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Kevin Michael Haigis, PhD

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Kevin Michael Haigis, PhD


  • Associate Professor of Medicine, Harvard Medical School
  • Chief Scientific Officer, Dana-Farber Cancer Institute

Contact Information

  • Office Phone Number857-215-0448


Dr. Haigis received his PhD from the University of Wisconsin in 2002 and continued training as a postdoctoral fellow in the laboratory of Tyler Jacks at MIT. He became a Harvard Medical School Assistant Professor of Pathology in 2007 and Associate Professor of Medicine in 2014. Additional appointments include Assistant Pathologist at Massachusetts General Hospital (2007-2014); Faculty Member of the HMS Biological and Biomedical Sciences Graduate Program and Full Member of the Gastrointestinal Malignancies Cancer Genetics Program of the DF/HCC (both 2007 – present); Investigator at the Center for the Study of Inflammatory Bowel Disease at MGH/BIDMC (2007-2016); Associate Member of the Center for Systems Biology at MGH (2010-2014); Member of the Harvard Digestive Disease Center and Faculty Member of the Bioinformatics and Integrative Genomics Graduate Program (both 2016- present). He served as Director of Cancer Genetics at Beth Israel Deaconess Cancer Center from 2014 until joining Dana-Farber as Chief Research Officer in 2020. He is an Associate Member of the Broad Institute (2017- present).

Recent Awards:

  • Grand Challenge, 2019
  • Nodal Award, 2009
  • Research Scholar Grant, 2008
  • Career Development Award, 2007-2008
  • Howard Temin Award, 2006
  • Robert Black Fellowship, 2003
  • Schlimgen Award for Dissertation Research, 2002


Cancer and inflammation in the gastrointestinal tract
My laboratory studies cancer and inflammation in the gastrointestinal tract by integrating genetically engineered mouse models with biochemistry and structural biology, proteomics and genomics, and bioinformatics and systems biology. Our primary cancer research goal over the past decade has been to understand the biology of the RAS family oncogenes at a level that will allow us to design and implement precision medicine approaches for RAS-mutant colorectal cancer (CRC) and pancreatic ductal adenocarcinoma (PDAC). Our work has helped to refine the fundamental principles of precision medicine, in particular by demonstrating that closely related cancer genes, and allelic forms of the same gene, can be functionally distinct and therefore require distinct therapeutic interventions. Through our work, my laboratory has strongly integrated into the HMS and Broad Institute cancer research community. Our ongoing work focuses on the application of mass spectrometry to mouse models of K-RAS driven cancer,  the identification of synthetic lethal partners with mutant forms of K-RAS, understanding allele-specific functions of K-RAS across gastrointestinal cancers, and the development of computational models of K-RAS signaling and genetics.
Our work on inflammation addresses two complementary and intertwined goals: (1) to understand inflammatory signaling at the level of protein networks and (2) to bring the concept of personalized medicine to the field of inflammatory bowel disease (IBD) research. Much of our early work in this domain was devoted to the development of methods to apply computational modeling approaches to signaling data from mouse models of inflammatory signaling driven by tumor necrosis factor alpha. In addition to studying general mechanisms of homeostasis, we have sought to characterize protein signaling mechanisms that drive chronic inflammation.

Research Departments:

Research Website:


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