Adjunct Associate Professor of Biochemistry and Molecular Medicine
Office Phone: 202-994-3539
Department: Biochemistry and Molecular Medicine
- B.Sc, University of Garhwal, India, 1981
- M.Sc, J.n. University, India, 1984
- MPhil, J.n. University, India, 1985
- PhD, J.n. University, India, 1990
Dr. Dimri received his PhD degree from the School of Environmental Sciences, Jawaharlal Nehru University, New Delhi India. He completed his postdoctoral studies from the Lawrence Berkeley National Laboratory, University of California Berkeley, where he discovered the senescence associated beta galactosidase (SABG) marker, a gold standard to identify senescent cells. He was a faculty member at the Department of Radiation Oncology, New England Medical Center, Tufts University Boston from 2000-2003. Prior to joining GWU in 2010, he was an assistant professor of medicine at the Northwestern University, Chicago, IL, a senior scientist at the Northshore University HealthSystem, Evanston, and an adjunct professor at the McCormic School of Engineering, Northwestern University, Evanston, IL. Dr. Dimri has authored more than 60 publications. He is also a founding and current Editor-in-Chief of the "Breast Cancer: Basic and Clinical Resaerch".
The major focus of my laboratory is to define the molecular mechanisms of cellular senescence, cell immortalization and oncogenesis in human cells. We are particularly interested in determining the role of a family of proteins that act as epigenetic gene silencers known as Polycomb Group (PcG) proteins in regulation of these processes. Cells must overcome senescence in order to further undergo genetic and phenotypic changes to become cancerous. We are focusing on candidate PcG genes such as BMI1 that can bypass senescence, induce immortal phenotype, and cooperate with other known oncogenes to transform human cells such as human mammary epithelial cells (HMECs). Currently, we are working on four related projects. In the first project, we aim to perform a global RNAi screen and an expression screen of a microRNA library to identify BMI1 cooperating oncogenic lesions. It is expected that BMI1 cooperating oncogenic lesions identified in RNAi library screening will include potential tumor suppressors, which when mutated/deleted in BMI1 overexpressing HMECs will result in transformation of such cells and progression of breast cancer in patients. In second project, we are studying signaling pathways that regulate BMI1 expression. In particular, our focus is transcriptional and posttranslational regulation of BMI1 in HMECs and breast cancer cells. We also plan to identify potential oncogenic mutations in BMI1 oncogene, which may make it more stable and potent, and study the oncogenic role of mutant BMI1 proteins in breast cancer and therapy resistance in breast cancer patients. In third project, we aim to define the role of c-Myc is a master regulator of PcG proteins including BMI1 and EZH2, and determine how c-Myc impacts chromatin conformation via regulation of PcG proteins. In project 4, we aim to study the role of PcG proteins in senescence, aging and the development of age-related pathologies.
Current Grants: None
Past Grants: 5RO1 CA094150 (The Role of BMI1 in Bresat Cancer) 2003-2014
BIOC6222 (Biochemical Genetics and Molecular Medicine)
Centers and Institutes
GWU Cancer Center
- GW Cancer Center
Sahasrabuddhe, A.A., Dimri, M., Bommi, P.V., and Dimri, G.P. (2011) ?TrCP regulates BMI1 protein turnover via ubiquitination and degradation. Cell Cycle 10(8):1322-1330.
Dimri, M., Bommi, P., Sahasrabuddhe, A.A., Khandekar, J.D., and Dimri, G.P. (2010) Dietary omega-3 polyunsaturated fatty acids suppress expression of EZH2 in breast cancer cells. Carcinogenesis, 31: 489-495.
Bommi, P., Dimri, M., Sahasrabuddhe, A.A., Khandekar, J.D., and Dimri, G.P. (2010) The polycomb group protein BMI1 is a transcriptional target of HDAC inhibitors. Cell Cycle, 9(13): 2663-2673.
Yadav, A.K., Sahasrabuddhe, A.A., Dimri, M., Bommi, P.V., Sainger, R., and Dimri, G.P. (2010) Deletion analysis of BMI1 oncoprotein identifies its negative regulatory domain. Mol. Cancer, 9: 158.
Hoenerhoff, M.J., Chu, I., Datta, S., Dimri, G.P., and Green, J.E. (2009) BMI1 Cooperates with H-RAS to Induce an Aggressive and Metastatic Phenotype with Spontaneous Brain Metastases. Oncogene. 28: 3022-3032.
Guo, W-J., Zeng, M-S., Yadav, A., Song, L-B., Guo, B-H., Band, V., and Dimri, G.P. (2007) Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression nad downregulating Akt activity in breast cancer cells. Cancer Res. 67(11): 5083-5089.
Datta, S., Hoenerhoff, M.J., Bommi, P., Sainger, R., Guo, W-J., Dimri, M., Band, H., Band, V., Green, J.E., and Dimri, G.P. (2007) Bmi-1 cooperates with H-Ras to transform human mammary epithelial cells via dysregulation of multiple growth regulatory pathways. Cancer Res. 67: 10286-10295. PMCID: PMC2424172.
Dimri, G.P. (2005) What has senescence got to do with cancer? Cancer Cell 7: 505-512.
Itahana, K., Ying, Z., Itahana, Y., Martinez, J.L., Beausejour, C., Jacobs, J.L., van Lohuizen, M., Band, V., Campisi, J., and Dimri, G.P. (2003) Control of replicative senescence in human fibroblast by p16 and the polycomb protein Bmi-1. Mol. Cell Biol. 23: 389-401.
Dimri, G.P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E.E., Rubelj, I., Pereira-Smith, O.M., Peacocke, M. and Campisi, J. (1995) A Novel biomarker identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl. Acad. Sci. USA 92: 9363-9367.
Industry Relationships and Collaborations
This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.