Ronald DePinho
Professor
The University of Texas MD Anderson Cancer Center
Department of Cancer Biology
Our basic and translational research program focuses on pathways and processes governing aging and age-related disorders, particularly cancer. Our experimental approach is built upon the use of unbiased computational analyses of multi-dimensional datasets, genetically engineered mouse models, and human-mouse comparisons on the molecular, cellular and physiological levels. Through MD Anderson’s Institute for Applied Cancer Science, we strive to drive basic discoveries to therapeutic and diagnostic endpoints in a systematic action-oriented culture. Our activities have focused on (i) defining the role of telomeres in governing cancer genome alterations, epithelial carcinogenesis, aging and degenerative disorder (both acquired and inherited), (ii) utilizing genetically engineered mouse (GEM) models to study human cancers with an emphasis on comparative oncogenomics and proteomics to discover and ultimately validate new genes for enlistment into drug discovery, early detection or prognostic biomarkers; there is a focus on glioma, pancreatic cancer, colorectal cancer and prostate cancer, and (iii) elucidating pathways orchestrating aging and age-related disorders with the goal of therapeutically manipulating such pathways to attenuate the incidence of age-associated diseases such as cancer, cardiomyopathy and neurodegeneration. Our mission is to convert basic knowledge into clinical endpoints that will impact on patient outcomes in meaningful ways.
Highlighted publications:
Lu X, et al. Effective combinatorial immunotherapy for castration-resistant prostate cancer. Nature. 2017; 543(7647): 728-732.
Liao W, et al., KRAS-IRF2 axis drives immune suppression and immune therapy resistance in colorectal cancer. Cancer Cell. 2019; 35(4): 559-572.e7
Zhao D, et al. Synthetic essentiality of chromatin remodeling factor CHD1 in PTEN-deficient cancer. Nature. 2017; 542(7642): 484-488.
Dey P, et al. Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Nature. 2017; 542(7639): 119-123.
Education & Training
M.D. - Albert Einstein College of Medicine - 1981