Douglas V. Faller

Professor

Education:

Ph.D., MIT
M.D., Harvard

General field of research:

Cancer Biology

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research
Cancer Center
Pediatrics
Pathology
Microbiology
Biochemistry

Contact information:

Office
K-701
Phone: (617)-638-4173

Lab
R-906
Phone: (617)-638-5610
Fax: (617)-638-4173

dfaller@bu.edu

Keywords:

cell cycle, control targeted therapies, translational research, epigenetics, drug development

Summary of research interest:

The major focus is the study of the basic molecular and cellular biology of transformed cells and tumors. We are determining the mechanisms by which retroviruses and their oncogenes cause tumors, defining the ways in which viruses and oncogenes control host cell gene expression.

One special interest of the laboratory involves viral regulation those cellular genes encoding cell cycle-regulating molecules, DNA repair and growth factors or and cytokines.  We analyze the molecular mechanisms by which oncogene-transformed cells become autonomous of growth factor requirements, elucidating growth-factor signal transduction pathways in normal and trans¬formed mesenchymal and lymphoid cells, and the ways in which signaling path¬ways are disrupted or circumvented in tumor cells.

We also study the role of oncogenic proteins in transcription, development, cell cycle control and arrest, and programmed cell death. Another area of focus is signaling by steroi  d hormones and antagonists in breast and prostate cancer cells. Our goal in all of this work is the translation of our basic research into clinically relevant applications, and consequently we develop small molecules as targeted therapeutics for malignant and inherited diseases.

Recent publications:

Xia, S., Forman, L.W., Chen, Z., and Faller, D.V.: PKCδ survival signaling in cells containing an activated p21Ras oncoprotein. 2009, Cell Signalling, 21(4):502-508. PMID: 19146951

Ghosh, Ruma Pal, Spanjaard, R.A., Faller, D.V. and Ghosh, S.K.: Identification of LTR-specific small non-coding RNA in FeLV infected cells. 2009, FEBS Letters, in press.

Perrine, S.P., Mankidy, R., Boosalis, M.S., Bieker, J.J., Faller, D.V.:  EKLF is recruited to the γ-globin promoter as a coactivator and is required for γ-globin gene induction by short-chain fatty acids.  2009, Eur. J. Haematology, in press.  PMID: 19220418

Zhang, B., Chambers, K.J., Maze-Rothstein, G.F., Archidiacono, A., Faller, D.V. and Wang, S.: Tumor suppressor HIC1 directly regulates E2F-driven transcription. 2009, Oncogene, 28:651-61. PMID: 19015639

Rankin, A., Spanjaard, R.A., and Faller, D.V.: Telomerase inhibitors versus T-Oligo; Contrasting mechanisms of cytotoxicity in cancer. Anti-Cancer Drugs, 2008, 19:329-338. PMID: 18454043

Florence, B. L. and Faller, D.V.: Drosophila Female Sterile Homeotic is a multi-functional transcriptional regulator that is modulated by Ras signaling. 2008, Developmental Dynamics, 237(3):554-64. PMID: 18264999

Dai, Y., Ngo, D.,  Jacob, J., Forman, L.W., and Faller, D.V.:  Prohibitin and the SWI/SNF ATPase subunit Brg1 are required for effective androgen-antagonist-mediated transcriptional repression of androgen receptor-regulated genes. 2008, Carcinogenesis, 29:1725-1733. PMID: 18487222

Zhang, B., Chambers, K.J., Maze-Rothstein, G.F., Archidiacono, A., Faller, D.V. and Wang, S.: Reprogramming of the SWI/SNF complex for co-activation or co-repression. 2007, Oncogene, 26:7153-7157. PMID: 17486062

Technologies available for sharing upon request:

Lentiviral vector production
Chromatin Immunoprecipitation Assays