Professor of Radiation Oncology, Institute for Academic Medicine
Full Member, Research Institute
Scientific Director, Department of Radiation Oncology
Weill Cornell Medical College
Dr. Pandita earned his Ph.D. in Cytogenetics from Panjab University in 1980. He held faculty appointments at Columbia University in New York, Washington University in St. Louis, Missouri, and The University of Texas Southwestern Medical Center in Dallas, Texas before becoming a member of the Houston Methodist Research Institute in 2014. As a member of the Cancer Research Program, he directs a research program focusing on DNA repair and radiotherapy. Dr. Pandita was elected the Fellow of the American Association of Advancement of Science in 2013. He has also been a member of several NIH study sections and review boards. He is the past Chairman of A-T Workshop 2012 (ATW2012) International meeting. Dr. Pandita serves on the editorial board for the journals Cancer Research, Genomic Integrity, BMC Genomics, and served as a chartered member of the CMAD NIH Study Section.
Dr. Pandita's research employs radiation genetics and biology to study the relationships between DNA sequence, chromatin structure and sensitivity to IR. The long-term goal of the research projects is to understand the mechanistic role of chromatin structure in regulating the cell survival response to IR-induced DNA damage. This knowledge base will be used by the laboratory to develop clinically relevant methods to increase tumor cell response to IR-based therapies while decreasing injury to adjacent, normal tissue.
Dr. Pandita's main areas of research are the following:
-To define, at the chromatin level, the function of H4K16ac in DNA DSB repair.
-To determine the role of ATM dependent MOF phosphorylation in the cellular response to IR.
-To determine the pathobiology of mutant mice defective for MOF T392 phosphorylation in order to test the hypothesis that Mof plays a critical role in oncogenic transformation in vivo.
-To determine the mechanisitic basis for enhanced tumor cell radiosensitivity following HP1ß loss or hyperthermia.