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Haoqiang Ying

Haoqiang Ying

Regular Member

Associate Professor

[email protected]
MDA Y8.6089 (Unit 0108)

The University of Texas MD Anderson Cancer Center
Department of Molecular and Cellular Oncology

My major research interest is the genetics and biology of pancreatic cancer, with an overarching goal to identify and characterize molecular vulnerabilities of pancreatic ductal adenocarcinoma (PDAC). Using a novel inducible PDAC mouse model, we have recently established that oncogenic Kras plays fundamental roles in the metabolism reprogramming of pancreatic cancer and is essential for tumor maintenance. Our studies indicate that Kras oncogene orchestrates the flux of glucose metabolism intermediates into various anabolic pathways to support PDAC growth. Part of our ongoing work is to use metabolomics and various biochemical approaches to characterize how Kras-driven glucose flux regulates novel hexose metabolism pathways which are important for nutrient salvage and protein homeostasis in pancreatic cancer. We are currently evaluating combination strategies to target metabolism pathways in PDAC, including co-targeting Kras-driven nutrient metabolism and mitochondrial respiration using a novel OXPHOS inhibitor.

While KRAS oncogene is required for PDAC maintenance, our study using the inducible PDAC model also demonstrated that a subset of tumor cells will bypass the addiction to KRAS and contributes to tumor growth following KRAS extinction. We have identified YAP1 oncogene as the major driver for the bypass of KRAS-dependency in PDAC. Importantly, our current study indicates that YAP1 is activated in a subset of human PDACs and is required for their tumorigenic activity. We are currently generating novel genetically engineered mouse (GEM) models that will allow us to characterize the role of YAP1 specifically in advanced tumors. We will use these novel mouse models in conjunction with patient-derived xenograft models to understand the molecular mechanisms for YAP1 function in PDAC. Since previous studies have shown that YAP1 is absolutely required for KRAS-driven tumor initiation, we are also using single cell technologies to decipher the YAP1-dependent cellular trans-differentiation program for the inception of pancreatic tumors. The outcome of these studies will provide preclinical evidence to target YAP1 for the treatment and prevention of PDAC.


MDACC Faculty

Education & Training

Ph.D. - Boston University School of Medicine - 2007
M.D. - Peking Union Medical College - 2000

Research Opportunities


Faculty Development