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Michael Vansaun, PhD

Michael Vansaun portrait
Assistant Professor, Cancer Biology
mvansaun@kumc.edu

Professional Background

The overall goal of my research is to identify novel therapeutics to prevent and/or reduce the mortality from pancreatic cancer. I have a broad background in cellular biology, with specific training and expertise in cancer biology. I have studied cancer for 15 years, of which I have spent the past 10 years specifically focused on liver and pancreatic cancer. My experience and qualifications in this field of study are exemplified by some of my recent peer reviewed publications, awarded grants, and through participation in meetings and associations with the Pancreatic Cancer Action Network, the American association for cancer research, the American Pancreatic Association and the American Gastroenterological Association. The focus of our studies is to determine how obesity impacts the development and progression of cancer. We are interested in factors released from adipose tissue that ultimately regulate mitogenic activity within cancer cells. Our studies rely heavily on the use of genetically engineered mouse models of pancreatic cancer focusing of the KPC (KrasG12D; LSL-p53R172H; Ptf1aCre) mice as well as advancement of in vitro co-culture model systems. The KPC mice closely recapitulate the human disease and provide a unique opportunity to test therapeutics in vivo as well as to test gain and loss of genetic modifiers in pancreatic cancer.

Education and Training
  • PhD, Neurobiology, University of Kansas Medical Center, Kansas City, KS
  • BS, Biology, University of Denver, Denver, CO
  • Post Doctoral Fellowship, Cancer Biology, Vanderbilt University, Nashville, TN
Professional Affiliations
  • IGPBS Admissions Committee, IGPBS Admissions Committee, Member, 2020 - Present
  • Institutional Biosafety Committee, Member, 2020 - Present
  • American Pancreatic Association, Member, 2010 - Present
  • American Association for Cancer Research, Member, 2004 - Present

Research

Overview

Dr. VanSaun's lab focuses on understanding the influence of adipose secreted cytokines (adipokines) on pancreatic cancer progression. The epidemic of obesity is a significant risk factor, associated with 40% of all cancers, including pancreatic cancer, which ranks as the third deadliest cancer with an approximate five-year survival rate of 9%. Obesity associated inflammation incites a yin/yang dysregulation of adipokines, whereby pro-tumorigenic adipokine (leptin, IL-6 and IL-1β) levels increase and anti-tumorigenic adipokine (adiponectin) levels decrease. This dysregulation results in enhanced activation of mitogenic pathways, such as KRAS, that drive cancer progression and promote the recruitment of innate inflammatory cells. We have spent the past eight years studying adipocyte-tumor crosstalk and understanding how secreted factors from the adipose tissue (adipokines) ultimately affect the tumor microenvironment. We have developed mouse and human in vitro PDAC-adipocyte co-culture models as well as in vivo genetically engineered mouse models of pancreatic cancer combined with high fat diet induced obesity to understand the impact of obesity on pancreatic cancer progression. We currently have multiple projects ongoing in the laboratory to understand: 1) role of adipose-tumor crosstalk in pancreatic cancer progression, 2) role of tyrosine phosphatases in regulation of MAPK signaling, 3) regulation of immune function in the tumor microenvironment, 4) metabolic alterations in response to phosphatase activity, 5) the potential use of adiponectin agonists as anti-cancer therapeutics.

Current Research and Grants
  • Counteracting molecular mechanisms of obesity dependent PDAC progression, NIH/NCI, PI
Publications
  • Vansaun, M., N. 2013. Molecular pathways: adiponectin and leptin signaling in cancer.. Clinical cancer research : an official journal of the American Association for Cancer Research, 19 (8), 1926-32
  • Messaggio, F, Mendonsa, A., M, Castellanos, J, Nagathihalli, N., S, Gorden, L, Merchant, N., B, VanSaun, M., N. 2017. Adiponectin receptor agonists inhibit leptin induced pSTAT3 and in vivo pancreatic tumor growth.. Oncotarget, 8 (49), 85378-85391
  • VanSaun, M., N, Lee, I., K, Washington, M., K, Matrisian, L, Gorden, D., L. 2009. High fat diet induced hepatic steatosis establishes a permissive microenvironment for colorectal metastases and promotes primary dysplasia in a murine model.. The American journal of pathology, 175 (1), 355-64
  • Mendonsa, A., M, Chalfant, M., C, Gorden, L., D, VanSaun, M., N. 2015. Modulation of the leptin receptor mediates tumor growth and migration of pancreatic cancer cells.. PloS one, 10 (4), e0126686
  • Manley, Sharon., J, Olou, Appolinaire, Messggio, Fanuel, Jack, Ambrose, Joseph, VanSaun, Michael., N. 2022. Synthetic adiponectin receptor agonist, AdipoRon, induces glycolytic dependence in pancreatic cancer cells. Cell Death and Disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817044/