Ronald A. DePinho

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Ronald A. DePinho

Ronald A. DePinho, M.D., president of The University of Texas MD Anderson Cancer Center in Houston, is internationally recognized for basic and translational research in cancer, aging and age-associated degenerative disorders. He was inducted into the National Academy of Sciences in 2012.

DePinho became president on Sept. 1, 2011.[1] He is only the fourth full-time president in the 70-year history of MD Anderson.[2]

Prior to joining MD Anderson, he spent 14 years at Dana-Farber Cancer Institute and Harvard Medical School in Boston. There, he was founding director of the Belfer Institute for Applied Cancer Science at Dana-Farber and was a professor in the Department of Medicine (genetics) at Harvard and an American Cancer Society Research Professor. Previously, he held numerous faculty positions during 10 years at Albert Einstein College of Medicine in New York.

Research

At Dana-Farber and Harvard, DePinho guided major basic-translational research programs focused on brain, colorectal, pancreatic and prostate cancers. Under his leadership, the Belfer Institute followed industry-like principles to systematically translate basic research findings into clinical endpoints.

His scientific program has made fundamental discoveries underlying cancer in the aged and factors governing acquired and inherited degenerative disorders. He established the concept of tumor maintenance, discovered a core pathway of aging and demonstrated that aging is a reversible process.[3] He has constructed and used refined mouse models of cancer to identify many new cancer targets and diagnostics.

Background

DePinho was born in the Bronx, N.Y in 1955 to Celeste and Alvaro DePinho. He is the third of five children. He earned a bachelor's degree in biological sciences in 1977 from Fordham University, where he graduated summa cum laude as class salutatorian. He received his medical degree with distinction in microbiology and immunology in 1981 from Albert Einstein College of Medicine.

He completed an internship and residency in internal medicine at Columbia-Presbyterian Medical Center, followed by postdoctoral fellowships in the Department of Cell Biology at Albert Einstein College of Medicine and in the Department of Biochemistry and Biophysics at Columbia-Presbyterian Medical Center.

DePinho's independent scientific career began at Albert Einstein College of Medicine, where he was the Feinberg Senior Scholar in Cancer Research. There, he established the first National Cancer Institute-supported shared transgenic and gene targeting facility, which enabled his laboratory and many other researchers to model and study the genetic basis of cancer and other complex diseases.

Awards and honors

Select publications

  • Viale A, Pettazzoni P, Lyssiotis CA, Ying H, Sánchez N, Marchesini M, Carugo A, Green T, Seth S, Giuliani V, Kost-Alimova M, Muller F, Colla S, Nezi L, Genovese G, Deem AK, Kapoor A, Yao W, Brunetto E, Kang Y, Yuan M, Asara JM, Wang YA, Heffernan TP, Kimmelman AC, Wang H, Fleming JB, Cantley LC, DePinho RA, Draetta GF. Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Nature. 2014 Oct 30;514(7524):628-32.[4]
  • Son J, Lyssiotis CA, Ying H, Wang X, Hua S, Ligorio M, Perera RM, Ferrone CR, Mullarky E, Shyh-Chang N, Kang Y, Fleming JB, Bardeesy N, Asara JM, Haigis MC, DePinho RA, Cantley LC, Kimmelman AC. Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway. Nature. 2013 Apr 4;496(7443):101-5.[5]
  • Ying H, Kimmelman AC, Lyssiotis CA, Hua S, Chu GC, Fletcher-Sananikone E, Locasale JW, Son J, Zhang H, Coloff JL, Yan H, Wang W, Chen S, Viale A, Zheng H, Paik JH, Lim C, Guimaraes AR, Martin ES, Chang J, Hezel AF, Perry SR, Hu J, Gan B, Xiao Y, Asara JM, Weissleder R, Wang YA, Chin L, Cantley LC, DePinho RA. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell. 2012 Apr 27;149(3):656-70.[6]
  • Paik JH, Ding Z, Narurkar R, Ramkissoon S, Muller F, Kamoun WS, Chae SS, Zheng H, Ying H, Mahoney J, Hiller D, Jiang S, Protopopov A, Wong WH, Chin L, Ligon KL and DePinho RA. FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis. Cell Stem Cell. 2009 Nov 6;5(5):540-53.
  • Zheng H, Ying H, Yan H, Kimmelman AC, Hiller DJ, Chen AJ, Perry SR, Tonon G, Chu GC, Ding Z and others. p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation. Nature. 2008 Oct 23;455(7216):1129-33.[7]
  • Paik JH, Kollipara R, Chu G, Ji H, Xiao Y, Ding Z, Miao L, Tothova Z, Horner JW, Carrasco DR and others. FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostatsis. Cell. 2007 Jan 26;128(2):309-23.
  • Maser RS, Choudhury B, Campbell PJ, Feng B, Wong KK, Protopopov A, O'Neil J, Gutierrez A, Ivanova E, Perna I and others. Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. Nature. 2007 Jun 21;447(7147):966-71.[8]
  • Stommel JM, Kimmelman AC, Ying H, Nabioullin R, Ponugoti AH, Wiedemeyer R, Stegh AH, Bradner JE, Ligon KL, Brennan C and others. Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies. Science. 2007 Oct 12;318(5848):287-90.
  • Wong KK, Maser RS, Bachoo RM, Menon J, Carrasco DR, Gu Y, Alt FW, DePinho RA. Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates aging. Nature. 2003 Feb 6;421(6923):643-8.[9]

References

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External links

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