Marilyn E. Thompson, Ph.D.
Associate Professor
Department of Cancer Biology,
Department of Biomedical Sciences

(615) 327-6787
WBS, Room 2135
1005 Dr. D.B. Todd Boulevard
Nashville, TN  37208

methompson@mmc.edu

Lab URL

CV or Bio (PDF)

University of South Alabama, Mobile, AL         B.S.     Respiratory Therapy
University of South Alabama, Mobile, AL         Ph.D.   Pharmacology
Vanderbilt University, Nashville, TN     Postdoctoral Training    Cell Biology

The Thompson laboratory is interested in molecular events within cells that are causal for initiation or progression of cancer. In particular, they examine the relationship between the expression of the BRCA1 gene product and its cellular localization on the proliferative status of cells. It is known that sustained activation of cancer-provoking signaling pathways leads to a decrease in BRCA1 expression and alters its relative distribution in the cytosol and the nucleus.  Other environmental “cues” that accompany proliferation and metastasis, such as hypoxia, also alter the localization and expression of BRCA1.  These laboratory studies are complemented by clinical investigations of the tumors of patients who over-express the oncogenes, like BRCA1 or  HER2, on the effectiveness of treatment with the anticancer agent,  Herceptin, allowing the development of hypotheses concerning disease both pathogenesis and the therapeutic efficacy of Herceptin in modifying the expression of candidate disease genes.

Thompson, M.E., C. Robinson-Benion and J.T. Holt.  An amino-terminal motif functions as a second nuclear export sequence in BRCA1.  J. Biol. Chem. 280: 21854-21857, 2005

Abbott DW, ME Thompson, C Robinson-Benion, G Tomlinson, RA Jensen, JT Holt. BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement of transcription-coupled DNA repair. Journal of Biological Chemistry , 274, 18808-18812, 1999

Thompson, ME, RA Jensen, PS Obermiller, DL Page, JT Holt. Decreased expression of BRCA1 accelerates growth and is often present during sporadic breast cancer progression. Nature Genetics, 9, 444-450, 1995