Abhik Saha

Assistant Professor

My current research is focused on virus mediated human cancers. During my post-doctoral tenure, I have made extensive use of various biochemicals, molecular as well as cell biology techniques, which helped me to understand how EBV, a ubiquitous human tumor virus, causes B-cell lymphomas in human, particularly in immuno-compromised individuals. My findings contributed immensely towards the understanding of the molecular basis of an essential nuclear antigen encoded by EBV, EBNA3C manipulates host machinery in the disease pathogenesis. Overall, my studies pointing to the unique ability of this particular EBV antigen functions in regulating both apoptosis and cell proliferation, further raise the possibility of enhancing efficacy of therapeutic strategies against EBV associated human cancers. Prior to this, as a PhD student, I primarily used techniques related to the field of biochemistry, molecular and structural biology to develop peptide inhibitors against Hsp16.3 protein, a virulence factor of latent Mycobacterium tuberculosis (TB). My studies led us to identify two potent peptide sequences, which could be used as lead compounds in future drug development against latent tuberculosis. 

As a principal investigator, I propose to study on human cancers particularly those which caused by tumor viruses. The study of tumor viruses has provided the foundation of our current understanding in cancer biology. Human tumor viruses associate with a prolonged latency and contribute to approximately 20% of the human cancers worldwide. Hence, the opportunity exists to fight against tumor viruses associated human cancers at the global scale by the development of effective vaccines against oncogenic viruses through identifying their underlying mechanisms.

Given the multifaceted scenario of cancer propagation, where autophagy was shown to counteract genomic instability as well as facilitate tumor resistance to therapy, which in general relies on the lack of ability to undergo apoptosis. Despite the important progress made in elucidating the basic features of autophagy and its interconnection with apoptosis, the function of this process in human cancer is still a matter of substantial debate. The final outcome of autophagy depends on the cancer cell type, the extracellular stimuli and the ability to evade or not apoptosis in response to drug treatment. Given the ability of autophagy to regulate diverse processes in cells, it is not surprising that viruses have evolved to interact with this process to promote their own survival. My research will focus to further define the molecular mechanisms by which different viruses manipulate autophagy and interact with autophagy-apoptosis network to enhance viral pathogenesis. Successful completion of my work may lead to the development of novel antiviral therapies that antagonize associated cancer development.


Presidency University,
86/1 College Street, Kolkata - 700073,
West Bengal, India

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Email: abhik.biotechnology at presiuniv.ac.in
alternate E-mail: abhik.dbs at presiuniv.ac.in

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