Journal of Experimental Pathology

Haitao Zhang

Department of Pathology and Laboratory Medicine

Tulane University School of Medicine

USA

Academic Editor

Biography

Dr. Zhang received his B.S. in molecular biology from the Nankai University, Tianjin, China, in 1992. He completed his doctoral training in the Department of Experimental Pathology at Roswell Park Cancer Institute, receiving his Ph.D. in 2000. Subsequently, he conducted postdoctoral research under the mentorship of Dr. Margot Ip, studying the mechanism of TNF alpha suppression of functional differentiation of mammary epithelial cells. From 2001 to 2003, Dr. Zhang worked at the Microarray and Genomics Core Facility at Roswell Park as a bioinformatics specialist. He was recruited to the Department of Cancer Chemoprevention at Roswell Park in 2003 as a research scientist and was promoted to research assistant professor in 2005. In 2008, he joined the faculty of Tulane University School of Medicine as a tenure-track assistant professor in the Department of Pathology and Laboratory Medicine, and was promoted to associate professor with tenure in 2014. Dr. Zhang’s research centers on targeting the androgen receptor signaling axis for the prevention and treatment of prostate cancer. He has severed on several DOD and NIH grant review panels.

Research Interest

Dr. Haitao Zhang, Associate Professor in the Department of Pathology and Laboratory Medicine at Tulane University School of Medicine, is an established investigator in translational research of prostate cancer. Dr. Zhang’s laboratory focuses on targeting the androgen receptor (AR) signaling axis in prostate cancer intervention. His lab has investigated the anticancer efficacies and mechanisms of several synthetic and natural compounds in prostate cancer. His recent search has established a role of AR splice variants (AR-Vs) in resistance to hormonal therapy and taxane-based chemotherapy in castration-resistant prostate cancer. Ongoing efforts in his lab include studies on the intracellular trafficking and the nuclear translocation of AR and its splice variants, and the impact of circadian disruption on stress response and therapeutic resistance in prostate cancer.