• Principle Investigator of Leukaemia Scheme (LTM Trust from National Cancer Institute, UK), Department of Medicine, Vanderbilt University Medical Center, USA
• Research Fellow, Haematology/Oncology, Vanderbilt University Medical Center, USA
• Post-doctoral Fellow, Department of Biochemistry and Molecular Biology, Medical University of South Carolina, USA
• Scientist Fellow, National Institute for Plant Genome Research, New Delhi, India

PhD : Jawaharlal Nehru University (JNU), New Delhi

• Lady Tata Memorial Trust International Award, 2010-2012 from NCI, United Kingdom (UK)
• Award in recognition of excellence in Cancer Research and an outstanding presentation at VICC Retreat on “System Biology” at Vanderbilt University Medical Center USA, 2011
• Professional award for outstanding presentation demonstrating “Best Use of Research Shared Recourses”, Vanderbilt University Medical Center, USA 2010
• Award in oral scientific presentation, Science Research Day; Medical University of South Carolina, USA, 2008

The research in the Biswas laboratory focuses on the studies of the molecular mechanisms that are responsible for differentiation of hematopoietic stem cell (HSC) lineages during liver injury and hepatocyte regenerations. This laboratory brought here a broad aspect of fundamental research on cell cycle and apoptotic pathways that modulate the hematopoietic stem and progenitor cells (HSPCs) accompanied with a progressive alteration of vasculature in bone marrow during development of fibrosis/ cirrhosis related to HBV (Hepatitis B), HCV (Hepatitis C) and alcohol hepatitis. Some project highlights are as follows:

• Identification of specific HSC progenitors and their potential involvement in favouring the hepatic regeneration during chronic liver diseases or acute insult on chronic liver failure: This study will determine the mechanistic paradigm underlying the specific contribution of CD34+ populations to support the survival of acute on chronic liver patients (Gastroenterology 2012; 142: 505–512). Using in vitro culture and animal studies, we are currently establishing the model systems to induce HSC differentiation that accompanies with liver injury.

• The contribution of apoptosis and proliferation during hepatocellular carcinoma (HCC) development: During HCC the liver cancer stem cells (tumor-initiating cells, TICs) mostly derive from normal liver stem/progenitor cells depending on micro-environmental context. Now, it is believed that inflection of apoptotic pathways involving Bcl-2 family members may offer an effective way to protect against hepatic injury and HCC development by reducing the pressure for clonal expansion. Recently, we settled the long term argument on the ambivalent role of the pro-apoptotic BH3-only protein Bid in tumorigenesis (Biswas et al. Cell Death Differ 2013; 20: 869–877) and PUMA in carcinogen i.e. DEN (diethylnitrosamine)-driven liver cancer model of mice (Cell Death Differ 2013; 20: 847–849). Using these cues, we are currently accumulating evidences to investigate the role of BH3-only proteins as potential therapeutic targets in injury-associated liver.

• The mechanism underlying immune tolerance in chronic hepatitis viruses: During liver injury the understanding of immune responses is based on the findings in patients who have cleared the virus versus those who did not. High viral load affects DNA damage and cell cycle check points leading to an exhaustion of CD8 T cells, Natural killer (NK) and dendritic cells from the system. Addressing the hypothesis has the potential to unravel how the pro-apoptotic and anti-apoptotic Bcl-2 family members are involved in removal of injured or infected hepatocytes by specific immune cells as an adaptive and beneficial process during different stages of chronic hepatitis progression.

Publications in peer reviewed journals

• Subhrajit Biswas, Qiong Shi , Aubrey Wernick, Alexis Aiello, Sandra Zinkel (2013) The Loss of the BH3-only Bcl-2 family member Bid delays T cell Leukemogenesis in Atm- deficient mice. Cell Death and Differentiation, Jul; 20(7):869-77 (Editorial Choice)
• Subhrajit Biswas, Qiong Shi, Lauren Matisse, Susan Cleveland, Utpal Dave and Sandra Zinkel (2010) A Role for Pro-apoptotic Bax and Bak in T- Cell Differentiation and Transformation. Blood 116: 5237-5246. PMID: 20813900
• Subhrajit Biswas and Deepak Bastia (2008) Mechanistic Insights into Replication Termination as Revealed by Investigations of the Reb1-Ter3 Complex of Schizosaccharomyces pombe Mol. Cell. Biol. 28: 6844-6857. PMID: 18794373
• Subhrajit Biswas, Patrick Van Dijck and Asis Datta (2007) Environmental sensing and signal transduction pathways regulating morphopathogenic determinants of Candida albicans. Microbiol. Mol. Biol. Rev. 71:348-376. PMID: 17554048
• Subhrajit Biswas, Monideepa Roy, and Asis Datta (2003) N-Acetylglucosamine-inducible CaGAP1 encodes a general amino acid permease which co-ordinates external nitrogen source response and morphogenesis in Candida albicans. Microbiology 149:2597-2608. PMID: 12949183