Wei G, Margolin A, Haery L, et al. Chemical genomics identifies small-molecule MCL1 repressors and BCL-xL as a predictor of MCL1 dependency. Cancer Cell. 2012;21(4):547-562.
Wei G, Twomey D, Lamb J, et al. Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL1 and glucocorticoid resistance. Cancer Cell. 2006;10(4):331-342.
Guo Wei, Ph.D.
Guo Wei is a group leader in the Cancer Program at the Broad Institute of MIT and Harvard. He joined the Broad Institute as a postdoc researcher in 2005 and became a research scientist in 2009. At the Broad, Guo has pioneered the research of targeting pro-survival proteins in cancer. He and his colleagues discovered that MCL1 is frequently amplified and highly expressed in cancer, and is required for the survival of cancer cells with low BCLxL expression, and thus identified MCL1 as a potential oncology target and revealed a potential patient population that would be benefit from MCL1 therapeutics. Since 2012, Guo has co-directed the research and development activities of the MCL1 therapeutics project within the Broad and also coordinated collaborations with other partner institutions.
Guo holds a B.S. in biology from Shandong University and a M.S. in plant physiology from the Chinese Academy of Sciences. He obtained his Ph.D. in molecular genetics from The Ohio State University, where he was awarded The Ohio State University Presidential Fellowship. Upon completion of his doctorate, Wei was awarded the Damon Runyon Cancer Research Foundation Postdoctoral Fellowship as he began his postdoctoral studies at Dana-Farber Cancer Institute and the Broad Institute. He is an active member of the American Association for Cancer Research.
Contact Wei via email at firstname.lastname@example.org.