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Bardeesy, N., Sinha, M., Lopez, L., Tuveson, D.A., Horner, J., Redston, M.S., and DePinho, R.A. (2003). Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. Genes Dev 17, 3112-3126 and has further refined models for pancreas Boutin, A.T., Liao, W.T., Wang, M., Hwang, S.S., Karpinets, T.V., Cheung, H., Chu, G.C., Jiang, S., Hu, J., Chang, K., et al. (2017). Oncogenic Kras drives invasion and maintains metastases in colorectal cancer. Genes Dev 31, 370-382, colon Ding, Z., Wu, C.J., Chu, G.C., Xiao, Y., Ho, D., Zhang, J., Perry, S.R., Labrot, E.S., Wu, X., Lis, R., et al. (2011). SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression. Nature 470, 269-273, and prostate cancer Maser, R.S., Choudhury, B., Campbell, P.J., Feng, B., Wong, K.K., Protopopov, A., O'Neil, J., Gutierrez, A., Ivanova, E., Perna, I., et al. (2007). Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. Nature 447, 966-971. Combining his oncogenic and telomerase knockout mouse models, his laboratory performed the first genome-wide comparative oncogenomic profiling, which facilitated the identification of new cancer targets in the early days of the cancer genome project. Maser, R.S., Choudhury, B., Campbell, P.J., Feng, B., Wong, K.K., Protopopov, A., O'Neil, J., Gutierrez, A., Ivanova, E., Perna, I., et al. (2007). Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. Nature 447, 966-971 Highlights from Dr. DePinhoâs mouse model work include the generation of CDKN2A knockout mice and providing proof of the tumor suppressor function of this gene, which is now known to be critical in diverse cancers â most prominently GBM, melanoma and mesothelioma. In addition, his lab used their metastatic prostate cancer model to develop a prognostication signature for metastatic potential in patients. Ding, Z., Wu, C.J., Chu, G.C., Xiao, Y., Ho, D., Zhang, J., Perry, S.R., Labrot, E.S., Wu, X., Lis, R., et al. (2011). SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression. Nature 470, 269-273. These studies provided the foundation for the development of a biomarker test, Promark, which is now in clinical use for the stratification of men with localized prostate cancer into high and low risk of prostate cancer-related death. Dr. DePinhoâs Kras inducible pancreas cancer model illuminated the role of oncogenic Kras in metabolic reprogramming Ying, H., Kimmelman, A.C., Lyssiotis, C.A., Hua, S., Chu, G.C., Fletcher-Sananikone, E., Locasale, J.W., Son, J., Zhang, H., Coloff, J.L., et al. (2012). Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell 149, 656-670 and identified a Kras-cytokine circuit underlying this reprogramming Dey, P., Li, J., Zhang, J., Chaurasiya, S., Strom, A., Wang, H., Liao, W.T., Cavallaro, F., Denz, P., Bernard, V., et al. (2020). Oncogenic KRAS-Driven
Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment. Cancer Discov 10, 608-625, yielding therapeutic targets for this cancer hallmark Dey, P., Li, J., Zhang, J., Chaurasiya, S., Strom, A., Wang, H., Liao, W.T., Cavallaro, F., Denz, P., Bernard, V., et al. (2020). Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment. Cancer Discov 10, 608-625. This work led to the discovery of resistance mechanisms enabling Kras-independent growth, which also involve the tumor microenvironment Hou, P., Kapoor, A., Zhang, Q., Li, J., Wu, C.J., Li, J., Lan, Z., Tang, M., Ma, X., Ackroyd, J.J., et al. (2020). Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer. Cancer Discov 10, 1058-1077. Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.J., Sadanandam, A., Hu, B., et al. (2019). Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer. Cell 179, 1239.
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reactivation in telomere dysfunctional adult mice with severe tissue degeneration actually reversed aging and degenerative phenotypes across many organs, including the brain. Unbiased gene expression profiling and functional studies led to identification of a core pathway of aging, linking for the first-time telomere dysfunction, diminished oxidative defense, and impaired mitochondrial function. Thus, three previously distinct theories of aging â focused on genotoxic stress, oxidative defense, or mitochondrial biology â were now integrated into a cohesive theory via a single pathway responsive to many pathways linked to aging. Zheng, H., Ying, H., Yan, H., Kimmelman, A.C., Hiller, D.J., Chen, A.J., Perry, S.R., Tonon, G., Chu, G.C., Ding, Z., et al. (2008). p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation. Nature 455, 1129-1133. Most recently, his lab has defied a mechanism by which telomere dysfunction induces tissue inflammation. Zhao D., DePinho, R. (2017). Synthetic essentiality: Targeting tumor suppressor deficiencies in cancer. Bioessays, 39(8).
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co-deletion of bystander genes in tumor suppressor gene loci, providing a cancer-specific vulnerability through the targeting of paralogs. Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.J., Sadanandam, A., Hu, B., et al. (2019). Yap1 Activation
Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer. Cell 179, 1239.. Dey, P., Baddour, J., Muller, F., Wu, C.C., Wang, H., Liao, W.T., Lan, Z., Chen, A., Gutschner, T., Kang, Y., et al. (2017). Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Nature 542, 119-123.
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Raven, felt differently: âPresident DePinho did exactly what he pledged to do--elevate the scientific enterprise through the recruitment and retention of world class researchers, accelerate the translation of intellectual property, develop new collaborations with other institutions and hospitals, and put internal teams of the worldâs best clinicians and researchers together to mobilize MD Andersonâs quest to speed up development for new and more effective treatments.
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Remodels the
Immunosuppressive Tumor Microenvironment in PTEN-Deficient Prostate Cancer. Cancer Discov 10, 1374-1387. Together with his establishment of tumor maintenance, the concepts of collateral lethality and synthetic essentiality have expanded the universe of cancer targets and the context in which these targets are rate-limiting.
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Dr. DePinhoâs experience as a clinician prompted him to pursue the use of mouse models in translational cancer medicine. In addition to his first inducible oncogene model in melanoma, Dr. DePinhoâs team produced several of the first genetically engineered mouse models for glioblastoma
Aguirre, A.J.,
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I would like to disclose here a conflict of interest. I write articles, including my update to his
Knowledge article, on behalf of Dr. DePinho and in consultation with him for a small fee. I have been carefully studying and intend to follow all of Knowledge's guidelines, including those on WP:COI,
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Similarly, his concept of âsynthetic essentialityâ provides a framework for the identification of essential effectors of tumors suppressor gene deficiencies Zhao, D., Cai, L., Lu, X., Liang, X., Li, J., Chen, P., Ittmann, M., Shang, X., Jiang, S., Li, H., et al. (2020). Chromatin
Regulator CHD1
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This page follows the structure and tone of the pages of several of Dr. DePinho's peers. All are notable scientists in their field, including a Nobel
Laureate with whom Dr. DePinho contributed to a breakthrough cancer target. His lab gained notoriety with the development of mouse models that can
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After last sentence, consider adding from the same article already cited this excerpt from among three counterpoint statements in the article. This one is from the
Chancellor William McRaven. Opening fragment added to explain who the quote is from: However some, including the Chancellor William
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Recent work by the DePinho lab has focused on precision oncology, with an emphasis on utilizing genomic deletions as points of cancer selective vulnerabilities. Dr. DePinhoâs concept of âcollateral lethalityâ further expanded the cancer gene target space. Collateral lethality is based on the
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After 2nd paragraph, add this important research description: âExploring the potential of telomerase therapy in aging, Dr. DePinho developed an inducible telomerase mouse model to test the regenerative potential of restoration of physiological levels of telomerase. Strikingly, telomerase
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Section 4: Research
Consider changing this title from âResearchâ to âBasic Research.â âBasicâ (or synonym âFundamentalâ) in this context means (from Knowledge page) âwith the aim of improving scientific theories for better understanding and prediction of natural or other phenomena.â It is
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2nd paragraph, 2nd sentence. After âtumor maintenanceâ here is the missing citation: Chin, L., Tam, A., Pomerantz, J., Wong, M., Holash, J., Bardeesy, N., Shen, Q., OâH. Depinho, R.A. (1999). Essential role for oncogenic Ras in tumor maintenance. Nature 400, 468-472.
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Hi, I am a new user and have been updating the Wiki article of Ronald DePinho. It has been flagged for a few issues (correcting external links and missing citations. I have made pretty major edits to address these issues. Can you please remove the "Issues" template?
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2nd paragraph, after last sentence: Here is a missing citation after âtargets and diagnosticsâ: Morgenbesser, SD., Williams, B. O., Jacks, T., DePinho, R.A. (1994), p-5, 3-dependent apoptosis produced by Rb-deficiency in the developing mouse lens. Nature 371,72-64.
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Career section: Last sentence: Consider removing âunprecedented from the phrase âunprecedented turbulenceâ This is an opinion, not a fact, and not included In any articles on the subject, including the article drawn from here, which uses only âfaculty turmoil.
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WP:RS, WP:V and WP:NPOV, very closely. My aim is simply to create a factual page. On any pages where I look for assistance, such as this one, I will always disclose my relationship to Dr. DePinho in the interests of transparency.
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Factual correction: placement of âformer presidentâ incorrectly describes Ronald DePinho as the former president of the
Department, when he was in fact former president of MD Anderson, as the next sentence describes.
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I have assembled a careful list of corrections and additions (e.g., citations). I have pasted it below. Is this the right place to ask for help? Because I have a conflict of interest, I cannot make these changes.
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31:) policy, even if it is not a biography, because it contains material about living persons. Contentious material about living persons that is unsourced or
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Honors and Awards Section This section is very outdated. Here is the complete list, and can replace what is there and is already ordered chronologicallyâ
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require that editors disclose their "employer, client, and affiliation" with respect to any paid contribution; see
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Leadership in Scientific Achievement Award, Portuguese-American Leadership Council of the United States (2018)
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distinguished from âappliedâ research, which is defined in Knowledge as âpractical application of science.â
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Member, Institute of Medicine (now Health and Medicine Division) of the National Academies (2004-present)
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M.D. with distinction in Microbiology & Immunology, Albert Einstein College of Medicine (1981)
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Commander of the Order of Saint James of the Sword (knighthood), Republic of Portugal (2015)
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Prize for Scientific Excellence in Medicine, American Italian Cancer Foundation (2012)
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Brien McMahon Award for Distinguished Public Service, Fordham University (2017)
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50 Most Influential Physician Executives and Leaders, Modern Healthcare (2016 )
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American Society for Clinical Investigation Award (now Korsmeyer Award) (2002)
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Ellis Island Medal of Honor, National Ethnic Coalition of Organizations (2017)
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Order of Saint James of the Sword (knighthood), Republic of Portugal (2015)
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2016 Luminary Award, The Texas Healthcare and Bioscience Institute (2016)
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American Cancer Society Edith A. Pistorino Research Professorship (2004)
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Albert Einstein College of Medicine Distinguished Alumnus Award (2004)
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NCI Physician Scientist Award (K08), National Cancer Institute (1984)
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First sentence: misspelling: Change âdisfunctionâ to âdysfunctionâ
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100 Most Influential People in Healthcare, Modern Healthcare (2015)
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Outstanding Phi Beta Kappa Alumnus Award, Fordham University (2013)
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Team Science Award, American Association for Cancer Research, 2020
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Fellow, American Association for the Advancement of Science (2014)
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Albert Szent-Györgyi Prize for Progress in Cancer Research (2009)
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American Heart Association Established Investigator Award (1992)
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Fellow, American Association for Cancer Research (2015-present)
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from the article and its talk page, especially if potentially
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Unknown-importance biography (science and academia) articles
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Member, American Academy of Arts and Sciences (2010-present)
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Salutatorian and Summa Cum Laude, Fordham University (1977)
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The Ellison Medical Foundation Senior Scholar Award (2003)
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American Cancer Society Research Professorship (1998-2008)
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The Humanitarian Award, The Latino Learning Center (2017)
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Foreign Member, Royal Academy of Science, Portugal (2017)
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Melini Award for Excellence in Biomedical Research (1993)
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Feinberg Senior Faculty Scholar in Cancer Research (1992)
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Steinbugler Award for Biology, Fordham University (1977)
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Start-Class biography (science and academia) articles
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Talk pages of subject pages with paid contributions
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Member, National Academy of Sciences (2012-present)
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Cancer Research Institute Investigator Award (1989)
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Outstanding Senior Award, Fordham University (1977)
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