2017 GRANTEE: Haoqiang Ying, MD, PhD
MD Anderson Cancer Center
Research Project: The Regulation of Oncogene Addiction by YAP Pathway in Pancreatic Cancer
Award: 2017 Pancreatic Cancer Action Network – AACR Career Development Award
Award Period: July 1, 2017 – June 30, 2019
Dr. Ying earned his MD degree from Peking Union Medical College, China, in 2000 and received his PhD in biochemistry from Boston University School of Medicine in 2006. He then worked as a postdoctoral fellow at Dana-Farber Cancer Institute, where he used genetically-engineered mouse models to study how advanced pancreatic cancer is dependent on KRAS –the most commonly mutated protein in the disease – and how KRAS influences the cells’ ability to break down (metabolize) nutrients for energy and tumor survival. Dr. Ying joined MD Anderson Cancer Center in 2014 as an assistant professor. His research program is focused on understanding context-specific regulation of KRAS dependency and its related metabolic programs in pancreatic cancer.
Whereas the vast majority of pancreatic cancer cases have a mutation in KRAS, a protein that causes many of the cancer-like features and behaviors of the cells, there is a subset of pancreatic tumors that becomes less dependent on KRAS activity for survival. Preliminary evidence has suggested that tumors that are KRAS-independent lead to poorer patient outcomes than those that remain dependent on the activity of mutant KRAS.
Dr. Ying and his colleagues have found that another oncogene (a protein that can become activated to instill cancer-like properties in cells), called YAP1, may become activated in cells that are independent of KRAS activity. The team hypothesizes that YAP1 activation may replace KRAS and promote aggressive tumor progression.
For his funded project, Dr. Ying aims to decipher the function of YAP1 in pancreatic tumors in mice, particularly in the context of KRAS independence. Potential clinical implications of this work could include precision medicine-type approaches to tailor a patient’s treatment to whether their tumor expresses mutant KRAS or YAP1 – pending the identification of therapeutic strategies that are particularly effective for each subtype of the disease.