Seeking new targets for development of preventive and treatment strategies in advanced breast cancer.
Laboratory studies are focused on understanding the role of a tumor promoting gene as a potential therapeutic target to prevent metastasis.
These studies may inform new drug development that could improve outcomes for patients with aggressive breast cancer.
Breast cancer is not one disease, but a variety of diseases driven by unique biologies. Some may be driven by hormones, such as estrogen, or growth factors such as HER2. Mutations in genes that control essential cell processes such as growth, metabolism and normal cell death also fuel tumor growth.
Whatever their "addiction", tumor cells learn how to manipulate the pathways they depend on in order to survive. Understanding the genes in these processes will help tremendously in the clinical management of the disease. One such gene is called YAP and has been shown to promote breast cancer cell growth, survival and metastasis.
Work by Dr. Wang revealed a unique function of YAP in the regulation of energy metabolism. Tumor cells are known to reprogram their metabolism to support their uncontrolled growth and survival during tumor progression, making YAP a promising therapeutic target. Dr. Wang is also working with a class of drug, called histone deacetylase (HDAC) inhibitors, already in clinical trials that may inhibit the actions of YAP. As part of his BCRF/AACR research, Dr. Wang will continue to study YAP as a biomarker for cancer cells and potential target to limit the growth and spread of cancer cells.
Dr. Wenqi Wang received his BS from Nanjing University in China in 2004. Mentored by Dr. Kan Liao, he obtained his PhD from the Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, in 2009. In October 2009, he joined Dr. Junjie Chen’s lab at MD Anderson Cancer Center to pursue postdoctoral training. Currently, Dr. Wang is assistant professor at University of California, Irvine. His research focuses on the Hippo-YAP signaling pathway that mediates organ size and tumor suppression.