Douglas V. Faller, M.D., Ph.D.
Professor OF Medicine, Pediatrics, Biochemistry, Microbiology, Pathology and Laboratory Medicine; Director of the Cancer Center; Vice-Chairman, Division of Medicine
M.D. Harvard Medical School
A major focus of our laboratory is the study of the basic molecular and cellular biology of virus- and oncogene-transformed cells and tumors. We are involved in determining the mechanisms by which retroviruses and their oncogenes cause tumors, through defining the ways in which oncogenes control host cell gene expression. A special interest of this laboratory involves viral regulation those cellular genes encoding proto-oncogenic molecules and cytokines. We are analyzing the molecular mechanisms by which oncogene-transformed cells become autonomous of growth factor requirements. This work involves the elucidation of growth-factor signal transduction pathways in normal and trans-formed mesenchymal and lymphoid cells, and study of the ways in which this signaling path-way is disrupted or circumvented in tumor cells. This work has resulted in new information regarding the transduction of growth factor signals by second messenger systems in both normal and transformed cells. My laboratory also studies the role of oncogenes in programmed cell death. A related area of his research is the interaction of retroviruses and the tumors they induce with cellular immune defense mechanisms. The means by which virus- or tumor-specific cytotoxic T lymphocytes, natural killer cells and monocytes recognize and destroy infected cells and tumors is under investigation, as are the molecular mechanisms by which tumors escape from immune surveillance. The mechanisms of aber-rant control of Class I Major Histocompatibility Antigen gene expression in oncogene-transformed cells, retrovirus-infected cells and naturally-occurring tumors are being deter-mined. A new transactivation property of murine leukemia viruses has been elucidated, which controls the expression of genes in the host cell important to the leukemogenic process. My laboratory also has a translational research program which develops molecular cancer therapeutics derived from his basic research, and tests them in clinical trials.
- Wang, S., Zhang, B., and Faller, D.V. 2002. Prohibitin requires BRG-1 and BRM for the repression of E2F and cell growth. EMBO J. 12:1-10.
- van de Mark, K., Chen, J.S., Steliou, K., Perrine, S.P., and Faller, D.V.: alpha-Lipoic acid induces p27Kip1-dependent cell cycle arrest in non-transformed cell lines and apoptosis in tumor cell lines. J. Cell Physiol. 2003, 194:325-340.
- Liou, J.S., Chen, J.S. and Faller, D.V. 2004. Characterization of p21Ras-mediated apoptosis induced by protein kinase C inhibition and application to human tumor cell lines. J. Cell Physiol. 198:277-294.
- Wang, S., Zhang, B., and Faller, D.V. 2004. Brg-1/Brm and prohibitin are required for the suppression of breast cancer cell growth by estrogen antagonists. EMBO J. 23:2293-303.
- Chen, J.S. and Faller, D.V. 2005. Histone deacetylase inhibition-mediated post-translational elevation of p27Kip1 protein levels is required for G1 arrest in fibroblasts. 2005, J. Biol. Chem. 202:87-99.
- Mork, C.A., Spanjaard, R.A., and Faller, D.V. 2005. A mechanistic approach to anticancer therapy: targeting the cell cycle with histone deacetylase inhibitors. Current Reviews in Pharmacology (in press).
- Perrine, S.P., Hermine, O., Small, T., O’Reilly, R., Fingeroth, J., Mentzer, S.J., and Faller, D.V. 2005. A Phase I/II Study of Arginine Butyrate and Ganciclovir in Patients with Epstein-Barr Virus-Associated Lymphoid Malignancies. (in press).To see additional publications by investigator click on any article and enter last name and initials in Query box.