Associate Professor of Pathology
Director of Center for Tumor Virus Research
Education:
1987, Ph.D. Louisiana State University
Postdoctoral Training:
1987-1990 Postdoctoral Fellow, Department of Pathology, Dana-Farber Cancer Institute
Academic Appointments:
1991-1995 Instructor in Pathology, Harvard Medical School
1995-2000 Assistant Professor of Medicine, Harvard Medical School
2000-Present Associate Professor of Pathology, Tulane Cancer Center, Tulane University
Current Funding:
1998-2002 NIH R01 Research Grant
2001-2002 US ARMY Breast Cancer Concept Award
U. S. Patents:
US 5759803 –Retinoblastoma-Associated Protein 1 (E2F-1) Polypeptides and cDNA.
Teaching Specialties:
Molecular virology of DNA tumor viruses
Research Interests:
Gene regulation, cell cycle control, role of Epstein Barr virus in cancer, tumor virology, tumor immunology, herpesvirus reactivation, pRb, E2F, Sp1, CBP, p300, E1A, Tag, Zta, Rta, p21, p27, c-myc, p53.
Tel: 504-988-1167
Fax: 504-988-5516
Web Site: www.flemingtonlab.com
- Rodriguez A, and Flemington EK. Transfection mediated cell cycle signaling. Anal Bio 1999; 272:171-181.
- Rodriguez A, Armstrong M, Dwyer, D and Flemington EK. Genetic dissection of cell growth arrest mediated by the Epstein-Barr virus lytic gene product, Zta. J Virol 1999; 73:9029-9038.
- Campanero MR, Armstrong M, and Flemington EK. Distinct cellular factors regulate the c-myb promoter through its E2F element. Mol Cell Biol 1999; 19:8442-8450.
- Campanero MR, Armstrong M, and Flemington EK. CpG methylation as a novel mechanism for the regulation of E2F activity. Proc Natl Acad Sci USA 2000; 97:6481-6486.
- Rodriguez A,Jung EJ, Flemington EK. Cell cycle analysis of Epstein Barr virus infected cells following treatment with lytic cycle inducing agents. J Virol 2001; 75:4482-4489.
- Flemington EK. Herpesviral lytic replication and the cell cycle: Arresting new developments. J Virol 2001; 75:4475-4481.
- Rodriguez A, Jung EJ, Yin Q, Cayrol, C, Flemington EK. Role of c-myc regulation in Zta mediated induction of the cyclin dependent kinase inhibitors, p21 and p27, and cell growth arrest. Virology; 2001; 284:159-169.
- Jung EJ, Flemington EK. Transfection Mediated Cell Synchronization: Acceleration of G1-S Phase Transition by Gamma Irradiation. Biotechniques; 2001; 31:2-6.
Dr. Flemington’s lab has been engaged in studies addressing transcriptional regulation and cell cycle control mechanisms. The cell cycle work has involved a number of studies including cloning the first member of the cell cycle transcription factor, E2F1, and a number of studies directed towards addressing the mechanisms through which E2F modulates gene expression, cell cycle checkpoint function, and apoptosis. Current E2F work involves addressing the role of the E2F co-activator, TRRAP, in E2F function.
Dr. Flemington’s lab is also actively involved in addressing the role of EBV in the development of several human cancers including Burkitt’s lymophoma, nasopharyngeal carcinoma, gastric carcinoma, post-transplant lymphoproliferative disease (PTLD), Hodgkin’s lymphoma, non-hodgkin’s lymphoma in AIDS patients. His lab previously discovered that although EBV encodes a number of genes that promote cell cycle progression, a distinct set of genes encoded by EBV, unexpectedly cause activation of a G1 checkpoint function through induction of p53, p21, p27 and suppression of c-myc expression. In EBV associated tumors, these genes are suppressed and this suppression is necessary for tumor survival. Dr. Flemington’s lab is currently addressing the transcriptional mechanisms involved in reactivation of these genes with the idea of understanding how directed activation of gene expression might be utilized in anti-tumor approaches. Additional studies along these lines involve utilizing the genetic diversity associated with phage display technology to identify novel peptides that engage surface receptors which signal activation of these genes.
Department of Pathology & Laboratory Medicine
Rev DDO 7/04