Ashok Kumar Giri (INSA-Senior Scientist)

Dr. Ashok Kumar Giri

INSA-Senior Scientist

M.Sc. (Zoology), 1976, 1st class, 1st rank.
Ph.D. (Zoology), 1981, University of Calcutta, Calcutta.
D.Sc. (Genetic Toxicology), 1995, University of Calcutta, Calcutta
Visiting Fellow at USA: US Environmental Protection Agency, Cincinnati USA from March 1984 to July 1984
Post Doctoral Fellow at USA: The University of Michigan, USA from 1987 to 1989
Visiting Scientist at USA; University of Texas Medical Branch at Galveston, USA from 1992 to 1994

  • Past President of the Asian Association for the Environmental Mutagen Societies (AAEMS) for the year 2014-2016.
    Elected as a Fellow of the National Academy of Sciences India, Science, Allahabad, with effect from 2015.
    Elected as a Fellow of the Indian National Science Academy, New Delhi, with effect from 2013.
    Elected as Member of the Editorial Board of Mutation Research from the Year 2009-2014.
    Elected Fellow of the West Bengal Academy of Sciences in 2005.
    Received prestigious D.Sc. Degree from Calcutta University in 1995.
    Young Scientist Award from Indian National Science Academy, New Delhi for the year 1984.
    Young Scientist Award from the Indian Science Congress Association for the year 1982.

  • Epigenetic studies to develop biomarkers and also mechanism of arsenic induced toxicity and carcinogenicity.
    Identification of different genes responsible for arsenic susceptibility and carcinogenicity.
    Molecular epidemiology and Environmental health.
    Gene expression studies of arsenic exposed individuals.
    Animutagenic and anticarcinogenic effects of black tea, Darjeeling tea and its polyphenols in multiple test systems.

  • Fellow/RA

    Debmita Chatterjee, SRF

    1. Chatterjee, D., Bandyopadhyay, A. K., Sarma, N., Basu, S., Roychaudhury, T., Roy, Sib Sankar, and Giri, A. K. (2017) Role of microRNAs in senescence and its contribution to peripheral neuropathy in the arsenic exposed population of West Bengal, India, Environmental Pollution, 233: 596-603.
    2. Babdyopadhyay, A. K., Paul, S., Adak, S. and Giri, A. K. (2016). Reduced LINE-1 methylation is associated with arsenic-induced genotoxic stress in children. 29 (4): 731-741.
    3. Chatterjee D, Bhattacharjee P, Sau TJ, Das JK, Sarma N, Bandyopadhyay AK, Roy SS, Giri AK. (2015). Arsenic exposure through drinking water leads to senescence and alteration of telomere length in humans: A case-control study in West Bengal, India. Mol Carcinogen. 54(9): 800-809.
    4. Banerjee N, Bandyopadhyay AK, Dutta S, Das JK, Roy Chowdhury T, Bandyopadhyay A,Giri AK. (2017). Increased microRNA 21 expression contributes to arsenic induced skin lesions, skin cancers and respiratory distress in chronically exposed individuals. Toxicology. 378: 10-16.
    5. Paul S and Giri A. K. (2015). Epimutagenesis: A prospective mechanism to remediate arsenic induced toxicity. Int. doi: 10.1016/j.envint.2015.04.002. Epub 2015 Apr 18. Review.
    6. Bhattacharjee P, Paul S, Banerjee M, Patra D, Banerjee P, Ghoshal N, Bandyopadhyay A, Giri AK. (2013) Functional compensation of glutathione S-transferase M1 (GSTM1) null by another GST superfamily member, GSTM2, Scientific Report. 3: 2704. doi: 10.1038/srep02704.
    7. Banerjee M, Banerjee N, Bhattacharjee P, Mondal D, Lythgoe PR, Martínez M, Pan J, Polya

    DA, Giri AK. (2013) High arsenic in rice is associated with elevated genotoxic effects in humans.Scientific Report, 3: 2195. doi: 10.1038/srep02195.

    1. Bhattacharjee, P, Banerjee, M and Giri, A. K. (2013) Role of genomic instability in arsenic-induced carcinogenicity. A review, Int. 53: 29-40.
    2. Banerjee N, Nandy S, Kearns J.K, Bandyopadhyay A.K, Das J.K, Majumder P, Basu S, Banerjee S, Sau T.J, States JC, Giri A.K. (2011) Polymorphisms in the TNF-α and IL10 gene promoters and risk of arsenic-induced skin lesions and other nondermatological health effects. Toxicol Sci. 121(1):132-139.
    3. Banerjee M, Banerjee N, Ghosh P, Das J. K, Basu S, Sarkar A. K, States J. C and Giri A. K. (2010), Evaluation of the serum catalase and myeloperoxidase activity in the chronic arsenic exposed individuals and concomitant cytogenetic damage. Toxicol Appl Pharmacol. 249: 47-54
    4. Banerjee N, Banerjee S, Sen R, Bandyopadhyay A, Sarma N, Majumder P, Das J.K, Chatterjee M, Kabir S.N and Giri AK (2009) Chronic arsenic exposure impairs macrophage functions in the exposed individuals. J Clin Immunol. 29(5): 582-94.
    5. Ghosh P, Banerjee M, Giri A. K. and Ray K. (2008) Toxicogenomics of Arsenic: Classical Ideas and Recent Advances, Reviews in Mutation Research, 659: 293-301.
    6. Ghosh P, Basu A, Singh K. K and Giri A. K. (2008) Evaluation of Cell Types for Assessment of Cytogenetic Damage In Arsenic Exposed Population, Molecular Cancer, 28: 45-49.
    7. De Chaudhuri S, Ghosh P, Sarma N, Majumdar P, Sau T.J, Basu S, Roychoudhury S, Ray K and Giri A.K. (2008) Genetic Variants Associated with Arsenic Susceptibility: Study of Purine Nucleoside Phosphorylase, Arsenic (+3) Methyl Transferase and Glutathione S-Transferase Omega Genes. Environmental Health Perspective, 116: 501-505.
    8. Banerjee M, Sarma N, Biswas R, Roy J, Mukherjee A and Giri A. K. (2008) Deficiency in DNA repair leads to arsenic susceptibility: Evidence from Comet assay and challenge assay. J cancer, 123: 283-287.
    9. Halder B, Bhattacharya U, Mukhopadhyay S and Giri A. K. (2008) Molecular mechanism of black tea polyphenols induced apoptosis in human skin cancer cells: involvement of Bax translocation and mitochondria mediated death cascade. Carcinogenesis, 29: 129-138.
    10. Banerjee M, Sarkar J, Das J. K, Mukherjee A, Sarkar A. K, Mondal L. K and Giri A. K. (2007) Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosomal aberrations. Carcinogenesis, 28: 672-676.
    11. Ghosh P, Basu A, Mahata J, Basu S, Sengupta M, Das J. K, Mukherjee A, Sarkar A. K,  Mondal  L. K,  Ray K and Giri A. K. (2006) Cytogenetic damage and genetic variants in the individuals susceptible to arsenic induced cancer through drinking water. Int. J.  Cancer, 118(10): 2470-2478.