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2. Research experience
Before moving to the field of clinical research, my work involved arsenic toxicogenomics and molecular genetics, addressing the issue of arsenic calamity in the Indian subcontinent. My research included genetic mechanisms and factors influencing inter-individual genetic susceptibility toward arsenic toxicity. During my seven years studying arsenic toxicology, I worked on various aspects of genetic and epigenetic regulations of arsenicosis and development of arsenic induced cancers. As a Research Associate after my Ph.D, I studied DNA methylation, epigenetic dysregulation, and miRNA profiling to identify arsenic-induced toxicity and carcinogenicity. My work included studying global and gene specific DNA methylation, epigenetic dysregulation caused by arsenic exposure, and miRNA profiles to see effect of arsenic on the regulation of gene expression networks. Later on I joined the University of Colorado nschutz Medical Campus as a Postdoctoral Fellow where I focused on genetic and epigenetic regulation of the mouse reproductive axis. During my second postdoctoral work at the University of Maryland, I worked on contact ediated cell signaling with special emphasis on live cell transcription imaging and analysis.
3. Research interest
A broad laboratory background has given me a unique perspective on integration of basic discovery research with rapid translation of novel therapies into the clinic. Management of the Clinical Research Unit at TTCRC gives me the opportunity to implement my understanding of biological research to integrate advancements in molecular biology with clinical trials. CRU is involved in the design, development, management, analysis and reporting of academic clinical studies in cancer, providing end-to-end facility for academic clinical trials. CRU also has a central role in various other biological studies and research approaches aimed at improving outcomes in ALL. The overarching goal of my work s to translate new mechanism-driven insights of cancer biology into bringing novel therapies to the clinic.
- Das N, Kumar T.R. (2019). Molecular regulation of follicle stimulating hormone. Journal of Molecular Endocrinology. 60(3):R131-R155. Das N, Kumar T.R. (2018). Molecular regulation of follicle stimulating hormone. Journal of olecular Endocrinology. 60(3):R131-R155.
- Das N, Chatterjee D, Paul S, Bhattacharjee P. (2017). Epigenetic signatures associated with increased risk of arsenic-induced pre-cancerous and cancerous skin lesion development in the arsenic exposed population of West Bengal, India. Environmental Pollution (submitted).
- Das N, Giri A, Chakraborty S, Bhattacharjee P. (2016). Association of Single Nucleotide Polymorphism with arsenic-induced skin lesions and genetic instability in exposed population of West Bengal, India. Mutation Research. 809:50 56.
- Das N, Sen D, Chakraborty B, Chaudhuri K, Bhattacharya S, Chowdhury R, Giri A.K. (2015). Bacterial arsenic resistance genes in a reducing environment significantly influences ground water arsenic concentration in the Ganga- rahmaputra-Barak basin. Environmental Science and Pollution Research (under review).
- Das N, Paul S, Chatterjee D, Banerjee N, Majumder N.S, Sharma N, Sau T.J, Basu S, Banerjee S, Majumder P, Bandyopadhyay A.K, States J.C, Giri A.K. (2012). Arsenic exposure through drinking water increases the risk of liver nd cardiovascular diseases in the population of West Bengal, India. BMC Public Health. 12:639.
- Bhattacharjee P, Das N, Chatterjee D, Banerjee A, Das J.K, Basu S, Banerjee S, Majumder P, Prashant Goswami, Giri A.K. (2013). Association of NALP2 polymorphism with arsenic induced skin lesions and other health effects. utation Research. 755(1):1-5.
- Paul S, Das N, Bhattacharjee P, Banerjee M, Das JK, Sarma N, Sarkar A, Bandyopadhyay AK, Sau TJ, Basu S, Banerjee S, Majumder P, Giri A.K. (2013). Arsenic-induced toxicity and carcinogenicity: a two-wave cross-sectional study in arsenicosis individuals in West Bengal, India. J Expo Sci Environ Epidemiol. 23(2):156-62