Weibiao Cao, MD
Associate Professor, Department of Medicine, The Warren Alpert Medical School of Brown University, Providence, RI, USA
https://vivo.brown.edu/display/wcao
Biography
Dr. Cao obtained his MD degree from Zhejiang Medical University in Hangzhou, China in 1986. Dr. Cao worked as a research associate and an assistant professor in Division of Gastroenterology, Rhode Island Hospital from 1996 to 2007. He was trained as a pathology resident from 2007 to 2011and a GI pathology fellow from 2011 to 2012 in the Department of Pathology, Rhode Island Hospital and Brown University. Since November, 2012 Dr. Cao has been an attending surgical and GI pathologist as well as an independent researcher in Department of Pathology, Rhode Island Hospital and Brown University. He has been an associate professor since 2013 and a director of autopsy service since 2017 in Department of Pathology and Laboratory Medicine, the Warren Alpert Medical School of Brown University, Providence, RI, USA. Dr. Cao has been a Member of Oncology C (ONCC) scientific peer review panel, Department of Veterans Affairs, USA and an editorial board member of Scientific Reports since 2015.
Research Interest
Dr. Cao is studying the mechanisms of the progression from Barrett esophagus to esophageal adenocarcinoma, focusing on the role of NADPH oxidases-derived reactive oxygen species. His research on NADPH oxidase NOX5-S shows that NADPH oxidase NOX5-S is overexpressed in esophageal adenocarcinoma cells and mediates acid-induced hydrogen peroxide production. Acid-induced NOX5-S expression depends on an increase in intracellular calcium and activation of a transcription factor CREB. NOX5-S contributes to increased cell proliferation and decreased apoptosis in esophageal adenocarcinoma cells.
Dr. Cao also studies the signal transduction pathways mediating contraction in normal esophageal smooth muscle and the inflammation-associated changes in signalling that occur in experimental esophagitis. In addition, he investigates inflammation-induced changes in contractile signal transduction pathways of human sigmoid colon and study the effect of inflammatory mediators on colonic motor function in ulcerative colitis.