The University of Texas MD Anderson Cancer Center
Department of Experimental Therapeutics
My interests are in mechanisms of drug resistance, particularly in cancers retaining the p53 tumor suppressor in its wild-type state. Normally, the presence of wild-type p53 in cancers provides an apoptotic stimulus and imparts high tumor cell sensitivity to therapeutic agents. In resistant cancers, however, wild-type p53 fails to activate cell cycle checkpoint response and induce the apoptotic stimulus. The goal in my laboratory is to undertake hypothesis-driven studies to define pathways responsible for this loss of p53 function and rationally investigate designer drugs to reactivate the tumor suppressor and provide a basis for translational opportunities. Such an approach is essential for improving response rates in the clinic. In our laboratory, we use a variety of analytical tools to assess pharmacological (e.g., drug concentration at the cellular level and target sites), biochemical (e.g., checkpoint kinase activity and proteomic analysis), and molecular (e.g., target activation, microarrays and siRNA) drivers of cytotoxic drug response and their modulation in sensitive and resistant tumor models. There are ample opportunities to network with other labs with mutual interests.
A tutorial under my guidance would provide an opportunity to understand the significance of drug resistance, its underlying mechanism and its circumvention through rational concepts utilizing novel therapeutic agents.
Education & Training
Ph.D. - University of London - 1975