Associate Professor, Department of BiochemistryTumor Cell Biology ProgramPhD, Biological Sciences, 1998, University of Texas at AustinPostdoc, 1998-2001, UT MD Anderson, Houston, TXPostdoc, 2001-04, Institut Andre Lwoff, France
Contact Information2500 N State St., Room G220Jackson, MS 39216Phone: (601) 984-1521E-mail: firstname.lastname@example.org
Resistance to DNA-damaging chemotherapeutic agents represents a major hurdle for the successful treatment of cancer. My lab is focused on understanding the role of two transcription factors, mutant p53 and E2F3, in the cellular response to DNA damage. p53 is the most frequently mutated tumor suppressor gene in human cancer. The vast majority of p53 mutations are a single base pair change that generally produces a mutant protein incapable of transactivating wildtype p53 target genes. However, substantial evidence indicates that mutant p53 has gain-of-function activity that is dependent on its de novo ability to regulate gene expression. We have previously demonstrated that suppression of mutant p53 expression can lead to cell death. We are presently investigating mutant p53's transcriptional regulatory activity and assessing the significance of this function in the promotion of chemotherapy resistance. The second major project revolves around the pro-apoptotic role of the E2F transcription factor family in the response to DNA damage. We have demonstrated that E2F3a can be induced by genotoxic stress and that in its absence, DNA damage induced apoptosis is severely compromised. We are presently investigating how E2F3 contributes to the response to DNA damage by identifying its transcriptional targets, and we are also assessing if changes in E2F3 activity contribute to chemotherapy resistance in cancer cells.
2500 North State Street
Jackson, MS 39216
General Information: 601-984-1000
Patient Appointments: 888-815-2005