Matthew Vander Heiden, MD, PhD

Director, Koch Institute for Integrative Cancer Research at MIT
Professor of Biology, MIT 
Lester Wolfe (1919) Professor of Molecular Biology
Instructor in Medicine, Dana-Farber Cancer Institute


Bio     Research Interests     Key Publications


Matthew Vander Heiden is the director of the Koch Institute at MIT, the Lester Wolfe (1919) Professor of Molecular Biology, and a member of the Broad Institute. He is also a practicing oncologist and Instructor in Medicine at the Dana-Farber Cancer Institute/Harvard Medical School. He earned his doctoral and medical degrees from the University of Chicago, where he worked in the laboratory of Craig Thompson. Vander Heiden then completed a residency in internal medicine at Brigham & Women’s Hospital and a Hematology-Oncology fellowship at Dana-Farber Cancer Institute/Massachusetts General Hospital. He was a postdoctoral fellow in the laboratory of Lewis Cantley at Harvard Medical School, where he was supported by a Mel Karmazin Fellowship from the Damon Runyon Cancer Research Foundation. In 2010, Vander Heiden joined the MIT faculty. He was promoted to a tenured position at MIT in 2017, and was appointed Director of the Koch Institute (an NCI-designated basic science cancer center) in 2021.
The Vander Heiden laboratory has been working to understand the relationship between metabolism and cancer, with work to understand how metabolic changes in cells contribute to cancer progression and response to therapy. A large fraction of his work has been dedicated to understanding the metabolism of pancreatic cancer, including how pancreatic cancer cells adapt their metabolism to support tumor growth in the pancreas and various metastatic sites, and how pancreatic cancer influences whole body metabolism to cause weight loss and tissue wasting.  
Over the course of his career, his work has been recognized by several awards including a Burroughs Wellcome Fund Career Award for Medical Sciences, the AACR Gertrude B. Elion Award, an HHMI Faculty Scholar Award, an NCI Outstanding Investigator Award, and election to the American Society for Clinical Investigation and the European Academy for Cancer Sciences. He serves on the external advisory boards for the Yale Cancer Center, the Ellen and Ronald Caplan Cancer Center at the Wistar Institute, and Salk Institute Cancer Center.

Research Interests

The long-term goal of the Vander Heiden Laboratory is to understand how mammalian cell metabolism is adapted to support cancer initiation and progression, with a major focus on pancreatic cancer.  Cancer cells have metabolic requirements that differ from most normal, non-proliferating cells. To proliferate, cancer cells must transform available nutrients into the varied array of macromolecules that are needed to build a new cell. Cancers also interact with host tissues, and the presence of cancer can alter whole-body physiology to cause changes that are affect survival and quality of life.  The Vander Heiden laboratory seeks to understand both how cancer cells use metabolism to support their growth in tumors, and how this impacts the other tissues to lead to phenotypes such as weight loss and tissue wasting. They use mouse and cell models of pancreatic cancer to dissect mechanisms underlying the metabolic changes observed in pancreatic cancer patients. 


Related to how metabolism support pancreatic cancer cell proliferation in tumors, work from the Vander Heiden laboratory and others has determined that environmental factors within tumors, including which nutrients are present, can constrain how those cells use metabolism to grow and divide. The Vander Heiden laboratory is working to define which nutrients are available in the pancreas, how those nutrients are affected by changes in diet and whole body metabolism and how the nutrients found in the liver and lung influence the ability of pancreatic cancer to metastasize. The Vander Heiden laboratory is also interested in how pancreatic cancer leads to weight loss and tissue wasting, particularly early in the disease. Their work has focused on how the cancer can affect the normal digestive function of the pancreas, and how this can lead to loss of both fat and muscle mass. They also are studying how diet and obesity affect pancreatic cancer initiation and progression, with a goal toward identifying interventions that might improve therapy for patients. Finally, in close collaboration with Brian Wolpin and other Hale Center Investigators, the Vander Heiden laboratory has found that tissue wasting can occur very early in pancreatic cancer disease progression, and a translational goal of the group is to explore how this might leveraged for earlier disease detection.

Key Publications

Babic A, Rosenthal MH, Sundaresan TK, Khalaf N, Lee V, Brais LK, Loftus M, Caplan L, Denning S, Gurung A, Harrod J, Schawkat K, Yuan C, Wang QL, Lee AA, Biller LH, Yurgelun MB, Ng K, Nowak JA, Aguirre AJ, Bhatia SN, Vander Heiden MG, Van Den Eeden SK, Caan BJ, Wolpin BM. Adipose tissue and skeletal muscle wasting precede clinical diagnosis of pancreatic cancer. Nat Commun. 2023 Jul 18;14(1):4317.
Interactions with stromal cells promote a more oxidized cancer cell redox state in pancreatic tumors. Datta R, Sivanand S, Lau AN, Florek LV, Barbeau AM, Wyckoff J, Skala MC, Vander Heiden MG. Sci Adv. 2022 Jan 21;8(3):eabg6383. doi: 10.1126/sciadv.abg6383. Epub 2022 Jan 21.
Low glycaemic diets alter lipid metabolism to influence tumour growth. Lien EC, Westermark AM, Zhang Y, Yuan C, Li Z, Lau AN, Sapp KM, Wolpin BM, Vander Heiden MG. Nature. 2021 Nov;599(7884):302-307. doi: 10.1038/s41586-021-04049-2. Epub 2021 Oct 20.
Dissecting cell-type-specific metabolism in pancreatic ductal adenocarcinoma. Lau AN, Li Z, Danai LV, Westermark AM, Darnell AM, Ferreira R, Gocheva V, Sivanand S, Lien EC, Sapp KM, Mayers JR, Biffi G, Chin CR, Davidson SM, Tuveson DA, Jacks T, Matheson NJ, Yilmaz O, Vander Heiden MG. Elife. 2020 Jul 10;9:e56782. doi: 10.7554/eLife.56782.
Altered exocrine function can drive adipose wasting in early pancreatic cancer. Danai LV, Babic A, Rosenthal MH, Dennstedt EA, Muir A, Lien EC, Mayers JR, Tai K, Lau AN, Jones-Sali P, Prado CM, Petersen GM, Takahashi N, Sugimoto M, Yeh JJ, Lopez N, Bardeesy N, Fernandez-Del Castillo C, Liss AS, Koong AC, Bui J, Yuan C, Welch MW, Brais LK, Kulke MH, Dennis C, Clish CB, Wolpin BM, Vander Heiden MG. Nature. 2018 Jun;558(7711):600-604. doi: 10.1038/s41586-018-0235-7. Epub 2018 Jun 20.
Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development. Mayers JR, Wu C, Clish CB, Kraft P, Torrence ME, Fiske BP, Yuan C, Bao Y, Townsend MK, Tworoger SS, Davidson SM, Papagiannakopoulos T, Yang A, Dayton TL, Ogino S, Stampfer MJ, Giovannucci EL, Qian ZR, Rubinson DA, Ma J, Sesso HD, Gaziano JM, Cochrane BB, Liu S, Wactawski-Wende J, Manson JE, Pollak MN, Kimmelman AC, Souza A, Pierce K, Wang TJ, Gerszten RE, Fuchs CS, Vander Heiden MG, Wolpin BM. Nat Med. 2014 Oct;20(10):1193-1198. doi: 10.1038/nm.3686. Epub 2014 Sep 28.
Direct evidence for cancer-cell-autonomous extracellular protein catabolism in pancreatic tumors. Davidson SM, Jonas O, Keibler MA, Hou HW, Luengo A, Mayers JR, Wyckoff J, Del Rosario AM, Whitman M, Chin CR, Condon KJ, Lammers A, Kellersberger KA, Stall BK, Stephanopoulos G, Bar-Sagi D, Han J, Rabinowitz JD, Cima MJ, Langer R, Vander Heiden MG. Nat Med. 2017 Feb;23(2):235-241. doi: 10.1038/nm.4256. Epub 2016 Dec 26.

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