- Areas of Research
- Grant Resources
- Research Centers
- Center for Comparative Effectiveness Analytics
- Center for Health Promotion and Prevention Research (CHPPR)
- Center of Biomedical Research Excellence (COBRE)
- North Dakota IDeA Network of Biomedical Research Excellence (INBRE)
- Rural Health Reform Policy Research Center
- Seven Generations Center of Excellence in Native Behavioral Health
- Clinical Centers
- Service Centers
- Center for Rural Health
- Fetal Alcohol Syndrome Center
- Health Workforce Information Center (HWIC)
- Mobile Simulation (SIM-ND)
- National Resource Center on Native American Aging
- North Dakota Area Health Education Center (AHEC)
- North Dakota Tobacco Quitline
- Rural Assistance Center (RAC)
- Simulation Center (ND STAR)
- About Us
- New Building
Archana Dhasarathy, Ph.D.
- Ph.D., (2004) Genetics Graduate Program, Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX. Advisor Dr. Michael Kladde.
- M.Sc., (1996) Biomedical Genetics, University of Madras, India
- B.Sc., (1994) Zoology, The Ethiraj College, University of Madras, India
Professional and Research Experience
- Research Fellow, Laboratory of Molecular Carcinogenesis (LMC), 2010-2011 NIEHS/NIH, RTP, North Carolina
- Visiting Fellow, Laboratory of Molecular Carcinogenesis (LMC), 2005-2009 NIEHS/NIH, RTP, North Carolina
Epigenetic modifications of our genome affect transcription regulation and are involved in a broad range of human diseases, including cancer metastasis. Metastasis is a critical event in cancer progression that involves the spread of tumor cells from a primary cancer to secondary sites in the body, thus rendering the effective management of cancer extremely difficult. The misregulation of several normal biological pathways contributes to metastasis.
In particular a process known as 'Epithelial to Mesenchymal Transition' (EMT), which causes cells to change their shape and migrate during development, is hypothesized to play an important role in metastasis. My research aims to understand the epigenetic and molecular basis of EMT. Specifically, I am interested in two highly related transcription factors, Snail and Slug, which regulate the expression of genes that are essential for EMT. Using breast cancer cells as a model system, I propose to investigate the mechanisms utilized by Snail and Slug to bring about gene repression leading to EMT. As our understanding of epigenetic mechanisms of EMT increases, the challenge will be to develop new drugs to specifically target and reverse each epigenetic lesion.
Dhasarathy A, Phadke D, Mav D, Shah RR, Wade PA. (2011) The transcription factors Snail and Slug activate the transforming growth factor-beta signaling pathway in breast cancer. PLoS One. 2011;6(10):e26514. Epub 2011 Oct 20
Dhasarathy A and Wade PA (2008). The MBD protein family‐ reading an epigenetic mark? Mutat Res. 647(1‐2):39‐43.
Dhasarathy A, Kajita M and Wade PA. (2007) The Transcription Factor Snail Mediates Epithelial to Mesenchymal Transitions by Repression of Estrogen Receptor Alpha. Mol Endocrinol. 21(12):2907‐18. *(This article was selected for the cover page of Molecular Endocrinology).
Dhasarathy A and Kladde MP (2005) Promoter occupancy is a major determinant of chromatin remodeling enzyme requirements. Mol Cell Biol. 25(7): 2698‐707
Jessen WJ, Dhasarathy A, Hoose SA, Carvin CD, Risinger AL and Kladde MP. (2004) Mapping chromatin structure in vivo using DNA methyltransferases. Methods, 33(1):68‐80.
Carvin CD, Dhasarathy A, Friesenhahn LB, Jessen WJ and Kladde MP. (2003) Targeted cytosine methylation for in vivo detection of protein‐DNA interactions. Proc. Natl. Acad. Sci. USA 100:7743‐7748.