis of the Life Expectancy of National Football League Players. International Journal of Financial Studies. 2. 168-178. 10.3390/ijfs2010168. Fung TT, van Dam RM, Hankinson SE, et al. Low-carbohydrate diets and all-cause and cause-specific mortality: two cohort studies.Ann Intern Med 2010, 153:289-298.Kaaks R. Nutrition, insulin, IGF-1 metabolism and cancer risk: a summary of epidemiological evidence.Novartis Found Symp 2004, 262:247-260; discussion 260-268.Salvioli S, Capri M, Bucci L, et al. Why do centenarians escape or postpone cancer? The role of IGF-1, inflammation and p53.Cancer Immunol Immunother 2009, 58:1909-1917.Levine ME, Suarez JA, Brandhorst S, et al. Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population.Cell Metab 2014, 19:407-417.Vergnaud AC, Norat T, Romaguera D, et al. Meat consumption and prospective weight change in participants of the EPIC-PANACEA study.Am J Clin Nutr 2010, 92:398-407.Brewer GJ. Iron and copper toxicity in diseases of aging, particularly atherosclerosis and Alzheimer's disease.Exp Biol Med 2007, 232:323-335.Brewer GJ. Risks of copper and iron toxicity during aging in humans.Chem Res Toxicol 2010, 23:319-326.Padler-Karavani V, Yu H, Cao H, et al. Diversity in specificity, abundance, and composition of anti-Neu5Gc antibodies in normal humans: potential implications for disease.Glycobiology 2008, 18:818-830.Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis.Nat Med 2013.Tang WH, Wang Z, Levison BS, et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk.N Engl J Med 2013, 368:1575-1584.de Lorgeril M, Salen P. New insights into the health effects of dietary saturated and omega-6 and omega-3 polyunsaturated fatty acids.BMC Med 2012, 10:50.Lunn JC, Kuhnle G, Mai V, et al. The effect of haem in red and processed meat on the endogenous formation of N-nitroso compounds in the upper gastrointestinal tract.Carcinogenesis 2007, 28:685-690.Zheng W, Lee SA. Well-done meat intake, heterocyclic amine exposure, and cancer risk.Nutr Cancer 2009, 61:437-446.Lagiou P, Sandin S, Lof M, et al. Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study.BMJ 2012, 344:e4026.Lagiou P, Sandin S, Weiderpass E, et al. Low carbohydrate-high protein diet and mortality in a cohort of Swedish women.J Intern Med 2007, 261:366-374.Young VR, Pellett PL. Plant proteins in relation to human protein and amino acid nutrition.Am J Clin Nutr 1994,59:1203S-1212S.Rand WM, Pellett PL, Young VR. Meta-analysis of nitrogen balance studies for estimating protein requirements in healthy adults.Am J Clin Nutr 2003, 77:109-127.

Is cancer its own separate organism? While we believe that it may not be most of the time, some instances of contagious cancer variants do not die with the host. Listen in to learn: How cancers may first arise Why metastatic sites hold vital clues to begin understanding metastasis  How to backtrack a tumor to see how it may have formed  Courtenay C. and Lucy Patten Davis Endowed Chair in Lung Cancer Research, James DeGregori, shares his expertise on various forms of cancer and the theoretical questions of the future. Many people think that random mutations may be the root cause of many forms of cancer. However, new research disputes this, and specialists have begun on a new research path of carcinogens and their effects on the body. While they may cause a higher rate of mutations in the area they affect, carcinogens seem to have many other impacts as well. The critical component of the speculation surrounding cancer is the "why?" of the developing tumors in specific areas that may not be favorable for it. By determining the traits present in particular cells where the tumor began, the genetics can be deciphered, providing a complete image of cancer's development. Visit degregori-lab for more information. Episode also available on Apple Podcasts: apple.co/30PvU9C

Trends in Immunology Volume 36, Issue 4, 2015, 217–228 Carcinogenesis 2015;36:1180-1192 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

With pre-print services, data sharing, open access, and the internet rapidly changing the journal publication landscape, Toxicological Sciences Editor-in-Chief Jeffrey M. Peters provides co-hosts Anne Chappelle and David Faulkner with perspective on how journals are adapting to the times. Dr. Peters also details how new training and guidance programs at ToxSci are aiming to enhance submissions and peer reviews. About the GuestJeffrey M. Peters, PhD, is a Distinguished Professor of molecular toxicology and carcinogenesis in the College of Agricultural Sciences and the Huck Institutes of the Life Sciences at the Pennsylvania State University (Penn State). He also serves as Deputy Director of the Penn State Cancer Institute, where his role is to catalyze collaborations among cancer researchers across Penn State's colleges and campuses.Dr. Peters has served on many editorial boards, including that of the Journal of Biological Chemistry, and he is the Editor-in-Chief of Toxicological Sciences, the official journal of the Society of Toxicology (SOT).Dr. Peters joined Penn State in 2000 after completing a postdoctoral fellowship at the National Cancer Institute (NCI) in Bethesda, Maryland. He holds a bachelor's degree in dietetics and a doctorate in nutrition science, both from the University of California Davis. Dr. Peters also completed postdoctoral fellowships in the Department of Cell Biology and Human Anatomy and the Institute of Toxicology and Environmental Health at UC-Davis.Dr. Peters holds long-standing NCI funding for his research program related to cancer and lipid metabolism. His laboratory studies the role of the peroxisome proliferator-activated receptors (PPARs) in the regulation of homeostasis, toxicology, and carcinogenesis. PPARs are members of the nuclear receptor superfamily and are critical modulators of environmental and dietary stimuli. The lab is particularly interested in delineating how natural compounds found in dietary constituents can activate PPARs, with the goal of identifying new molecules/proteins that can be targeted with existing approaches to improve the efficacy of chemoprevention and chemotherapy. These studies will likely lead to the identification of specific macronutrients that will effectively activate PPARs so that dietary formulations of agricultural products can be developed that will improve human and animal health and prevent serious diseases.Dr. Peters also is the Associate Director of the Center for Molecular Toxicology and Carcinogenesis at Penn State and was previously the co-leader of the Cancer Institute's Mechanisms of Carcinogenesis research program. DisclaimerThe viewpoints and information presented in Adverse Reactions represent those of the participating individuals. Although the Society of Toxicology holds the copyright to the production, it does not vet or review the information presented, nor does presenting and distributing the Adverse Reactions podcast represent any proposal or endorsement of any position by the Society.

050:  SUGAR and CANCER:  Are they Connected?  And What YOU CAN DO About it!In this episode, Dr. Thomas Hemingway will share both the history of SUGAR / glucose  as it relates to CANCER as well as its implications in PREVENTION AND TREATMENT of Cancer.Listen as Dr. Hemingway shares about Sugar and Cancer  AND, MUCH MUCH MORE.Learn more about Thomas Hemingway, MD and upcoming episodes, tips, tricks and more here: www.modernmedicinemovement.com on Instagram at @modermedicinemovement or @alohasurfdocAsk to join his FREE Private Facebook health Group with weekly LIVE educational sessions entitled:Modern Medicine Movement Health and Wellness Grouphttps://www.facebook.com/groups/2543880582493990/?ref=shareAlthough Dr. Thomas Hemingway is a physician, he is NOT your physician and is NOT to replace your primary care physician/health care provider. This podcast is NOT to be construed as medical advice by Dr. Thomas Hemingway or the guests comments as they are opinion only and NOT medical advice. Please consult your physician/health care provider should you have any medical questions or before trying any new practice. Check out reference he referred to in the podcast:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941741/. Cancer as a metabolic disease: implications for novel therapeutics. Carcinogenesis. 2014 Mar; 35(3): 515–527.  Published online 2013 Dec 16. Thomas N. Seyfried,* Roberto E. Flores, Angela M. Poff, 1 and Dominic P. D’Agostino https://pubmed.ncbi.nlm.nih.gov/31399389/ Ketogenic diet in the treatment of cancer - Where do we stand?  Molec Metab 2020 Mar;33:102-121. doi: 10.1016/j.molmet.2019.06.026. Epub 2019 Jul 27.  Daniela D Weber  1 , Sepideh Aminzadeh-Gohari  2 , Julia Tulipan  3 , Luca Catalano  4 , René G Feichtinger  5 , Barbara Kofler  6

Reference List: 1. Aune D, Chan DS, Vieira AR, et al. Dietary compared with blood concentrations of carotenoids and breast cancer risk: a systematic review and meta-analysis of prospective studies. Am J Clin Nutr 2012, 96:356-373. doi: 10.3945/ajcn.112.034165 2. Thomson CA, Rock CL, Thompson PA, et al. Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women's Healthy Eating and Living Study. Breast Cancer Research and Treatment 2011, 125:519-527. doi: 10.1007/s10549-010-1014-9 3. Lee SA, Fowke JH, Lu W, et al. Cruciferous vegetables, the GSTP1 Ile105Val genetic polymorphism, and breast cancer risk. Am J Clin Nutr 2008, 87:753-760. 4. Seow A, Yuan JM, Sun CL, et al. Dietary isothiocyanates, glutathione S-transferase polymorphisms and colorectal cancer risk in the Singapore Chinese Health Study. Carcinogenesis 2002, 23:2055-2061. doi: 10.1093/carcin/23.12.2055 5. Zhang X, Shu XO, Xiang YB, et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality. Am J Clin Nutr 2011, 94:240-246. doi: 10.3945/ajcn.110.009340 6. Darmadi-Blackberry I, Wahlqvist ML, Kouris-Blazos A, et al. Legumes: the most important dietary predictor of survival in older people of different ethnicities. Asia Pac J Clin Nutr 2004, 13:217-220. doi: 7. Piccolo E, Vignati S, Maffucci T, et al. Inositol pentakisphosphate promotes apoptosis through the PI 3-K/Akt pathway. Oncogene 2004, 23:1754-1765. doi: 10.1038/sj.onc.1207296 8. Galeone C, Pelucchi C, Levi F, et al. Onion and garlic use and human cancer. Am J Clin Nutr 2006, 84:1027-1032. doi: 10.1093/ajcn/84.5.1027 9. Thompson LU, Chen JM, Li T, et al. Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer. Clin Cancer Res 2005, 11:3828-3835. doi: 10.1158/1078-0432.CCR-04-2326 10. McCann SE, Thompson LU, Nie J, et al. Dietary lignan intakes in relation to survival among women with breast cancer: the Western New York Exposures and Breast Cancer (WEB) Study. Breast Cancer Res Treat 2010, 122:229-235. doi: 10.1007/s10549-009-0681-x 11. Anand P, Sundaram C, Jhurani S, et al. Curcumin and cancer: an "old-age" disease with an "age-old" solution. Cancer Lett 2008, 267:133-164. doi: 10.1016/j.canlet.2008.03.025 12. Giovannucci E, Rimm EB, Liu Y, et al. A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst 2002, 94:391-398. doi: 10.1093/jnci/94.5.391 13. Grainger EM, Schwartz SJ, Wang S, et al. A combination of tomato and soy products for men with recurring prostate cancer and rising prostate specific antigen. Nutr Cancer 2008, 60:145-154. doi: 10.1080/01635580701621338

"A tumor is certainly smarter than humans," says researcher Jyotsna Batra, discussing the ability of some tumors to change behaviors and progress through mutations. But she and other researchers are doing their best to utilize genome-wide associated studies to understand the genetic basis of stages of carcinogenesis. Listen and learn How her lab has identified 150 risk variants associated with prostate cancer, Why matching these variants with the aggressiveness and metastases of disease is an important step, How they must take into account the role of heterogeneity in these stages of research, and Why it's vital when assessing carcinogenesis and oncogenesis to combine multiple diagnostic methods, like PSA tests alongside genetic tests, to better understand potential for disease progression. Jyotsna Batra is an associate professor with the Faculty of Health and School of Biomedical Sciences at Queensland University of Technology (QUT). She works in genetics, biochemistry, and cell biology and is currently focusing on prostate cancer research. Her lab has recently joined a large prostate cancer consortium known as the Practical Consortium led by the Institute of Cancer Research in London. This teaming up offers the world a major cooperative workforce undertaking genome-wide association studies to understand the genetic basis of cancer. She describes one of her major projects: a germ-line study involving chip technology that has allowed her to identify 150 risk variants associated with prostate cancer risk. As Richard asks about possible directions prostate cancer research could take, she illustrates the challenges and breakthroughs, from the role of heterogeneity as research progresses to what liquid biopsies can offer.Her work with biomarkers is directed at identifying aggressiveness as she looks at plasma and blood for secretory tumor cells and microRNAs. She is able to give a succinct reason for why prostate cancer might evade treatment, namely the possibilities of multiple origins for a tumor as well as developed resistance to drugs. Finally she shares an important finding from her lab involving what diagnostic tests should be combined. Listen in for more about this exciting and life-saving work. Available on Apple Podcasts: apple.co/2Os0myK

Episode 4. Have you ever had a health scare (for you or a loved one) and been frustrated with yourself that it didn't propel you to make a big lifestyle change? On today's episode of the Motivation Made Easy podcast, I talk about our family's experience learning of our high genetic risk of cancer. I share this as one example of how external fear based motivation can be shifted to internal autonomous motivation and what this has looked like for us. A Personal Story Today we are getting personal. I talk first about about having basal cell carcinoma last year and how a recent experience brought up fears about our family history. I share that my husband has Lynch syndrome, a genetic mutation that greatly increases his risk (and potentially our kids) of many types of cancer. How to Transform Fear into Positive Progress When (Fear-Based) External Motivation Does Not Motivate Have you had a health scare in the past where you really hoped it would propel you to make habit changes in your life, but it didn't? I know this is extremely common, because I would often talk to patients about this. They might have recently had a heart attack and be incredibly frustrated with themselves that they weren't "taking it more seriously." I can relate to this, as I think many of us can. In the past, before I stopped dieting, I always hoped that health scares would motivate me to live a healthier life. I would try to use them as a reason for eating differently ("I have high cholesterol, I shouldn't have that") but really when push came to shove, it didn't work. The motivation was solidly in the external category. "A should" that was not transforming into any internal motivation any time soon. How to Merge the Eating Disorder & Weight Management Worlds in a Healthy Way We happened to find out about my husband having Lynch syndrome when I was working in a Preventive Cardiology clinic that recommended plant-based eating. Therefore, I decided to try out the Forks Over Knives Meal Planner as this was often being recommended to our patients. The Most Shocking Thing I Learned in My Plant-Based Eating Class I have written about this in the past, but I share again some of the data on how percentage of calories from animal protein is highly linked to cancer risk. This is another example of how our over focus on weight loss distracts us from the things we actually do have control over (e.g., our habits, how many fresh fruits and vegetable we have on a regular basis). Take Home Message I urge you to consider the information you have gotten about your health and your weight. Are you over emphasizing your weight and how much it impacts your health risk? If you are having a lot of shoulds or fears about your health, I urge you to just notice that, but then turn inward and ask yourself the question, "What do I really want for my life?" "Why is my health important to me?" Usually our health is important to use because of the things it will allow us to do, now or in the future. If you want more help clarifying this, download my free guide here. References Campbell, T. & Campbell, T. C. (2006). The China Study: The Most Comprehensive Study of Nutrition Ever Conducted and the Startling Implications for Diet, Weight Loss, and Long-term Health. Dunaif, G. E. & Campbell, T. C. (1987). Dietary protein level and aflatoxin B1-induced preneoplastic hepatic lesions in the rat. The Journal of Nutrition, 117, 1298–1302. Madhavan, T. V. & Gopalan, C. (1968). The effect of dietary protein on carcinogenesis of aflatoxin. Archives of Pathology & Laboratory Medicine, 85, 133-137. Youngman, L.D., & Campbell, T. C. (1992). Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential. Carcinogenesis, 13, 1607–1613. Youngman, L. D., & Campbell, T. C.

Chemical Carcinogenesis - Carcinogen | Carcinogen & Cancer | Types Of Carcinogen - Are Carcinogens Hiding in Products You Use Most? https://marcelamagdapopamd.com/about/ https://www.intrinsicmotivation.life/ Everyone uses such products as deodorant, shampoo, hand soap, body wash, moisturizer, shaving cream, cologne or makeup. But few consider whether doing so might be harmful to their health. The same goes for laundry and cleaning products. Marcela Magda Popa, M.D., has done the research and she knows that we are putting a lot of toxic ingredients on our skin, which as the body's largest organ, absorbs a lot of these poisons. Let Dr. Popa explain how to find healthier readily available alternative products. The author of “Keep Away from GRAS: Why Safe Everyday Products Are Making You Sick and Simple Strategies to Recover Your Health” was forced to take early retirement from her job as an internal medicine physician because of her stubborn autoimmune arthritis. Although a difficult period for her, it brought the time to research the suspicion she had formed that “generally recognized as safe” ingredients used in foods, cosmetics, cookware, hygiene products, and other products may be making people sicker. Marcela Magda Popa graduated from Carol Davilla Medical School in Bucharest, Romania, and completed residency training in the United States. She's been featured on MSN Lifestyle, SheKnows, Elite Daily, Bustle, and in Business Insider. carcinogenesis and carcinogens - usmle step 1 pathology neoplasia , dr g bhanu prakash. “chemical carcinogenesis and cancer preventive effects of anticarcinogenic foods”. The liver's role in vinyl chloride toxicity and carcinogenicity is providing a better understanding of the chemical carcinogenesis mechanism Chemical Carcinogenesis Pathology Simplified The unified hypothesis, for the carcinogenic properties of polycyclic aromatic hydrocarbons (PAH), predicts that the 7- hydroxymethyl sulfate ester, SMBA, plays... Proceedings of a Workshop on Approaches to Assess the Significance of Experimental Chemical Carcinogenesis Data for Man organized by IARC and the ... Jun 27, 2017 - ... Rat Liver Preneoplastic Lesions Induced by Chemical Carcinogenesis ... altered hepatic foci induced by carcinogens, in most animal models, ... Jan 1, 2016 - 3 The Millers and Chemical Carcinogenesis. In: The Understanding, Prevention and Control of Human Cancer. Author: Robert G. McKinnell. (Syracuse), the Kresge Laboratory of Physical Chemistry, the Wentworth ... and Animal Laboratory Correlations in Chemical Carcinogenesis, Ablex, Norwood, ... Chapter 8: Chemical Carcinogenesis ... A carcinogen is an agent whose administration to previously untreated animals leads to a statistically significant ... Mar 17, 2016 - These animal models resemble human skin cancer development, in that genetic changes caused by carcinogens and pro‑inflammatory cytokines ... Ames' test to detect the mutagenic property of a chemicals. CHEMICAL. CARCINOGENESIS. Which classes of chemicals tend to be carcinogens? _ Epoxides:. Carcinogen, any of a number of agents that can cause cancer in humans. They can be divided into three major categories: chemical carcinogens (including ... Skin Hyperproliferation and Susceptibility to Chemical Carcinogenesis in ... mice to the development of skin tumors upon exposure to chemical carcinogens. Chemical carcinogenesis: Too many rodent carcinogens*. (tumor promotion/mutagenesis/mitogenesis/anlmal cancer tests). BRUCE N. AMEStt AND Lois ... Applied Tumor Biology · Virotherapy · Virus-associated Carcinogenesis ... Chemical Biology Core Facility · Electron Microscopy · Flow Cytometry · Genomics and ... May 31, 2017 - Early cancer research focused primarily on chemical carcinogenesis in rat models and helped establish clear causal links between ... Read chapter Historical and Theoretical Aspects of Chemical Carcinogenesis: Particulate Polycyclic Organic Matter... Amazon.in - Buy Chemical Carcinogenesis and Mutage --- Support this podcast: https://anchor.fm/intrinsic-motivation/support

Are Carcinogens Hiding in Products You Use Most? https://marcelamagdapopamd.com/about/ https://www.intrinsicmotivation.life/ Everyone uses such products as deodorant, shampoo, hand soap, body wash, moisturizer, shaving cream, cologne or makeup. But few consider whether doing so might be harmful to their health. The same goes for laundry and cleaning products. Marcela Magda Popa, M.D., has done the research and she knows that we are putting a lot of toxic ingredients on our skin, which as the body’s largest organ, absorbs a lot of these poisons. Let Dr. Popa explain how to find healthier readily available alternative products. The author of “Keep Away from GRAS: Why Safe Everyday Products Are Making You Sick and Simple Strategies to Recover Your Health” was forced to take early retirement from her job as an internal medicine physician because of her stubborn autoimmune arthritis. Although a difficult period for her, it brought the time to research the suspicion she had formed that “generally recognized as safe” ingredients used in foods, cosmetics, cookware, hygiene products, and other products may be making people sicker. Marcela Magda Popa graduated from Carol Davilla Medical School in Bucharest, Romania, and completed residency training in the United States. She’s been featured on MSN Lifestyle, SheKnows, Elite Daily, Bustle, and in Business Insider.

Back on the podcast with me this week is sleep expert, Greg Potter, PhD. Through his articles, podcasts and live talks, Greg is helping an international audience understand the critical role sleep plays in health and wellbeing. Most recently, Greg has been studying the impact of circadian rhythm disruption, including sleep duration and meal timing, on the development of common cancers. In this interview, Greg and I discuss Alexey Guzey’s scathing critique of Matthew Walker’s book, Why We Sleep. We also talk about some of the biological processes affected by sleep restriction, including cognition, immune health, athletic performance, and appetite. Greg shares some of the ways poor sleep is associated with cancer formation, including the damaging effects of sleep restriction on DNA and metabolism. Here’s the outline of this interview with Greg Potter: [00:00:09] Greg's 4-part series of articles on sleep: 1. Having trouble sleeping? A primer on insomnia and how to sleep better; 2. Sleep-maintenance insomnia: how to sleep through the night; 3. Sleep-onset insomnia: how to get to sleep fast; 4. Sleep for athletes: are athletes a different breed? [00:00:28] Greg's previous podcasts: How to Entrain Your Circadian Rhythm for Perfect Sleep and Metabolic Health; Morning Larks and Night Owls: the Biology of Chronotypes; What to Do When You Can’t Sleep; Better Sleep for Athletes. [00:01:11] 2020 Metagenics International Congress on Natural Medicine. [00:03:36] Book: Why We Sleep, by Matthew Walker, PhD. [00:03:38] Article: Matthew Walker's "Why We Sleep" Is Riddled with Scientific and Factual Errors, by Alexey Guzey. [00:04:12] Book: Thinking, Fast and Slow by Daniel Kahneman. [00:10:23] Dimensions of sleep; Article: Buysse, Daniel J. "Sleep health: can we define it? Does it matter?." Sleep 37.1 (2014): 9-17. [00:12:34] The transtheoretical model of behavior change. [00:16:34] Stephan Guyenet’s Red Pen Reviews. [00:18:40] Chronotypes and the Sentinel Hypothesis. [00:19:39] Are people not sleeping enough? [00:21:56] Sleep duration in the US might be increasing; Study: Basner, Mathias, and David F. Dinges. "Sleep duration in the United States 2003–2016: first signs of success in the fight against sleep deficiency?." Sleep 41.4 (2018): zsy012. [00:26:12] People overestimate their sleep duration; Study: Lauderdale, Diane S., et al. "Self-reported and measured sleep duration: how similar are they?." Epidemiology (2008): 838-845. [00:28:29] Insulin sensitivity and testosterone higher after extended sleep; Killick, Roo, et al. "Metabolic and hormonal effects of ‘catch‐up’sleep in men with chronic, repetitive, lifestyle‐driven sleep restriction." Clinical endocrinology 83.4 (2015): 498-507. [00:29:00] Plasma IL-6 higher after sleep restriction; Study: Pejovic, Slobodanka, et al. "Effects of recovery sleep after one work week of mild sleep restriction on interleukin-6 and cortisol secretion and daytime sleepiness and performance." American Journal of Physiology-Endocrinology and Metabolism 305.7 (2013): E890-E896. [00:29:25] Better cognitive function with more sleep; Study: Kazem, Yusr MI, et al. "Sleep deficiency is a modifiable risk factor for obesity and cognitive impairment and associated with elevated visfatin." Open access Macedonian journal of medical sciences 3.2 (2015): 315. [00:29:37] Effects of sleep on appetite; Study: Al Khatib, H. K., et al. "The effects of partial sleep deprivation on energy balance: a systematic review and meta-analysis." European journal of clinical nutrition 71.5 (2017): 614-624. [00:30:02] Sleep extension and exercise performance; Study: Mah, Cheri D., et al. "The effects of sleep extension on the athletic performance of collegiate basketball players." Sleep 34.7 (2011): 943-950. [00:32:45] Assessing current sleep status. [00:33:11] Podcast with Ashley Mason: How to Use Cognitive Behavioral Therapy for Insomnia. [00:36:14] WHO (five) Well-Being Index; Short Form 12; Short Form 36. [00:38:55] NBT’s Health Assessment Questionnaire. [00:39:57] Sleep and all-cause mortality. [00:46:56] Sleep restriction leads to worse performance; Van Dongen, Hans, et al. "The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation." Sleep 26.2 (2003): 117-126. [00:47:31] Josh Turknett's 4-Quadrant Model; Podcast: How to Win at Angry Birds: The Ancestral Paradigm for a Therapeutic Revolution. [00:48:30] Sleep duration and cancer. [00:49:20] Short sleep duration associated with cancer among asians; long sleep duration associated with colorectal cancer; Study: Chen, Yuheng, et al. "Sleep duration and the risk of cancer: a systematic review and meta-analysis including dose–response relationship." BMC cancer 18.1 (2018): 1149. [00:51:02] Sleep deprivation and DNA damage: Study: Cheung, V., et al. "The effect of sleep deprivation and disruption on DNA damage and health of doctors." Anaesthesia 74.4 (2019): 434-440; and Carroll, Judith E., et al. "Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans." Brain, behavior, and immunity 51 (2016): 223-229. [00:51:16] Article: Seyfried, Thomas N., et al. "Cancer as a metabolic disease: implications for novel therapeutics." Carcinogenesis 35.3 (2014): 515-527. [00:56:22] Matthew Walker's website. [00:59:47] Greg’s website; Instagram, Twitter, LinkedIn. [01:02:55] Sleepio. (SHUTi no longer available).

Norris Cotton Cancer center Grand Rounds February 25, 2020 Ilana Cass, MD

It would be nearly impossible using current methods to test all the chemicals in use for toxic effects. So how do we prioritize which ones to study? In this podcast, Martyn Smith describes how he and his colleagues are developing lists of “key characteristics” shared by toxicants that cause specific adverse health effects, such as cancer or male or female reproductive toxicity. Risk assessors can use this information to predict the toxicity of other chemicals in an organized, systematic way. This approach may be useful in prioritizing chemicals for more detailed evaluation. Visit the podcast webpage to download the full transcript of this podcast. 

The Shot heard round the world. “… the origin of carcinogenesis resides with the mitochondria in the cytoplasm, not the with the genome in the Nucleus.”Researchers have transplanted the nucleus (it’s DNA) of a cancer cell into a healthy cell that had its nucleus removed. When that new combined cell with healthy cytoplasm and mitochondria but DNA from the cancer was injected into mice no cancer developed. But when the cancer cell with the nucleus of a healthy cell was injected into mice, those mice developed cancer. No one saw this coming or dared to predict such an outcome. It is evidence that the promoter of cancer was not the ‘cancerous DNA’ genes of the cancer cells, but the mitochondria in the cytoplasm of the cancer cells. This event, repeated many time since, invalidates the assumption upon which cancer treatment is based today. Books: Cancer As A Metabolic Disease, Hardcover Tripping Over The Truth Buy C8Keto MCT Oil on AmazonOur Facebook Group Keto NaturopathUntil next time, Dr. Karl

Dr Rosemary Waring is a toxicologist interested in gut dysfunction and endocrine disruption. Rosemary is currently using metabonomics to investigate the effects of diet on the gut microbiome in man and horses. We discuss Equine Gut Dysfunction and how enzymes help, plus a new product called EquiNectar which is based on groundbreaking microbiome research, improving equine health and performance through enhanced digestion.Dr Rosemary Waring is a Director of 'Tharos' and an observer on the Board of Ateria Health, both part of the Animal Microbiome Company. Plus independent toxicologist member of the COC (Committee on Carcinogenesis in Food, Consumer Products and the Environment), which is a UK government committee.You can follow Tharos and their progress with Equinectar at : www.tharos.co.ukInvest in Tharos and Equinectar here: https://tharos.envestry.comJoin in the conversation on Twitter 8pm-9pm GMT just use #HorseHour in your tweets. Follow us @HorseHour on Twitter, Facebook and Instagram and get more education, podcasts, pictures and videos at HorseHour.co.uk. See acast.com/privacy for privacy and opt-out information.

Dr. Ajay Goel will join Dr. Lise Alschuler to discuss his research of curcumin. His study published in the journal Carcinogenesis has shown several pathways curcumin can increase the effectiveness of chemotherapy and radiation against pancreatic cancer cells. The preventive benefits of curcumin are also discussed.This show is broadcast live on Tuesday's at 7PM ET on W4CS – The Cancer Support Network (www.w4cs.com) part of Talk 4 Radio (http://www.talk4radio.com/) on the Talk 4 Media Network (http://www.talk4media.com/).

Check out Dr. Ellie and her Food Allergy Formula: http://dr-ellie.teachable.com/p/the-food-allergy-formula Changing Diets http://learntruehealth.com/changing-diets/ Changing Diets Smoothly   Changing diets can be both intimidating and overwhelming. I have gone through over 30 diets, and trust me; it can get frustrating, too. However, changing diets doesn't have to be a negative experience. Dr. Ellie Heintze is my guest today who will show us the right mindset once you decide to start changing diets. Previous Life Dr. Ellie Heintze was a chemist in her 'previous life,' as she likes to call it. Earning her master's degree 12 years ago, it was a time when anything about food allergy was not a prevalent health issue. It was also around that time that Dr. Ellie Heintze happened to suffer from digestive health issues.  Hence, she decided to consult with a Gastroenterologist which consequently turned out to be a bad experience. As fate would have it, Dr. Ellie Heintze happened to chance upon a Naturopathic Doctor's clinic who also knew how to perform Acupuncture techniques. This moment, according to Dr. Ellie Heintze, changed her life. Changing Careers Dr. Ellie Heintze was surprised that on just her initial visit, she felt immediate relief from her health issues.  The Acupuncture technique was terrific! Because of that positive experience, she became curious about that doctor's natural approach to healing. While her health issues were traced to food allergies to gluten, dairy, and eggs, Dr. Ellie Heintze likewise became inspired to follow in that doctor's footsteps. The doctor was a graduate of Bastyr University, the same university where Dr. Ellie Heintze eventually earned her Master's degree in Acupuncture and a Doctorate in Naturopathic Medicine. Changing Diets "A lot of people with digestive issues get Acupuncture now. Others are curious about how to start changing diets to a gluten-free one. I call it the gluten-free switch," said Dr. Ellie Heintze. Dr. Ellie Heintze says that ideally, she encourages her patients to shift to whole foods as well as low-carb foods.  Apparently, this is because she says the gluten-free food is still considered processed. Label Reading When you plan on changing diets, Dr. Ellie Heintze says that getting into the habit of reading labels is a good start. This way, you can scrutinize all the ingredients. However, it's not only in food. Apparently, even supplements need to be scrutinized because it is usually filled with fillers. Some supplements have food dyes and ingredients like titanium dioxide. "Reading labels can also apply to supplements. There is much information on labels," said Dr. Ellie Heintze. "Focus on the bottom where it indicates other ingredients. If it only has a few words, it's ok. Put it back if there are a lot of ingredients. Also be wary of ingredients that are not familiar." Eating Right Dr. Ellie Heintze however, clarifies that changing diets is not just about switching to whole foods. To create a balanced meal, she says it is best to incorporate more vegetables and good fats. Learning to substitute the right foods is also essential to a successful diet. "Try to take away bread and pasta gradually. Replace it with quinoa and brown rice. Likewise, increase protein," Dr. Ellie Heintze suggests. "Have small, frequent meals and add good fats like avocado, olive oil, and coconut oil. You'll feel full longer, and your blood sugar won't crash." I agree with Dr. Ellie Heintze's recommendations.  Based on my personal experiences with diets, I tend to feel grumpy and experience moods swings due to unregulated blood sugar. Essentially, when we set ourselves up for success in the morning starting with a good, healthy breakfast, we set up ourselves emotionally and mentally for the rest of the day. To know what are the right foods to eat, Dr. Ellie Heintze incidentally has a book called, 'A Starting Point: Guide to Gluten-Free Living and Healthy Digestion.' Making A Smooth Transition Dr. Ellie Heintze suggests that before changing diets, better do a thorough research. You will feel more empowered if you know the reason behind your actions. "I see to it that I educate my patients on the 'why' behind changing diets. That way, they are more likely to stick to the process," explains Dr. Ellie Heintze. Next step is planning correctly. Dr. Ellie Heintze says changing diets can be initially overwhelming because we are so used to eating a certain way. Hence, we must go back to basics. A good example is knowing how to shop at the grocery. "It can be overwhelming not knowing what to buy. However, once you do know how to shop for the right ingredients, planning meals becomes easier," assures Dr. Ellie Heintze. "Making meals is simple and easy. Personally, I am a fan of making things in bulk by using a slow cooker. Another way of making a smooth diet transition is to make it a routine. Always be prepared. According to Dr. Ellie Heintze, if there is no food available at home, people tend to fall back on their old habits. "If you are eating out, know where to stop and eat. Make Sundays your meal planning day. Most likely, it will gradually become second nature," Dr. Ellie Heintze said. Mindset Shift Changing diets can work for you especially if you can get people in your household to be your support system. According to Dr. Ellie Heintze, educating the whole family is necessary so they can understand that even they can benefit from changing diets. "My patients have mostly digestive issues or chronic migraines. Because they want to eradicate taking medication, they are usually receptive to change. Many factors are involved. My patients' health improves after shifting their mindset towards eating right." How Well Acupuncture Works Acupuncture is suitable for a wide range of health conditions. According to Dr. Ellie Heintze, it helps the body's natural ability to heal itself. Furthermore, it can activate our parasympathetic nervous system when we are sleeping. Dr. Ellie Heintze likewise reassures that although people usually feel sleepy after treatment, this means the treatment is working. People can zone out and take a nap to get things back in balance. Consequently, Acupuncture helps the body to adapt better. "Acupuncture helps with digestive issues as well as help the body heal itself. Seven percent of our immune system is in our gut, and it is also connected to our brain," Dr. Ellie Heintze explains.  "Acupuncture is a whole body medicine, and since our body is a unit, it makes the technique effective." In addition to that, Acupuncture works well with pain since it addresses pain systematically. Dr. Ellie Heintze says that our 'Chi' moves our blood, nourishes our muscles, nerves, tissues. So if our 'Chi' is blocked, Acupuncture techniques get the energy moving freely. Hence, the pain decreases.   Ignite Health Program   Dr. Ellie Heintze's fantastic program lasts for six weeks. The program teaches patients how to make changes in their diet, how to incorporate meals and how to have the right mindset to make the transition successful.   A component of the program also includes stress reduction techniques.  However, because achieving optimal health does not only mean changing diets, Dr. Ellie Heintze included a module in the program, wherein you will be taught the right kind of physical exercises needed to maximize the effects of your diet change.   The Daily Cup   Dr. Ellie Heintze's The Daily Cup podcast is an excellent resource for maximizing your productivity and achieving your goals.  Primarily aimed at educating wellness providers and small business owners, Dr. Ellie Heintze invites fantastic experts on the show who provide a wealth of information.    "I want our medicine to survive. So we need sustainable and profitable businesses. This way, Natural Medicine can become more mainstream," said Dr. Ellie Heintze. Dr. Ellie Heintze completed a B.S. in Chemistry and Master’s degree in Chemical Toxicity and Carcinogenesis from Northern Arizona University. She attended Bastyr University where she received her Doctorate in Naturopathic Medicine and Master’s degree in Acupuncture.    Dr. Ellie Heintze sees patients with a wide range of ailments but specializes in digestive health (Irritable Bowel Syndrome, Celiac Disease), and food allergies. She is a licensed Naturopathic Doctor and Acupuncturist (East Asian Medical Practitioner) in the state of Washington.   Get Connected with Dr. Ellie Heintze:   Official Website   Simplify Your Practice A Starting Point Book   Facebook  Youtube Google  Recommended Reading by Dr. Ellie Heintze Heal Your Body by Louise Hay Book by Dr. Ellie Heintze A Starting Point Guide To Gluten-Free Living And Healthy Digestion   The Links You Are Looking For: Become A Health Coach Learn More About The Institute for Integrative Nutrition's Health Coaching Certification Program by checking out these four resources: 1) Integrative Nutrition's Curriculum Guide: http://geti.in/2cmUMxb 2) The IIN Curriculum Syllabus: http://geti.in/2miXTej 3) Module One of the IIN curriculum: http://geti.in/2cmWPl8 4) Get three free chapters of Joshua Rosenthal's book: http://geti.in/2cksU87 Watch my little video on how to become a Certified Health Coach! https://www.youtube.com/watch?v=CDDnofnSldI ------------------------------------------------------------------------------- Do you have a blood sugar issue? I can help you achieve healthy, normal and balanced blood sugar naturally! Visit BloodSugarCoach.com for your free 30min coaching call with Ashley James! http://www.BloodSugarCoach.com ------------------------------------------------------------------------------- If this episode made a difference in your life, please leave me a tip in the virtual tip jar by giving my podcast a great rating and review in iTunes! http://bit.ly/learntruehealth-itunes Thank you! Ashley James http://bit.ly/learntruehealth-itunes ------------------------------------------------------------------------------- Enjoyed this podcast episode? Visit my website Learn True Health with Ashley James so you can gain access to all of my episodes and more! LearnTrueHealth.com http://learntruehealth.com ------------------------------------------------------------------------------- Need Help Ordering The Right Supplements For You? Visit TakeYourSupplements.com, and a FREE health coach will help you! http://takeyoursupplements.com ------------------------------------------------------------------------------- Learn How To Achieve Optimal Health From Naturopathic Doctors! Get Learn True Health's Seven-Day Course For FREE! Visit go.learntruehealth.com http://go.learntruehealth.com/gw-oi ------------------------------------------------------------------------------- I made a low-carb, gluten-free cookbook just for you! Download your FREE copy today! Visit learntruehealth.com/free-health-cookbook http://learntruehealth.com/free-health-cookbook ------------------------------------------------------------------------------- Join Learn True Health's Facebook community group! Visit https://www.facebook.com/groups/LearnTrueHealth or search Learn True Health on Facebook! ------------------------------------------------------------------------------- Follow the Learn True Health podcast on social media! 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Prof Kyrtopoulos speaks with ecancertv at Childhood Cancer 2016 about the NewGeneris project, monitoring maternal diet and establishing biomarkers associated with childhood disease. He outlines the presence of micronuclei, among other biomarkers, as a 'warning sign' for childhood disease, and discusses food groups known to contain oncogenic chemicals. In summary, Prof Kyrtopoulos describes dietary awareness and changes by customers and food manufacturers that can reduce exposure.

This is the audio recording of the study guide Molecular basis of carcinogenesis, available here -> http://www.letstalkmed.com/molecular-basis-of-carcinogenesis.html . Facilitated and organized by Jinan AlRashoud

Have you ever wondered how science is used in real-life spy games? How accurately is science and medicine being portrayed in movies, books, and other forms of pop culture? Dr. Curtis Harris, a world-renowned cancer scientist and chief of the Laboratory of Human Carcinogenesis at the NIH National Cancer Institute and author of the new spy thriller, HIGH HAND, joins us to discuss how science is used in real-life spy games.We’ll learn about the kinds of technology being used to make people reveal information, the kinds of lethal poisons that are used in espionage, and how beloved characters like James Bond have influenced the science of spying.Dr. Harris serves as editor in chief of the scientific journal Carcinogenesis. His novel, High Hand, written with co-authors James Rosen (an award-winning Pentagon journalist) and James Ellenberger (a former senior official of a national labor federation), using the pseudonym Curtis J. James, takes on hot-button issues and opens up the covert worlds of the CIA and SVR.

Have you ever wondered how science is used in real-life spy games? How accurately is science and medicine being portrayed in movies, books, and other forms of pop culture? Dr. Curtis Harris, a world-renowned cancer scientist and chief of the Laboratory of Human Carcinogenesis at the NIH National Cancer Institute and author of the new spy thriller, HIGH HAND, joins us to discuss how science is used in real-life spy games. We’ll learn about the kinds of technology being used to make people reveal information, the kinds of lethal poisons that are used in espionage, and how beloved characters like James Bond have influenced the science of spying. Dr. Harris serves as editor in chief of the scientific journal Carcinogenesis. His novel, High Hand, written with co-authors James Rosen (an award-winning Pentagon journalist) and James Ellenberger (a former senior official of a national labor federation), using the pseudonym Curtis J. James, takes on hot-button issues and opens up the covert worlds of the CIA and SVR

Have you ever wondered how science is used in real-life spy games? How accurately is science and medicine being portrayed in movies, books, and other forms of pop culture? Dr. Curtis Harris, a world-renowned cancer scientist and chief of the Laboratory of Human Carcinogenesis at the NIH National Cancer Institute and author of the new spy thriller, HIGH HAND, joins us to discuss how science is used in real-life spy games. We’ll learn about the kinds of technology being used to make people reveal information, the kinds of lethal poisons that are used in espionage, and how beloved characters like James Bond have influenced the science of spying. Dr. Harris serves as editor in chief of the scientific journal Carcinogenesis. His novel, High Hand, written with co-authors James Rosen (an award-winning Pentagon journalist) and James Ellenberger (a former senior official of a national labor federation), using the pseudonym Curtis J. James, takes on hot-button issues and opens up the covert worlds of the CIA and SVR.

Have you ever wondered how science is used in real-life spy games? How accurately is science and medicine being portrayed in movies, books, and other forms of pop culture? Dr. Curtis Harris, a world-renowned cancer scientist and chief of the Laboratory of Human Carcinogenesis at the NIH National Cancer Institute and author of the new spy thriller, HIGH HAND, joins us to discuss how science is used in real-life spy games.We’ll learn about the kinds of technology being used to make people reveal information, the kinds of lethal poisons that are used in espionage, and how beloved characters like James Bond have influenced the science of spying.Dr. Harris serves as editor in chief of the scientific journal Carcinogenesis. His novel, High Hand, written with co-authors James Rosen (an award-winning Pentagon journalist) and James Ellenberger (a former senior official of a national labor federation), using the pseudonym Curtis J. James, takes on hot-button issues and opens up the covert worlds of the CIA and SVR

The intestine is a pivotal organ which is divided into two anatomical parts: the small intestine and the large intestine (colon and rectum). Both parts are made up of single layered epithelium. This epithelium is composed of villi (protrusions) – found only in the small intestine - and crypts (invaginations) leading to an increase of the surface of the intestinal lumen whereby the uptake of nutrients and water is improved. Every five days, the intestinal epithelium is renewed whereby both, crypts and eventually villi, are filled up with new cells. The homeostasis of the crypts/villi relies on adult stem cells (SCs), especially crypt base columnar (CBC) cells, which are located at the base of the crypts. These are regulated by an active Wnt signaling pathway. A deregulation of the Wnt signaling pathway leads to cancer formation found in humans almost exclusively in the colon and rectum. Colorectal cancer (CRC) is worldwide the third most common cause for cancer related deaths. In the majority of CRC, origin and progress are caused by mutations in the adenomatous polyposis coli (APC) gene which encodes an essential component of the β-catenin destruction complex that is the central element of the Wnt signaling pathway. As a consequence of these mutations, the executor of the Wnt signaling pathway, β-catenin, which is in this context a transcription factor, cannot be downregulated any more. As a consequence target genes of β-catenin are expressed in an unregulated manner. These target genes regulate features of stem cell biology which confer cancer stemness, metastasis, EMT (epithelial-mesenchymal transition), chemoresistance and other characteristics to colorectal tumor cells. Interestingly, APC mutations have only an effect when they occur in the adult stem cells. Thus, the descendend tumor cells show characteristics of these cells and have been termed cancer stem cells (CSCs). Like adult stem cells in the normal crypt CSCs are the origin of cancer and are characterized by an activated - here deregulated - Wnt signaling pathway and thus, by the aforementioned features. Clinically, cancer death is caused in most cases by metastasis which is treated by chemotherapy from which most if not all CRCs escape by the development of chemoresistance which is an intrinsic feature of the CSCs. Therefore, CSC specific targeted therapies might be a promising therapeutic tool for a successful treatment of CRCs. One possibility is the interference of CSC sustaining molecules as these molecules are involved in the induction and maintenance of CSCs. Here, a promising molecule is olfactomedin-4 (OLFM4) which was discussed to be a CSC marker. But the role of OLFM4 as a CSC marker and important factor for tumorigenesis has been controversially described. Therefore, I investigated in the first part of my thesis the role of OLFM4 in CRC cells. I demonstrate that OLFM4 was expressed only in two out of 14 CRC cell lines. The assumption that OLFM4 was only expressed in cells with characteristics of CSCs and thus, was not detected in the cell lines as they possess only a small proportion of CSCs, was not confirmed. I found that CSCs showed a reduced OLFM4 expression and thus, OLFM4 was not coexpressed with other SC markers. These results indicate that OLFM4 is not a marker of CSCs in CRC. In order to analyze the functional role of OLFM4 in CRC cells, I overexpressed OLFM4 lentivirally. However, the overexpression of OLFM4 and thus, high OLFM4 protein levels did not influence the expression of CSC, EMT or differentiation marker. Likewise, OLFM4 did not play a functional role for proliferation, stemness and metastatic features. Therefore, this study demonstrates that OLFM4 is not a CSC marker and has no functional role for the driving activity in the process of colorectal carcinogenesis. Additionally, I evaluated in the second part of my thesis the role of the microRNAome (miRNAome) in colorectal carcinogenesis, the influence on CSC features and whether the miRNAome might be a tool for specific CSC targeted therapies. microRNAs (miRNAs) are generally downregulated in tumors whereby the miRNA loss promotes tumorigenesis. As the majority of the CRC cases are driven by an APC mutation in the SC compartment, I used for my investigations a mouse model with a conditional Apc knockout in CBC cells which develops efficiently intestinal adenomas. This mouse model was crossed with another mouse model harboring a conditional knockout of the essential miRNA generator Dicer1 to investigate the role of a loss of the miRNAome in murine Wnt driven intestinal tumors. In this part of my study I demonstrated that hetero- and homozygous deletion of Dicer1 in CBC cells, in combination with an Apc knockout, enhances significantly the number of adenomas. Moreover, deletion of Dicer1 resulted in smaller adenomas caused by reduced proliferation. Further analysis of DICER1 deletion in human CRC cell lines revealed that loss of DICER1 and thus, miRNAs led likewise to a decreased proliferation. Additionally, I showed that loss of miRNAs increased the expression/protein levels of CSC markers and CSC features indicating that loss of DICER1 promotes tumorigenesis. Moreover, I translated these mouse model/cell culture results into human colonic normal and tumor tissue as well as CRC. In a collection of different tissues (normal tissue, adenomas and cancers of stages I to IV), increased DICER1 levels were seen from normal tissue to adenomas followed by decreased levels during carcinoma progression. Increased levels of DICER1 were also found in the murine Wnt driven adenomas. In support with this I provided finally evidence that DICER1 expression is regulated by the Wnt signaling pathway thus already early in the beginning of the colorectal tumorigenesis. Thus, this data showed that DICER1 is a tumor suppressor in intestinal cancer and the loss of DICER1 and hence, of the miRNAome, influences CSC marker expression and marker protein levels as well as proliferation and CSC features. Therefore, the miRNAome might possibly become a therapeutic target for CSC targeted therapy.

Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin The doctors TWiP solve the case of the Woman with White Worms, and explain the role of a secreted growth factor from a carcinogenic parasite in wound healing and angiogenesis.   Links for this episode: Wound healing growth factor from carcinogenic parasite (PLoS Path) Opisthorchis (CDC) Opisthorchis life cycle (CDC) Image credit Letters read on TWiP 101 Listener Pick Ramon - Ancient Rome was infested with parasites Case study for TWiP 101 This week's case involves an uncommon parasite. Young girl,

In this presentation, James Cleaver of UC San Francisco shares some surprising results from studies of mutagenesis from UV light in two hereditary syndromes -- xeroderma pigmentosum (XP) and Cockayne syndrome (CS) -- which have mutations in the nucleotide excision repair (NER) pathway. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Science] [Show ID: 30212]

In this presentation, James Cleaver of UC San Francisco shares some surprising results from studies of mutagenesis from UV light in two hereditary syndromes -- xeroderma pigmentosum (XP) and Cockayne syndrome (CS) -- which have mutations in the nucleotide excision repair (NER) pathway. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Science] [Show ID: 30212]

This symposium brings together scientists representing evolutionary biology, genetics, dermatology, anthropology, and physiology to share their knowledge and questions about human skin in an explicitly evolutionary framework. Mark Shriver begins with a discussion about The Genetics of Skin Pigmentation, followed by Nina Jablonski on Naked, Colorful Skin and Its Role in Human Social Interactions, and James Cleaver on The Skin and Ultraviolet Radiation: Effects on DNA and Carcinogenesis Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Science] [Show ID: 30205]

This symposium brings together scientists representing evolutionary biology, genetics, dermatology, anthropology, and physiology to share their knowledge and questions about human skin in an explicitly evolutionary framework. Mark Shriver begins with a discussion about The Genetics of Skin Pigmentation, followed by Nina Jablonski on Naked, Colorful Skin and Its Role in Human Social Interactions, and James Cleaver on The Skin and Ultraviolet Radiation: Effects on DNA and Carcinogenesis Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Science] [Show ID: 30205]

Norris Cotton Cancer Center Grand Rounds - Brock C. Christensen PhD

The vast majority of colorectal cancer (CRC)-related deaths is caused by the metastatic spread of tumor cells to distant organs rather than by the growth of the primary tumor. However, until today the mechanisms involved in CRC metastasis are not completely understood. For cancer cells the epithelial-mesenchymal transition (EMT) is thought to represent a prerequisite to invade adjacent tissue and form metastases at distant sites. Transcription factors, cytokines or oncogenic signaling pathways play an important role in the regulation of the EMT program. Recently, the oncoprotein c-MYC was shown to induce EMT, e.g. by enhancing SNAIL expression. Previously an interaction between c-MYC and the transcription factor ZNF281/ZBP-99 has been described. However, so far it remained elusive which upstream signals regulate ZNF281 levels or activity and furthermore, what functions are mediated by ZNF281, which may contribute to the c-MYC-mediated tumor progression. Here, it could be shown that SNAIL and miR-34a/b/c control the expression of ZNF281 in a coherent feed-forward-loop: the EMT-transcription factor SNAIL directly induced ZNF281 transcription and repressed miR-34a/b/c, thereby alleviating ZNF281 from direct down-regulation by miR-34. Moreover, p53 activation led to a miR-34a-dependent down-regulation of ZNF281 expression. Additionally, in CRC cells it could be demonstrated, that ectopic ZNF281 expression induces EMT. This process was mediated by and dependent on the direct induction of SNAIL. Furthermore, ectopic ZNF281 increased migration/invasion, and enhanced β-catenin activity. Expression of the stemness markers LGR5 was directly and CD133 indirectly induced by ectopic ZNF281 expression, which also increased sphere formation. Conversely, in CRC cells the experimental down-regulation of ZNF281 resulted in a mesenchymal-epithelial transition (MET), inhibited migration/invasion and decreased sphere formation. Additionally, repression of ZNF281 led to decreased formation of lung metastases by CRC cells in a xenograft mouse tumor model. Furthermore, ZNF281 protein expression was indirectly elevated by ectopic c-MYC expression. Inactivation of ZNF281 prevented the induction of EMT by c-MYC or SNAIL. The analysis of tumor samples revealed that ZNF281 expression increases during CRC progression and correlates with tumor recurrence. Taken together, the results identify ZNF281 as a new EMT-promoting transcription factor, which contributes to metastasis formation in CRC. In the future, this knowledge may be exploited for therapeutic and diagnostic purposes in cancer therapy.

This work employed a mouse model of liver specific depletion of the gene Cdh1 and its respective protein E cadherin to study the role of this protein in liver homeostasis and pathophysiology. The experiment was done with specific focus on the effects concerning hepatocellular carcinoma (HCC) development. Background: Cadherins are present in all higher organisms, and have been studied rigorously in the past. The cadherin family is huge, encompassing more than 400 (known) members. E cadherin is the name-giver of that family and is considered to be of great importance to a broad range of physiological and pathophysiological functions. Known functions include cell-cell adhesion and deregulation of E-cadherin (in almost all cases a down-regulation) is associated with increased aggressiveness in both human and animal tumors. Aside from that, E-cadherin is of great importance during embryogenesis. Worldwide, HCC is an important disease in humans, especially in certain countries (mostly developing countries). While females are only occasionally affected by HCC, it ranks among the top 3 tumor-related death causes in males. The difficulties in treating this tumor curatively make research of genes or proteins relevant to HCC important for human medicine improvement. The existence of a connection between Cdh1 or E Cadherin and HCC has been suggested, but more research is still required. Methods: Employing Cre/loxP technology, a mouse model of liver specific E cadherin depletion was created (L Cdh1del/del). The mice were compared to littermates with normal Ecadherin levels (L Control). Mice body and organ weight was documented at different ages, and liver tissue was analyzed using qRT-PCR (cDNA), Western blot, histochemistry and immunohistochemistry. To test effects of the reduced E-cadherin on tumor development, a cohort of male mice was injected with a chemical carcinogen (DEN) at two weeks of age to induce HCC, and mice were analyzed 4, 8 or 12 months later. Results: Aside from a slight retardation in weight gain, L Cdh1del/del did not suffer from severe health effects or spontaneous tumor development. Histology showed some alterations around the small bile ducts in the liver (in the periportal fields) and RNA analysis showed that mice underwent a phase of considerably altered RNA activity (429 significantly regulated genes at 3 weeks of age), but later only a few up/down-regulated genes remained (28 genes at 6 weeks of age). Aside from Cdh1, no genes considered cadherin family members were regulated. Western blot analysis, qRT-PCR and IHC confirmed that E cadherin was down regulated on RNA level and on protein level in this animal model. All mice injected with DEN developed tumors, but L Cdh1del/del were affected more heavily, with tumors reaching large diameters faster. If mice were kept longer than 8 months, L Cdh1del/del had to be euthanized significantly earlier than L Control. A spin-off of the model was the establishment of a permanent cell line, developed from a liver tumor of a L Cdh1del/del mouse. PCR requiring a functional primer binding site on exon 10 of Cdh1 could not produce DNA product, indicating that the cell line was a derivative of an E-cadherin negative liver cell. Conclusion: Liver specific E cadherin reduction had a surprisingly small effect in the present mouse model (compared to the effects of E cadherin loss in organs like the skin or intestine, as documented in the literature) if mice were not challenged with a chemical carcinogen. If mice were challenged with experimental HCC induction, lack of E cadherin had a strong effect on the tumor growth. These findings attest, by an experimental animal model, the importance of E cadherin for tumor development in the liver. This data reinforces previous observations concerning E cadherin effects on tumors in studies working with resected human tumors of the liver or with conditional organ specific mouse models studying carcinoma in other organs (like the mammary gland, for example). Therefore, this animal model could help improve the understanding of mechanisms regulating aggressiveness in human tumors.

Ask Dr. Wise: The Child of Carcinogenesis Now playing at a theater near you....just in time for Halloween, The Child of Carcinogenesis! No, sorry to say, this segment of the Ask Dr. Wise Radio Show is not the stuff of fiction.  It's an in depth examination of one of the most widely used and controversial [...]

Sat, 21 Jul 2012 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/14944/ https://edoc.ub.uni-muenchen.de/14944/1/grill_jessica.pdf Grill, Jessica ddc:59

Thoracic & Lung Cancers

Background: Global histone modifications have been implicated in the progression of various tumour entities. Our study was designed to assess global methylation levels of histone 4 lysine 20 (H4K20me1-3) at different stages of prostate cancer (PCA) carcinogenesis. Methods: Global H4K20 methylation levels were evaluated using a tissue microarray in patients with clinically localized PCA (n = 113), non-malignant prostate disease (n = 27), metastatic hormone-naive PCA (mPCA, n = 30) and castration-resistant PCA (CRPC, n = 34). Immunohistochemistry was performed to assess global levels of H4K20 methylation levels. Results: Similar proportions of the normal, PCA, and mPCA prostate tissues showed strong H4K20me3 staining. CRPC tissue analysis showed the weakest immunostaining levels of H4K20me1 and H4K20me2, compared to other prostate tissues. H4K20me2 methylation levels indicated significant differences in examined tissues except for normal prostate versus PCA tissue. H4K20me1 differentiates CRPC from other prostate tissues. H4K20me1 was significantly correlated with lymph node metastases, and H4K20me2 showed a significant correlation with the Gleason score. However, H4K20 methylation levels failed to predict PSA recurrence after radical prostatectomy. Conclusions: H4K20 methylation levels constitute valuable markers for the dynamic process of prostate cancer carcinogenesis.

Meme kanserine dair çalışması Türk basınında yer bulan Doç. Dr. Tan İnce ile araştırmaları hakkında görüştük. Doç. Dr. Tan İnce Dr. Tan İnce şu anda Miami Üniversitesi'ne bağlı Miller Tıp Fakültesi'nde Multidisipliner (Çokyaklaşımlı) Kök Hücre Enstitüsü'nde Tümör Kök Hücreleri bölümünü yönetiyor. Kendisine söyleşi için yeniden teşekkür ederiz. Notlar Dr Tan İnce ve ekibinin, bu söyleşide tartıştığımız son makalesi şu: Sandra Santagata vd., 2011. High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer. Proceedings of the National Academy of Sciences of the United States of America 108:18378-18383. Bu makaleye dair İngilizce basın açıklamasını buradan okuyabilirsiniz. Dr İnce'nin daha önce geliştirdiği kanser hücresi kültürünün makalesi: Tan A. Ince vd., 2007. Transformation of Different Human Breast Epithelial Cell Types Leads to Distinct Tumor Phenotypes. Cancer Cell 12:160-170. HSF1'in bu makalede tartışılan rolünün tarif edildiği makale: Chengkai Dai vd., 2007. Heat Shock Factor 1 Is a Powerful Multifaceted Modifier of Carcinogenesis. Cell 130:1005-1018. Bu makale Dr İnce ile işbirligi yapan Dr Susan Lindquist ekibinin çalışmasını tarif ediyor. HSF1'in rolünü Şekil 1'deki çizimle anlatmaya çalıştım: (A) HSF1, hücre içinde ama çekirdek dışında HSP70 ve HSP90 gibi protenlerle bir arada bulunur. Bu esnada HSF1 henüz etkin değildir. Hücre çeşitli olumsuz fiziksel/kimyasal şartlar altındayken hücre içindeki elverişsiz ortam, çeşitli proteinlerin yapısal özelliklerini ve işlevlerini kaybetmesine yol açar. (B) Bu bozuk proteinlerin temizlenmesi görevi HSP70 ve HSP90 gibi proteinlere düşer. Bu sırada HSF1 bunlarla temasını kaybeder, çekirdek içine aktarılır, etkinleştirilir ve oradaki DNA'ya bağlanır. (C) HSF1, hücreye daha çok HSP70 ve HSP90 ürettirerek elverişsiz ortam ile başa çıkmasını sağlar. Bu esnada hücrenin içindeki ortamın kötüleşmesine (ya da iyileşmesine) bağlı olarak çekirdek içindeki HSF1 miktarı da artacaktır (veya azalacaktır). Şekil 1. HSF1,in hücre içindeki rolü (ölçeksiz çizilmiştir)

animatie over het ontstaan van plaveiselcelcarcinomen, animatie, carcinogenesis, hoofd-halstumoren, KNO,

animatie over het ontstaan van plaveiselcelcarcinomen, animatie, carcinogenesis, hoofd-halstumoren, KNO,

Toxic reactions with the molecules of life.

Lecture Slides in PDF format

Toxic reactions with the molecules of life.

Lecture Slides in PDF format

Enhanced Audio PodcastAired date: 10/4/2006 3:00:00 PM Eastern Time

Enhanced Video PodcastAired date: 10/4/2006 3:00:00 PM Eastern Time

Models for the dose and age dependence of radiation induced cancer have been based primarily on the follow-up of the atomic bomb survivors. Two different concepts have been deduced for leukaemias and for other cancers. The excess leukaemias appear in a distinct temporal wave with a maximum 5 to 10 years after radiation exposure; the distribution is more narrow for younger ages, but there is little dependence of the total attributable risk on age at exposure. For other cancers the latent periods are longer and, according to the current interpretation, the excess rates are then proportional to the age specific spontaneous rates, so that most excess cases would arise at old age. The factors of proportionality, and thus the attributable risks, are assumed to be markedly higher for young ages at exposure. It is argued here that there is no firm support for this interpretation. The present analysis compares the current model for cancers other than leukaemia to a more meaningful alternative than the so-called additive model which is usually invoked as a standard of comparison. The analysis is performed in terms of analytical expressions, to make the characteristics of the different concepts more transparent. It is seen that the Japanese data are equally well fitted by a model that assumes no dependence of sensitivity on age at exposure but merely accounts for a dependence of the excess risks on dose and on age attained. This 'age attained model' corresponds, in essence, to formulations that have been used earlier for the analysis of lung cancers in uranium miners. The data up to 1985 for the atomic bomb survivors do not yet permit a decision between the different models. But the acceptability of the age attained model shows that age dependencies for leukaemias and other cancers to be less fundamentally different than commonly assumed. The age attained model leads to risk projections for young ages at exposure that are substantially lower than present estimates. In fact it predicts essentially the same lifetime attributable risk for exposures at young and intermediate ages; decreased risks result only for exposures at advanced ages where the expression periods are already substantially reduced.

Research on radiation carcinogenesis requires a twofold approach. Studies of primary molecular lesions and subsequent cytogenetic changes are essential, but they cannot at present provide numerical estimates of the risk of small doses of ionizing radiations. Such estimates require extrapolations from dose, time, and age dependences of tumor rates observed in animal studies and epidemiological investigations, and they necessitate the use of statistical methods that correct for competing risks. A brief survey is given of the historical roots of such methods, of the basic concepts and quantities which are required, and of the maximum likelihood estimates which can be derived for right censored and double censored data. Non-parametric and parametric models for the analysis of tumor rates and their time and dose dependences are explained.

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Fri, 1 Jan 1982 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8978/1/8978.pdf Rossi, Harald H.; Kellerer, Albrecht M. ddc:610, Medizin

Fri, 1 Jan 1982 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8717/1/8717.pdf Kellerer, Albrecht M. ddc:610, Medizin

Sun, 1 Jan 1978 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8408/1/8408.pdf Kellerer, Albrecht M. ddc:610, Medizin

Thu, 1 Jan 1976 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8385/1/8385.pdf Kellerer, Albrecht M.

Wed, 1 Jan 1975 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8349/1/8349.pdf Rossi, Harald H.; Kellerer, Albrecht M. ddc:610, Medizin

Female 61 to 63 - day - old Sprague-Dawley rats were exposed once to a single dose of either 0.43 - MeV neutrons or 250 - kVX - rays . For neutrons 23 rats were exposed in plastic tubes rotated around and 31 c m from a water-cooled tritium impregnated target bombarded with 2.45 - MeV protons from a V a n de Graaff generator. The mean kerma was measured at the rat location by integrating the response of a rat - sized homogeneous tissue equivalent ionization chamber of minimum mass. The ratio between absorbed dose and kerma is under investigation and is anticipated to be approximately 0.7. A compensated GM gamma-ray dosimeter indicated that the gamma - ray doses were 3.5% of the total dose. All rats were examined weekly for the presence of breast tumours and these were removed, fixed, stained and verified histologically as mammary neoplasms. At 10 months after exposure 98

An analysis of experimental findings indicates that the induction of a manmmary neoplasm in the Sprague-Dawley rat is dependent on the action of radiation on more than one cell. Although a linear relation between incidence and x-ray dose might be consistent with available data, such a relation would be fortuitous and linear extrapolation to lower doses is unjustified.