Dr. Peng Huang
The University of Texas MD Anderson Cancer Center
Department of Molecular Pathology
- Molecular mechanisms of apoptosis
- Role of mitochondria in ROS generation and drug-induced apoptosis
- Free radical/redox regulation and signaling
- Role of p53 in DNA damage and apoptosis
- Anticancer agents
The major objectives of my research programs are to investigate the biochemical and molecular mechanisms of drug-induced apoptosis and to design mechanism-based strategies to enhance therapeutic activity and selectivity of anticancer drugs. We investigate the role of mitochondria in drug-induced apoptosis, and examine the effect of oncogenic signals on mitochondrial free radical generation/regulation and apoptotic response to anticancer agents. One important focus is the role of p53 and associated molecules in sensing DNA damage by reactive oxygen species (ROS) and other genotoxic agents and the subsequent signaling for apoptosis. The understanding of the difference between cancer cells and normal cells in their ROS/redox regulation and apoptotic signaling will provide a basis for designing new strategies to selectively kill cancer cells and improve therapeutic activity and selectivity.
The tutorial students in this laboratory will learn cell culture techniques, assays of apoptosis, isolation of mitochondria and their functional analysis, measurement of cellular ROS, enzyme/protein purification and characterization, mtDNA sequencing analysis, in vitro DNA replication and repair assays, and a variety of biochemical and molecular pharmacology techniques.
Office: MDA 2SCR4.3029 (Unit 951)
M.D. - Zhongshan Medical University - 1982
Ph.D. - The University of Texas Graduate School of Biomedical Sciences at Houston - 1990