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Thomas R. Berton

Thomas Berton Name: Thomas R. Berton Ph.D.
University/Institution: University of Texas MD Anderson Cancer Center Department of Carcinogenesis
Hometown: El Paso, TX
Project Name: The Role of E2F1 in UV-induced DNA Damage Response
Research Interests: E2F1, DNA damage, DNA repair, Tumorigenesis
Mentor: David Mitchell, Ph.D. and David Johnson, Ph.D.

I received my bachelor's degree from the University of Houston in 1988 in Biophysical and Biochemical Sciences. After a three year stint as a professional triathlete I entered the graduate program in the Department of Human Ecology at the University of Texas at Austin where I earned my doctoral degree in 1998 in Nutritional Sciences. I investigated how dietary fat and vitamin E affected biomarker expression and tumorigenesis in mice.

My first post-doctoral position was in the Department of Cell Biology at Baylor College Medicine in Houston, Texas. I tested the feasibility of using conditional knockout animals in biomedical research, as well as gene therapy. In 1999, I did a second Postdoctoral Fellowship in the Department of Carcinogenesis at UT MD Anderson Cancer Center Science Park-Research Division. I investigated the roles of E2f1, Brca1, and p53 in DNA repair, apoptosis, and spontaneous and UV-induced tumor development as well as cell cycle regulation under genotoxic stress conditions. I was funded through an NCI-funded T32 Carcinogenesis Training Grant. In 2001, I was awarded, a Postdoctoral Minority Supplement through the CMBB.

In 2004 I was promoted to Instructor as a non-tenured track faculty member in the Department of Carcinogenesis, and in 2005 I was awarded a K01 Mentored Career Development Award to study the role of E2F1 in UV-induced DNA damage response. I have taught courses on Mechanisms of Carcinogenesis for our Summer Undergraduate Research Program as part of the Community Outreach and Education Program of the Center for Research on Environmental Disease.

My future research interest is to determine if silencing E2F1 has the capability to sensitize p53 mutant tumor cells to apoptosis, which may lead to a potential modality for chemotherapy.

Updated: 05/15/13