Journal of Pharmacovigilance

Q Ping Dou

Q Ping Dou
Professor, Department of Oncology, Pharmacology & Pathology, School of Medicine
Wayne State University, USA

Biography

Dr. Q. Ping Dou is Professor of Oncology, Pharmacology and Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI. Dr. Dou obtained his B.S. degree in chemistry from Shandong University in 1981, Ph.D. degree in chemistry from Rutgers University in 1988, and postdoctoral training at the Dana-Farber Cancer Institute and Harvard Medical School from 1988 to 1993 (Mentor: Arthur B. Pardee). Dr. Dou has extensive experience in the fields of drug discovery, chemoprevention, natural products, proteasome inhibitors, cell cycle and apoptosis. He has published ~200 peer-reviewed research and review articles, many of those in journals of the highest quality, and also holds ~10 patents. He has extensive experience in professional service, including various study sections, several advisory and editorial boards, and committees. He has mentored numerous graduate students, post-doctoral fellows and junior faculty.

Research Interest

The main objective in Dr. Dou’s laboratory is aimed at discovering molecular targets of natural products in pre-clinical studies, followed by validation in targeted cancer intervention clinical trials. Dr. Dou's laboratory is one of the first to report that proteasome inhibitors rapidly induce tumor cell apoptosis, selectively activate the cell death program in oncogene-transformed, but not normal or untransformed cells, and are able to trigger apoptotic death in human cancer cells that are resistant to various anticancer agents. Dr. Dou's laboratory has shown that some tea polyphenols and medicinal compounds potently and specifically inhibit the chymotrypsin-like activity of the proteasome in vitro and in vivo at physiological concentrations. His laboratory has established, for the first time, a computational molecular model that shows how these natural compounds bind and target the proteasome chymotrypsin subunit. This innovative computational model has been validated by comparison of predicted and actual activities of tea polyphenol analogs, either naturally occurring or rationally designed and synthesized. Also, Dr. Dou and collaborators have reported that (i) some old copper-binding drugs (such as the antialcoholism drug Disulfiram) could converting the pro-angiogenic copper to a specific cancer cell death inducer, (ii) Disulfiram also promotes the conversion of carcinogenic cadmium to a proteasome inhibitor with pro-apoptotic activity in human cancer cells, and (iii) environmental toxic organotins target the proteasome in human cells and proteasome inhibition by organotins contributes to their cellular toxicity. Most recently, Dr. Dou and collaborators have found that (i) novel epigallocatechin gallate (EGCG) analogs and BR-DIM activate AMP-activated protein kinase (AMPK) pathway, target cancer stem cells and induce apoptosis, and (ii) novel EGCG and curcumin analogs increase efficacy of bortezomib (BTZ) in human multiple myeloma (MM) cells.