Talk:Ronald DePinho
This article must adhere to the biographies of living persons (BLP) policy, even if it is not a biography, because it contains material about living persons. Contentious material about living persons that is unsourced or poorly sourced must be removed immediately from the article and its talk page, especially if potentially libellous. If such material is repeatedly inserted, or if you have other concerns, please report the issue to this noticeboard.If you are a subject of this article, or acting on behalf of one, and you need help, please see this help page. |
![]() | This article is rated Start-class on Wikipedia's content assessment scale. It is of interest to the following WikiProjects: | ||||||||||
|
![]() | The Wikimedia Foundation's Terms of Use require that editors disclose their "employer, client, and affiliation" with respect to any paid contribution; see WP:PAID. For advice about reviewing paid contributions, see WP:COIRESPONSE.
|
REQUEST FOR DELETION OF THE "ISSUES" BOX TEMPLATE
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?
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 reverse aging.
I would like to disclose here a conflict of interest. I write articles, including my update to his Wikipedia 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 Wikipedia's guidelines, including those on WP:COI, 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.
Thanks, jasmit53
Another request
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. Jasmit53 (12/17/21 Requests from Janet Smith for corrections And for an additional section for Ronald DePinho
Early Life and Education section
Last sentence citation needed: insert this footnote:
https://einsteinmed.org/alumni/alumni.aspx?ID=1870
Career section, 2nd paragraph, first sentence:
Factual correction: placement of “former president” 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.
Fix this error by removing “and former president”
Career section: Last sentence: Consider removing “unprecedented from the phrase “unprecedented turbulence” 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 “faculty turmoil.
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 Raven, felt differently: “President 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 world’s best clinicians and researchers together to mobilize MD Anderson’s quest to speed up development for new and more effective treatments.
Section 4: Research
Consider changing this title from “Research” to “Basic Research.” “Basic” (or synonym “Fundamental”) in this context means (from Wikipedia page) “with the aim of improving scientific theories for better understanding and prediction of natural or other phenomena.” It is distinguished from “applied” research, which is defined in Wikipedia as “practical application of science.”
First sentence: misspelling: Change “disfunction” to “dysfunction”
1st paragraph, last sentence: Add ‘and inflammatory disease.”
2nd paragraph, 2nd sentence. After “tumor maintenance” here is the missing citation: Chin, L., Tam, A., Pomerantz, J., Wong, M., Holash, J., Bardeesy, N., Shen, Q., O’H. Depinho, R.A. (1999). Essential role for oncogenic Ras in tumor maintenance. Nature 400, 468-472.
2nd paragraph, after last sentence: Here is a missing citation after “targets and diagnostics”: 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.
After 2nd paragraph, add this important research description: “Exploring 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 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 – focused on genotoxic stress, oxidative defense, or mitochondrial biology – were now integrated into a cohesive theory via a single pathway responsive to many pathways linked to aging. [source] 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. [source] Zhao D., DePinho, R. (2017). Synthetic essentiality: Targeting tumor suppressor deficiencies in cancer. Bioessays, 39(8).
Dr. DePinho’s 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. DePinho’s team produced several of the first genetically engineered mouse models for glioblastoma [source] Aguirre, A.J., 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 [source] 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, [source] 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. [source] 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. DePinho’s 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 – 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. [source] 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. DePinho’s Kras inducible pancreas cancer model illuminated the role of oncogenic Kras in metabolic reprogramming [source] 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 [source] 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 [source] 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 [source] 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.
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. DePinho’s concept of “collateral lethality” further expanded the cancer gene target space. Collateral lethality is based on the co-deletion of bystander genes in tumor suppressor gene loci, providing a cancer-specific vulnerability through the targeting of paralogs. [source] 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.
Similarly, his concept of “synthetic essentiality” provides a framework for the identification of essential effectors of tumors suppressor gene deficiencies [source] 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 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.
Honors and Awards Section This section is very outdated. Here is the complete list, and can replace what is there and is already ordered chronologically”
Honors
- Honorary MS Degree, Harvard Medical School (1998)
- Commander of the Order of Saint James of the Sword (knighthood), Republic of Portugal (2015)
- Honorary PhD Degree, Hofstra University (2017)
- Ellis Island Medal of Honor, National Ethnic Coalition of Organizations (2017)
Awards
- Phi Beta Kappa, Fordham University (1976)
- Chemistry Award, Fordham University (1977 )
- Outstanding Senior Award, Fordham University (1977)
- Salutatorian and Summa Cum Laude, Fordham University (1977)
- Steinbugler Award for Biology, Fordham University (1977)
- Eli H. Rubin Award in Medicine (1981)
- M.D. with distinction in Microbiology & Immunology, Albert Einstein College of Medicine (1981)
- NCI Physician Scientist Award (K08), National Cancer Institute (1984)
- James S. McDonnell Foundation Scholar Award (1988)
- Cancer Research Institute Investigator Award (1989)
- March of Dimes Basil O'Connor Scholar Award (1989)
- American Heart Association Established Investigator Award (1992)
- Feinberg Senior Faculty Scholar in Cancer Research (1992)
- Melini Award for Excellence in Biomedical Research (1993)
- Irma T. Hirschl Career Scientist Award (1995)
- American Cancer Society Research Professorship (1998-2008)
- American Society for Clinical Investigation Award (now Korsmeyer Award) (2002)
- AACR-G.H.A. Clowes Memorial Award (2003)
- The Ellison Medical Foundation Senior Scholar Award (2003)
- Albert Einstein College of Medicine Distinguished Alumnus Award (2004)
- American Cancer Society Edith A. Pistorino Research Professorship (2004)
- Member, Institute of Medicine (now Health and Medicine Division) of the National Academies (2004-present)
- Albert Szent-Györgyi Prize for Progress in Cancer Research (2009)
- Member, American Academy of Arts and Sciences (2010-present)
- Prize for Scientific Excellence in Medicine, American Italian Cancer Foundation (2012)
- Thought Leader Award, Agilent Technologies (2012)
- Member, National Academy of Sciences (2012-present)
- Outstanding Phi Beta Kappa Alumnus Award, Fordham University (2013)
- Fellow, American Association for the Advancement of Science (2014)
- 100 Most Influential People in Healthcare, Modern Healthcare (2015)
- Fellow, American Association for Cancer Research (2015-present)
- Order of Saint James of the Sword (knighthood), Republic of Portugal (2015)
- 2016 Luminary Award, The Texas Healthcare and Bioscience Institute (2016)
- 50 Most Influential Physician Executives and Leaders, Modern Healthcare (2016 )
- Brien McMahon Award for Distinguished Public Service, Fordham University (2017)
- Foreign Member, Royal Academy of Science, Portugal (2017)
- The Humanitarian Award, The Latino Learning Center (2017)
- Leadership in Scientific Achievement Award, Portuguese-American Leadership Council of the United States (2018)
- Team Science Award, American Association for Cancer Research, 2020