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Christopher Shawn Williams, M.D., Ph.D.

  • Associate Professor of Medicine
  • Associate Dean, Physician-Scientist Education and Training
  • Director, Physician Scientist Training Program
  • Director, Medical Scientist Training Program
  • Staff Physician, VA Health System

Phone

615-322-3642

Email

christopher.s.williams@Vanderbilt.Edu
Vanderbilt University Medical Center, Gastroenterology Division
1030-C Medical Research Building IV
Nashville, TN 37232-0252

Christopher Shawn Williams, M.D., Ph.D.

  • Associate Professor of Medicine
  • Associate Dean, Physician-Scientist Education and Training
  • Director, Physician Scientist Training Program
  • Director, Medical Scientist Training Program
  • Staff Physician, VA Health System

615-322-3642

christopher.s.williams@Vanderbilt.Edu

Vanderbilt University Medical Center, Gastroenterology Division
1030-C Medical Research Building IV
Nashville, TN 37232-0252

Profile

Christopher Williams, M.D., Ph.D., is an Associate Professor of Medicine. His research interests focus on understanding how epithelial wound healing responses promote cancer development. His laboratory studies a recently discovered tight junction protein called BVES, and have determined that BVES is suppressed in colon cancer and that this promotes the spread of cancer. His research program is structured at determining how BVES promotes metastasis with the goal being to develop therapeutics to block metastasis.

Dr. Williams received a Bachelor’s Degree (1992) from Brigham Young University. He enrolled in the Medical Scientist Training Program (MSTP) at Vanderbilt University in 1994 and matriculated with a doctorate in Cell Biology and Medicine in 2002. He received the Albert Weinstein Prize in Medicine and elected the ABIM Research Pathway for a Medicine Residency, completing a residency in Medicine and Fellowship in Gastroenterology in 2007. Prior to that, he performed a post-doctoral fellowship in Dr. Scott Hiebert’s laboratory in the Department of Biochemistry at Vanderbilt University. He joined the faculty at Vanderbilt University School of Medicine July of 2007 as an Assistant Professor in Medicine and Cancer Biology and is a Staff Gastroenterologist at the VA Medical Center affiliated with Vanderbilt University Medical Center.

Education

  • M.D., Vanderbilt University, Nashville, Tennessee (2002)
  • Ph.D., Vanderbilt University, Nashville, Tennessee (2000)
  • B.Sc., Brigham Young University, Provo, Utah (1992)

Research Emphasis

1) Epigenetic control of intestinal epithelial wound healing and repair programs and relationship to colorectal oncogenesis.
2) Junctional signaling in mucosal wound healing responses and inflammatory carcinogenesis.
3) Oxidative injury defenses in Inflammatory Bowel Disease (IBD) and colitis associated carcinoma (CAC).

Research Description

Our research program focuses on understanding how the epithelium responds to injury and how normal injury response processes are subverted in the development of malignancy. The research activities span the basic to translational spectrum. We have three major research programs within the lab: 1) Epigenetic control of intestinal epithelial wound healing and repair programs and relationship to colorectal oncogenesis. We are studying the role of the Myeloid Translocation Gene (MTGs) family in intestinal biology with emphasis on gut development, stem cell function, wound healing and malignancy. MTGR1 (Myeloid Translocation Gene, Related-1), MTG8 and MTG16 are members of a gene family originally identified as targets of chromosomal translocation in acute myeloid leukemia (AML). MTG family members act as transcriptional repressors and interact with other corepressors mSin3, N-CoR/SMRT and histone deacetylases (HDAC1-3). Chromosomal translocations often target master regulatory genes that affect growth, differentiation and apoptosis. Using unique mouse models we are characterizing MTGs as modifiers of WNT dependent tumorigenesis in the gut and deterring how the regulate stem cell programs. 2) Junctional signaling in mucosal wound healing responses and inflammatory carcinogenesis. We recently determined that a tight junction associated protein called BVES was suppressed by promoter methylation in colon cancer and that it regulates epithelial to mesenchymal transition (EMT) influencing metastasis. We are currently cataloging the BVES protein interactome as a means to understand how BVES transduces "Out to In" signaling. In addition, using Bves-null mice, we are dissecting its role in intestinal wound healing using chemical, infectious, and mechanical colonic injury modeling and its role in colitis associated cancer. 3) Oxidative injury defenses in Inflammatory Bowel Disease (IBD) and colitis associated carcinoma (CAC). Little is known about the role of selenium and selenoproteins in inflammatory bowel disease (IBD), a condition of intermittent severe oxidative stress. We have shown that selenium deficiency results in increased mucosal injury and progression to colitis-associated dysplasia (CAD). Likewise, germ line Sepp1 and Gpx3 mutant mice had increased tumor burden with major effects on proliferation, apoptosis and DNA damage. We hypothesize that intestinal Sepp1 alters the inflammatory microenvironment via clearance of reactive oxygen species thus affecting epithelial stem cell and differentiation programs. We are determining which stem cell pathways are modified by selenoproteins in influencing tumorigenesis.

Publications

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