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To serve patients, health care providers, research scientists, scholars, and society by providing excellence and innovation in diagnostic services and educational resources in a respectful, professional and culturally diverse atmosphere.

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To become a preeminent leader in academic anatomic and clinical pathology while translating basic science discovery to improved clinical care.

Erika T. Brown, PhD

Erika T. Brown, Ph.D.

Assistant Professor, Department of Pathology & Laboratory Medicine
Office: Walton Research Bldg., Rm. 703
Lab: Walton Research Bldg., Rm. 702
Phone: (843) 792-8424


B.S., Biology/Biochemistry, 1993, Spelman College, Atlanta, GA
Ph.D., Medical Genetics, 1999, University of Alabama at Birmingham, Birmingham, AL
PostDoctoral Fellow, 1999-2002, Vanderbilt University Medical Center, Nashville, TN
Senior Research Associate, 2002-2004, University of Colorado Health Sciences Center, Denver, CO


My research interests are in the areas of cancer biology and DNA damage and repair. My work primarily focuses on the tumor suppressor BRCA2. Mutations in the BRCA2 gene are responsible for 30-40% of inherited, early-onset forms of breast cancer. Furthermore, C-terminal truncations of the BRCA2 protein prevent it from interacting with and regulating the DNA repair protein RAD51. Disruption of this interaction has been heavily implicated as one of the major causes of BRCA2-derived tumors. Therefore, the goals of this laboratory are to elucidate the more intricate details of the BRCA2-RAD51 interaction and further examine the effect of BRCA2 mutations on inefficient DNA repair and tumor formation.


Pending: DOD Breast Cancer Research Program
Active: R01 supplement (NIH/NIDDK)
Completed: K01 (NIH/NCI)


  1. Toole, William P. and Erika T. Brown, “Alterations in chemotherapeutic sensitivity of carcinoma cells that overexpress the DNA repair protein RAD51”, (in preparation).
  2. Hwang, HeeYoung, Patel, Vedang R. and Erika T. Brown, “Inhibition of RAD51 activity during S phase increases the chemotherapeutic sensitivity of carcinoma cells”, (in preparation).
  3. Hwang, HeeYoung, Patel, Vedang R. and Erika T. Brown, “An in vitro study of inhibition of RAD51 as a target for chemotherapeutic treatment of breast carcinomas”, (under review).
  4. Brown, Erika T. and Jeffrey T. Holt. “Rad51 overexpression rescues radiation resistance in BRCA2-defective cancer cells”. Mol Carcinog. 2009 Feb; 48(2):105-9.
  5. Holt, Jeffrey T., Toole, William P., Patel, Vedang R., Hwang, HeeYoung, and Erika T. Brown, “Restoration of CAPAN-1 cells with functional BRCA2 provides insight into the DNA repair activity of individuals who are heterozygous for BRCA2 mutations”, Cancer Genet Cytogenet. 2008 Oct 15; 186(2):85-94.
  6. Brown, Erika T., Robinson-Benion, Cheryl and Jeffrey T. Holt, “Radiation Enhances Caspase 3 Cleavage of Rad51 in BRCA2-Defective Cells”, Radiat Res. 2008 May; 169(5):595-601.
  7. Brown, Erika T. and Gerald M. Fuller, “Detection of a Protein Complex Associated with the G-455-A Polymorphism”, Blood, Vol. 92, No. 9, Nov. 1, 1998: pp. 3286-3293.
  8. Elhammer, Ake P., Poorman, Roger A., Brown, Erika, Maggiora, Linda L., Hoogerheide, John G., and Ferenc J. Kezdy, “The Specificity of UDP-GalNAc:Polypeptide N-Acetylgalactosaminyltransferase as Inferred from a Database of in Vivo Substrates and from the in Vitro Glycosylation of Proteins and Peptides”, The Journal of Biological Chemistry, Vol. 268, No. 14, May 15, 1993: pp. 10029-10038.

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