Abhik Saha

Assistant Professor

Research:

• Assistant Professor: 2012-current; Institute of Health Sciences, Presidency University, Kolkata, India
• Postdoctoral Fellow: 2007-2012; Dept. of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA. 
• PhD Fellow: 2001-2007; Dept. of Microbiology, Bose Institute, Kolkata, INDIA; Awarded from Jadavpur University, Kolkata, India

Academic:

• MSc: 1998-2000; Biochemistry with special paper Microbiology, University of Calcutta, Kolkata, India
• BSc: 1995-1998; Chemistry (Major) with Physics and Mathematics, University of Calcutta, Kolkata, India

Awards:

• DBT/Wellcome Trust India Alliance Intermediate Fellowship: 2015.
• Ramanujan Fellowship (DST, Govt. of India): 2013. 
• Senior Research Associateship (CSIR, Govt. of India): 2012. 
• Travel Award (Wellcome Trust, UK): 2020 (for Wellcome Researcher Meeting: Cell Biology, Immune Cells and Pathogens, on May 6-7, 2020 at London, UK. The meeting has been cancelled due to COVID-19 outbreak).
• Travel Award (Royal Society, London, UK): 2017 (for “Early Career Scientists” to attend the ‘Commonwealth Science Conference 2017’ at Singapore on June 13-16, 2017).
• Travel Award (DBT/Wellcome Trust India Alliance): 2016 (for 1st DELTAS Annual Meeting, Nairobi, Kenya, Africa to be held on July 5-6, 2016).
• Travel Award (DBT/Wellcome Trust India Alliance): 2016 (for “Epidemiological Transition” at Nairobi, Kenya, Africa, jointly organized by The African Academy of Sciences and the Royal Society of Tropical Medicine and Hygiene to be held on July 7-8, 2016).

I never thought that I will end up in biological research as I always wanted to be an artist. What I find now, I became an artist while I prepare my research figures in Corel Draw. I have graduated in Chemistry from University of Calcutta in 1998 and at that time only Chemistry students had option to opt Biochemistry afterward as their MSc degree. I was discussing with one of my cousin brothers about potential future opportunities after completion of my graduation and he was constantly telling or rather forcing me to join Biochemistry department at University of Calcutta by saying “if you want to do something in your life, just go there”. “Do you know, scientists can manipulate your DNA….express foreign proteins in bacteria (giving insulin as example)…etc”. I know, it sounds extremely childish now as well as unethical too…however, these were perhaps the words that brought me to join the Biochemistry department and changed my life’s perspective since then. I will never forget the day when I saw for the first time an ethidium bromide stained plasmid DNA and copied it on a piece of transparent sheet for our record. Despite the initial difficulties in following the classes, understanding the intricate biological phenomena, I had determined my mind within few months that I will pursue a research based career. Nevertheless, it would be completely unjustified if I do not mention some of the great teacher’s names – Prof. Maitrayee DasGupta and Prof. Dhrubajyoti Chattopadhyay (Currently Vice-Chancellor at Sister Nivedita University) whose classes and interactions were the source of my inspiration for which I am what I am today.    

It was my incessant passion on learning Molecular Biology techniques started from reading the Watson’s book “The Double Helix”, I decided to join Prof. Sujoy DasGupta’s lab at Bose Institute, Kolkata. The objective of my project was to develop peptide inhibitors against Hsp16.3 protein, a virulence factor of latent Mycobacterium tuberculosis and a member of human a-crystallin family. During my PhD tenure, I had also opportunity to work with two eminent biophysicists – Prof. Siddhartha Roy and Prof. Bhabatarak Bhattacharyya. My doctoral degree has provided me a flavour of interdisciplinary research and made me learn the magnitude of it in order to understand the right way to approach any basic biology questions.   

To venture into more interdisciplinary research arena, I have decided to further work on tumor virology and joined Prof. Erle S Robertson’s Lab at University of Pennsylvania School of Medicine, USA in 2007. It has been a tremendous experience to work with Erle. As a postdoctoral researcher my broad objective was to explore the role of EBNA3C, one of the essential latent antigens of EBV (Epstein–Barr virus) in the development of viral associated B-cell lymphomas, predominantly in immune-compromised individuals. Overall, my studies demonstrate the unique ability of this particular EBV antigen functions in regulating both apoptosis and cell proliferation, raises the possibility of exploring other interconnected pathways in order to enhance the current therapeutic means against multiple EBV-linked human cancers.

With these experiences, in 2012, I decided to come back to India and joined at the Dept. of Biotechnology, Presidency University (erstwhile Presidency College), Kolkata (College Street Campus). Like me, several enthusiastic and talented researchers all over the world joined Presidency around similar time when it was transitioning to a University from a well-known under-graduate College and under the right guidance of two consecutive Vice-Chancellors (Prof. Malabika Sarkar and Prof. Anuradha Lohia) started working towards making it a research-intensive University committed to research as a central part of its mission. After eight years, some of the faculty members including me from the biological division moved to the newly built second campus (Institute of Health Sciences) at New Town in 2020 during lockdown period. My group at the Institute of Health Sciences, is broadly engaged in deciphering the roles of microbial infection or dysbiosis in the development of several human cancers both of lymphoid and epithelial in origin. In addition, our group also focuses in decoding the impact of genomics and eigenomics in cancer development. Our group utilizes various biochemical, cell biology, molecular biology and computational tools along with advanced next-generation sequencing technologies in answering the pertinent research questions.

Research at Presidency University:

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EBV induced B-cell lymphomagenesis: One of the research interests of my group at Institute of Health Sciences, Presidency University, Kolkata (second campus at New Town) lies in understanding the underlying mechanisms that govern Epstein-Barr virus (EBV) induced B-cell lymphomagenesis. EBV, the first human tumor virus discovered, contributes to approximately 1% of all human cancers including several B-cell neoplasms. A characteristic feature of EBV life cycle is its capability to transform metabolically quiescent B-lymphocytes into hyperproliferating B-cell blasts with the establishment of viral latency, while intermittent lytic cycle induction is necessary for the production of progeny virus. Recently, our group demonstrated that dynamic alterations of a membrane associated carbonic anhydrase isoform CA9 expression and its activity in regulating pH homeostasis act as one of the major drivers for EBV induced B-cell transformation and subsequent B-cell lymphomagenesis. We showed that an essential viral oncoprotein EBNA2 mediated CA9 transcriptional activation is essential for virus infected B-cell survival, while during lytic cycle reactivation CA9 expression is transcriptionally suppressed by the key EBV lytic cycle transactivator, BZLF1 through its transactivation domain (PLOS Pathogens, 2024; DST-SERB 2019-22 Project). Currently our group is investigating the precise roles of specific cellular components that regulate both EBV latent and lytic cyle replications. Successful completion of this project will not only in general greatly advance our knowledge regarding involvement of cell proteins in viral latent-lytic switch and its importance in EBV induced oncogenesis, but also in long run this will offer potential therapeutic expansion in other human diseases including cancers generated by different viral infections (DBT 2022-25 and DST-SERB 2024-27 Projects). 

Autophagy mediated degradation of EBV oncoproteins: EBV encoded EBNA3 family of nuclear latent antigens comprising of EBNA3A, EBNA3B, and EBNA3C are unique to immunoblastic lymphomas, those are generated in an immunocompromised background. While EBNA3A and EBNA3C are involved in blocking many important tumor suppressive mechanisms, EBNA3B exhibits tumor suppressive functions. During my postdoctoral tenure, I have demonstrated that EBNA3 proteins, in particular EBNA3C, interact with and employ different protein degradation machineries to induce B-cell lymphomagenesis, while these viral proteins are extremely stable in growing B-lymphocytes. Here at Presidency University, my group demonstrated that proteasomal inhibition leads to specifically degradation of oncogenic EBNA3A and EBNA3C proteins, whereas EBNA3B remains unaffected. Upon proteasomal inhibition, EBNA3C degradation occurs via autophagy-lysosomal pathway, through labelling with K63-linked polyubiquitination and participating in p62-LC3B complex involved in ubiquitin-mediated autophagy substrate selection and degradation through autolysosomal process. While proteasomal inhibition reduces EBNA3C’s oncogenic property, it induces both latent and lytic gene expressions and promotes viral reactivation from EBV transformed B-lymphocytes. This is the first report where we demonstrated that a viral oncoprotein degrades through autophagy-lysosomal pathway upon proteasomal inhibition. Our results promise development of novel strategies specifically targeting proteolytic pathway for the treatment of EBV associated B-cell lymphomas (PLOS Pathogens, 2020; DST-SERB 2019-22 and DBT/Wellcome Trust IA 2015-20 Projects).

Role of EBV oncoprotein EBNA3C in modulating autophagy: Previous studies demonstrated that EBV encoded oncoprotein EBNA3C is indispensable for primary B-cell transformation and maintenance of lymphoblastoid cells outgrowth. During my postdoctoral tenure, I have demonstrated that EBNA3C usurps two putative cell pathways-cell-cycle and apoptosis, essentially through modulating ubiquitin-mediated protein-degradation or gene transcription. In cancer cells, these two pathways are interconnected with autophagy, a survival-promoting catabolic network in which cytoplasmic material including mis/un-folded protein aggregates and damaged organelles along with intracellular pathogens are degraded and recycled in lysosomal compartments. Our lab demonstrated that EBNA3C elevates autophagy, which serves as a prerequisite for apoptotic inhibition and maintenance of cell growth. We showed that EBNA3C globally accelerates autophagy gene transcription under growth limiting conditions. EBNA3C recruits histone epigenetic marks for transcriptional activation of several autophagy genes, notably ATG3, ATG5, and ATG7 responsible for autophagosome formation. Together our data highlight a new role of an essential EBV oncoprotein in regulating autophagy cascade as a survival mechanism and offer novel-targets for potential therapeutic expansion against EBV induced B-cell lymphomas (Cell Death Dis, 2018; DBT/Wellcome Trust IA 2015-20 Project).

Microbial signatures associated with oral and prostate cancers development: The relationship between humans and microbes dates back to ancient times. Robert Koch's ground-breaking work on ‘Pure Culture’ technique illuminated specific role of microbes in causing various human diseases. This technique, however, later met a challenge known as 'The Great Plate Count Anomaly' where many visible microbes under the microscope couldn't be cultivated in pure culture, leading to the concept of 'Uncultivable Microbes'. Advanced sequencing techniques, such as metagenomics sequencing, shotgun sequencing, whole genome sequencing and 16S rRNA amplicon-based sequencing emerged as powerful tools to explore the uncultivable microbial world. In this study, we aimed to uncover the integral connections of microbial communities with both prostate cancer (PCa) and oral squamous cell carcinoma (OSCC) development through utilizing uncultivated sequencing technology along with various bioinformatics analysis. Prostate and oral cancers pose significant health challenges globally as well as with respect to Indian patients. Meticulous analysis of commensal bacteria compositions in both benign prostatic hyperplasia (BPH) and PCa patients’ revealed P. copri, C. campinensis and P. acnes dominated in diseased prostate lesions. While PCa samples exhibited elevated levels of C. taiwanensis and M. organophilum, BPH samples were enriched with K. palustris and C. mixtus. Several human tumor viruses like EBV, HBV and high-risk HPV strains HPV-16 and HPV-18 were also strongly associated with PCa development, correlating with its bacterial signature (Front Oncol. 2021). OSCC represents the most common oral malignancy. In contrast to adjacent normal samples, malignant oral tissues showed decreased bacterial genera of Actinomyces, Sutterella, Stenotrophomonas, Anoxybacillus and Serratia along with increased bacterial genera of Prevotella, Corynebacterium, Pseudomonas, Deinococcus and Noviherbaspirillum. In addition, high-risk HPV-16 strain was significantly linked to OSCC progression (Front Cell Infect Microbiol. 2022). Collectively, these findings reveal the complex interaction of bacterial and viral signatures with PCa and OSCC development (Front Oncol. 2021 and Front Cell Infect Microbiol. 2022; WB-DST-BT Project 2020-21).

Novel autophagy inducers: In addition to our ongoing projects we collaborated with the Chemistry Dept. at our University with an aim to identify small molecules that specifically induce autophagy in cancer cells. Natural compounds isolated from different medicinal plants remain one of the major resources of anticancer drugs due to their enormous chemical diversity. Previous studies suggested therapeutic potential for various tanshinones, key bioactive lipophilic compounds from the root extracts of Salvia miltiorrhiza Bunge, against multiple cancers. We designed, synthesized and evaluated anti-cancer properties of a series of condensed and doubly condensed furophenanthraquinones of tanshinone derivatives on two breast cancer lines - MCF7 and MDA-MB-231. We identified two thiophene analogues - compounds 48 and 52 with greater anti-proliferative efficiency (~4 fold) as compared to the natural tanshinones. Mechanistically, we showed that both compounds induced autophagy mediated cell death and partial but significant restoration of cell death in the presence of autophagy inhibitor further supported this notion. Both compounds transcriptionally activated several autophagy genes responsible for autophagosome formation along with two death regulators - GADD34 and CHOP for inducing cell death. Altogether, our studies provide strong evidence to support compounds 48 and 52 as promising leads for further development as anticancer agents through modulating autophagy mechanism (Bioorg Med Chem. 2021).

Methylation driven tumor suppressor genes against prostate adenocarcinoma: Prostate cancer (PCa) is the second most chronically diagnosed cancer among male and the fifth leading cause of cancer associated deaths worldwide. Frequent genome-wide as well as locus specific DNA methylation modifications and its subsequent impact on gene expressions potential are critical in PCa development. It has been suggested that promoter hypermethylation of a number of tumor suppressor genes (TSGs) involved in important cell pathways offer as attractive diagnostic and/or prognostic biomarkers for PCa. Restitution of expression of these genes could thus serve as a therapeutic strategy for the treatment of aggressive PCa patients. Studies have identified several methylation driven tumor suppressor markers potentially associated with PCa risk. Our genome-wide methylation analyses using ‘Infinium Human Methylation 850K BeadChip array’ identified several potential DNA-methylation driven TSGs associated with PCa development. In this project, we aim to define the underlying molecular mechanisms of the identified TSG silencing and their potential role in PCa development. Recently, our group in collaboration with Dr. Amlan Ghosh (Dept. of Life Sciences, Presidency University, Kolkata) showed that upregulation of DNA methylase enzyme DNMT1 and epigenetic silencing of demethylases TET1 and TET2 were associated with advanced clinicopathological features (a higher PSA level/Gleason score) and increased risk of PCa bone metastasis (Pathol Res Pract. 2024; WB-DST-BT 2020-21 and CSIR 2023-26 Projects).

Postdoctoral Research:

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Introduction to tumor virology: After being substantially experienced in protein chemistry and mycobacterial pathogenesis, I have decided to further work on other human diseases such as viral pathogenesis in human cancer field. To venture into such area, I have joined Dr. Erle S Robertson’s Lab at University of Pennsylvania School of Medicine in 2007. As a postdoctoral researcher my broad objective is to explore the role of EBNA3C, one of the essential latent antigens of EBV in the development of virus mediated B-cell lymphomas, particularly in immunocompromised individuals. Previous studies from Erle’s lab established that EBNA3C facilitates degradation of several important cell-cycle regulators, including pRb and p27KIP1 proteins, by recruitment of the SCFSkp2 E3 ubiquitin ligase complex. EBNA3C was also shown to be ubiquitinated at its N-terminal residues. In addition, although EBNA3C can bind to and be degraded in vitro by purified 20S proteasomes, surprisingly, it seems to be extremely stable in latently infected B-cells. The aim of this project was to find the mechanistic details of EBNA3C stabilization and its oncogenic potential particularly in regulating cell-cycle and apoptotic pathways.

Role of EBV oncoprotein EBNA3C in modulating p53-mediated apoptosis: My work demonstrated that EBNA3C can function as a deubiquitination enzyme (DUB) which was capable of deubiquitinating itself. Functional mapping using deletion and point mutational analysis showed that both the N- and C-terminal domains of EBNA3C contribute to the DUB activity. In addition, our data demonstrated that EBNA3C can deubiquitinate Mdm2, an important cell oncoprotein. EBNA3C forms a ternary complex with Mdm2 and p53 tumor suppressor protein, which in turn facilitates p53 degradation by recruiting Mdm2 E3 ligase activity (J Virol. 2009). In a parallel project, I have also shown that EBNA3C blocks p53 mediated transactivation as well as apoptotic activities through inhibiting its DNA-binding activity. It has been controversial for a long time that whether p53 is functional in EBV positive cells. My work has clearly revealed for the first time that an EBV oncoprotein EBNA3C interferes with the p53’s biological activity (Virology. 2009). Later, I have further shown that EBNA3C can negatively modulate p53-mediated functions by interacting with its regulatory proteins, the inhibitor of growth family proteins, ING4 and ING5, which are shown to be frequently deregulated in different cancer types. Functional mapping revealed that both ING4 and ING5 bound to similar N-terminal domain of EBNA3C previously demonstrated to associate with p53. In addition, I showed that a conserved domain of either ING4 or ING5 bound to both p53 and EBNA3C in a competitive manner, suggesting a potential mechanism whereby the ING4-5/p53 pathway is modulated by EBNA3C in EBV infected cells. Subsequently, we demonstrated that EBNA3C significantly suppresses both ING4 and ING5 mediated regulation of p53 transcriptional as well as the negative regulatory effects on cell proliferation activity. This work demonstrates a possible role for the candidate tumor suppressor ING genes in the biology of EBV-associated cancers (J Virol. 2010).

Role of EBV oncoprotein EBNA3C in regulating G1-S phase transition: This initial work along with the previous efforts led me to believe that EBNA3C might be involved in deregulating the entire mammalian cell-cycle machinery for EBV associated cancer progression. So far, studies probing EBNA3C functions provide perhaps the best link between latent EBV infection and the pRb regulated checkpoint which controls the G1-S phase transition. EBNA3C was previously shown to either directly target pRb for ubiquitin-proteasome mediated degradation or may indirectly target the pRb function by associating with Cyclin A/CDK2 complex. Additionally, studies have shown that EBNA3C bypasses the ability of the CDK inhibitor - p16INK4A to block transformation. Despite this body of evidence, a clear molecular mechanism accountable for disrupting the G1-S phase blockage by EBNA3C is yet to be established. My studies demonstrated several potential mechanisms in order to promote G1 to S transition: a) EBNA3C stabilizes Cyclin D1 through inhibition of its poly-ubiquitination; b) EBNA3C increases Cyclin D1 nuclear localization by blocking GSK3β activity; c) EBNA3C enhances the kinase activity of Cyclin D1/CDK6 which enables subsequent ubiquitination and degradation of pRb; 4) EBNA3C coupled with Cyclin D1/CDK6 complex efficiently nullifies the inhibitory effect of pRb on cell growth (Plos Pathogens. 2011).

Role of EBV oncoprotein EBNA3C in regulating E2F1 mediated apoptosis in response DNA-damage: The role of the pRb/E2F pathway in the regulation of cell-cycle progression, particularly the G1 to S phase transition, is well established. Previous studies have suggested distinct roles for individual members of the E2F family in the control of cell proliferation and cell fate. Interestingly, only E2F1 appears to be involved in both cell proliferation as well as inducing apoptosis. My study has demonstrated that EBNA3C knocked down LCLs induced more apoptosis compared to control cells. The induction of the apoptotic pathways could be associated with the ability of both E2F1 and p53 encoded apoptotic activities. We hypothesized that EBNA3C may also be involved in modulating E2F1 mediated apoptotic functions. Using exogenous system here we subsequently showed that EBNA3C blocks E2F1 mediated apoptosis in Saos-2 cells (p53-/-). Analyses from proliferation assay and colony formation assays demonstrate EBNA3C strongly competes with the anti-proliferative effects of E2F1. EBNA3C forms a pRb independent complex with E2F1 and represses E2F1 transcriptional activity. Mechanistically, we show using ChIP and dsDNA oligo-pulldown experiments that the specific DNA-binding ability of E2F1 towards p73 and Apaf-1 promoter regions is significantly reduced in the presence of EBNA3C (Plos Pathogens 2012). Overall, these observations pointing to the unique ability of EBNA3C function in regulating both apoptosis and cell proliferation, further raise the possibility for the development of effective therapeutic strategies against EBV associated human cancers.

Epigenetic modulation of tumor suppressor genes during early EBV infection in B-lymphocytes - DNA methylation at the CpG islands is a common epigenetic modification which contributes to the regulation of gene expression in mammalian cells. Thus, hypo or hyper-methylation of oncogene activation and tumor suppressor gene silencing was extensively shown to be associated with development of multiple human cancers. As similar to other oncogenic viruses, EBV-associated human cancers were also shown to be regulated by epigenetic modifications both on viral genome as well as cellular gene expressions. In this project, we investigated EBV infection of resting B lymphocytes, which leads to continuously proliferating lymphoblastoid cell lines through examination of the expression pattern of a comprehensive panel of TSGs and the epigenetic modifications, particularly methylation of their regulatory sequences. EBV infection of primary B lymphocytes resulted in global transcriptional repression of TSGs through engagement of hypermethylation. Therefore, CpG methylation profiles of TSGs may be used as a prognostic marker as well as development of potential therapeutic strategies for controlling acute infection and EBV-associated B-cell lymphomas (PNAS, 2015).

Doctoral Research:

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Peptide inhibitors against TB: I have begun my research career at Dept. of Microbiology, Bose institute as a PhD student under the guidance of an eminent microbiologist Dr. Sujoy K Das Gupta in 2001. The objective of my project was to develop inhibitors against Hsp16.3 protein, a virulence factor of latent Mycobacterium tuberculosis (TB). Hsp16.3, a member of a-crystallin family (a-HSPs), is known to be one of the factors responsible for inducing dormancy in M. tuberculosis. This study has been initiated with proposition that development of an inhibitor against this protein may help in arresting latent TB. With this goal in mind a detailed biochemical characterization of this protein has been done. Hsp16.3 was found to act as an efficient chaperone in vitro and also in vivo and a systematic deletion analysis revealed that the central a-crystallin domain is absolutely necessary for its activity. Next, the ‘phage display technique’ has been applied to select out peptide sequences that specifically interact with Hsp16.3 in order to developing inhibitors against that protein. Several peptide sequences have been identified having a consensus core comprising of His-X-X-X-His and peptides corresponding to that sequences inhibit the in vitro chaperone activity of Hsp16.3 and also destabilize Hsp16.3- substrate protein complexes, whereas little or no effect of these peptides was observed on aB-crystallin, a human homologous protein, indicating that there is an element of specificity in the observed inhibition. Although a drug is far away, the identified peptides could be used as lead compounds in future development of anti-TB drugs. This work has been published in a reputed ASM journal (Appl Environ Microbiol. 2005).

Peptide mimotope as TB-diagnostic tool: Apart from my own project I was also involved in another assignment, where we have successfully isolated several peptide mimotopes of a highly immunogenic non-protein mycobacterial antigen LAM using same phage display technique. These identified LAM mimotopes have shown a considerable extent of diagnostic as well as immunomodulatory potentials (Clin Vaccine Immunol. 2006).

TB chaperone blocks tubin self-assembly: In addition, I was also actively engaged in many collaborative projects with other labs. I have one co-authorship publication with Dr. Bhabatarak Bhattacharaya, who is a distinguished figure in tubulin-biochemistry field. In this project, we have shown that a number of chaperones including mycobacterial Hsp16.3 inhibit tubulin self-assembly in a dose dependent manner (Proteins. 2007).

Teaching Philosophy:

Since I was a student, I have intensely observed that the best teachers were those who truly concerned about their teaching. One can easily notice this zeal which collectively comes from systematic homework, constant evolution of teaching skills and most importantly the pleasure of watching students learn. While the eventual goal for a teacher is to spread new information among students, not just memorizing particulars, but to teach them how to think. This is absolutely possible only when both the teacher and the students are enjoying what they are learning.

Teaching assignments:

• 2012 – 2020: MSc in Biotechnology (Dept. of Biotechnology, Presidency University, Kolkata, College Street Campus) and MSc in Life Sciences (Dept. of Life Sciences, Presidency University, Kolkata, College Street Campus) - Molecular Biology, Genetics, Recombinant DNA Technology, Microbiology and Genomics theory and lab sessions.
• 2020 – Present: MSc in Biotechnology (School of Biotechnology, Presidency University, Kolkata, New Town Campus) and MSc in Biotechnology, Molecular Microbiology and Virology and Immunology (School of Biotechnology, Institute of Health Sciences, Presidency University, Kolkata, New Town Campus) - Microbiology & Recombinant DNA Technology (VRIM 0702, BITG 0702, MLMB 0702), Advanced Virology (VRIM 0802), Bioinformatics & Genomics and Proteomics (VRIM 0803, BITG 0803, MLMB 0803), Medical Virology (VRIM 0902), Clinical Immunology and Neuroimmunology (VRIM 0903) and lab sessions (VRIM 0892, VRIM 1091, VRIM 1092, VRIM 1093, VRIM 1094).

Other Experiences:

• Outreach: Invited Paper-Setter, Examiner, Moderator, External evaluator of M.Sc curriculum in various College/Universities - Tripura University, St. Xavier’s College, Amity University and Sister Nivedita University).
• Member Secretary: Institutional Biosafety Committee (IBSC), Presidency University, Kolkata (2023 – Present)
• Centre-in-Charge: MSc Biotechnology Examinations 2012-2013 at Presidency University, Kolkata
• Convener: ‘Integrative Biology’ PhD Committee, Dept. of Life Sciences, Presidency University, Kolkata (2014 15). 
• Member: Departmental PhD Committee, Dept. of Life Sciences, Presidency University, Kolkata (2015 – 2017); Institutional Annual Report Committee, Presidency University, Kolkata (2014 – 2020); Institutional Biosafety Committee (IBSC), Presidency University, Kolkata (2014 – 2023); Departmental PhD Committee, School of Biotechnology, Presidency University, Kolkata (2020 – 2022); Departmental PhD Committee, Institute of Health Sciences, Presidency University, Kolkata (2022 – Present).
• Joint Coordinator: DBT-BUILDER program for establishment of Central Instrumentation Research Facility at Dept. of Life Sciences, Presidency University, Kolkata (2014 - 15).
• Invited Peer Reviewer: Infectious Agents and Cancer (2013 – present); Future Microbiology (2015 – present); Current Drug Metabolism (2016 - present); PloS Pathogens (2017 – present); Scientific Reports (2018 – present); Journal of Cancer Treatment and Diagnosis (2018 – present); Cancer Management and Research (2018 – present); Frontiers in Cellular and Infection Microbiology (2020 – present); Frontiers in Oncology (2020 – present); Virus Disease (2020 – present); Cell Death and Disease (2020 – present); Frontiers in Pharmacology (2021 – present); Frontiers in Immunology (2021 – present); Cells – MDPI (2021 – present); Future Virology (2021 – present); Tumor Biology (2021 – present); Molecular Cancer Therapeutics (2021 – present); Frontiers in Molecular Biosciences (2022 – present); Journal of Clinical Medicine – MDPI (2022 – present); Cancers – MDPI (2022 – present); Biomedicines – MDPI (2022 – present); Biology – MDPI (2022 – present); Biochimie (2022 – present); Bioorganic and Medicinal Chemistry (2022 – present).
• Review Editor: Frontiers in Immunology (Section: Microbial Immunology); Frontiers in Molecular Biosciences (Section: Molecular Diagnostics and Therapeutics) (2022 – Present).
• Invited Grant Reviewer: DST-SPARC, Govt. of India (2019 – Present); DST-SERB, Govt. of India (2019 – Present).

Meetings/Seminars/Conferences Organized:

• Mini symposium on ‘Nutrition & Chronic Disease’, organized by the Department of Life Sciences, Presidency University, Kolkata in association with the Department of Nutrition and Food Science, Wayne State University, USA, on December 4, 2019 at Presidency University, Kolkata.
• National symposium on ‘Frontiers in Biological Sciences’ co-organized by St. Xavier's college, Presidency University and Indian Institute of Chemical Biology (IICB) on September 21-22, 2019 at St. Xavier's college, Kolkata.
• 6th Molecular Virology Meeting organized by Indian Institute of Technology (IIT) Kharagpur in association with Presidency University, Kolkata, Amity University, Kolkata, Indian Institute of Chemical Biology (IICB) and National Institute for Cholera and Enteric Diseases (NICED) on February 28 – March 2, 2019 at Indian Institute of Technology (IIT), Kharagpur.
• Regional Young Investigators’ Meeting Kolkata organized by Presidency University, Kolkata in association with Indiabioscience, Bose Institute, Indian Association for the Cultivation of Science (IACS), National Institute for Biomedical Genomics (NIBMG) and Indian Institute of Chemical Biology (IICB) on February 5-6, 2019 at Presidency University, Kolkata at Presidency University, Kolkata.
• Public Lecture by Prof. Venkatraman Ramakrishnan, Nobel laureate in Chemistry 2009 on “From Chidambaram to Cambridge: a life in science” at Presidency University, Kolkata on January 22, 2019.
• “Illumina Technology” by Premas Life Sciences Pvt. Ltd. at Presidency University. Kolkata on October 3, 2018.
• “The application of Semiconductor Sequencing in basic and translational health research” by Thermo Fisher Scientific, at Presidency University. Kolkata on September 19, 2018. 
• Indian Science National Academy (INSA) Golden Jubilee Commemoration Medal Lecture 2018 by Prof. Partha P Majumder, “Riding the Genomics Wave to Reach New depths of Human Health and History”, at Presidency University, Kolkata on August 20, 2018.
• Seminar by Prof. Barbara Pauly, Director of Fellowships, Human Frontier Science Program (HFSP), University on “HFSP: Funding International Research Collaborations in the Life Sciences” on March 12, 2018 at Presidency University, Kolkata.
• Seminar by Prof. Usha Menon, University of College London, UK on “Ovarian cancer screening: the long journey” on March 30, 2016 in weekly departmental colloquium at Presidency University, Kolkata.
• Seminar by Dr. Sangram Bagh, Saha Institute of Nuclear Physics, Kolkata on "Can we program a cell like an engineer programs a device?: Synthetic  biology and its application in cellular robotics, programmed therapeutics and space travel" on March 2, 2016 in weekly departmental colloquium at Presidency University, Kolkata.
• One-day symposium “Life Sciences Symposium” jointly sponsored by Wellcome Trust/ DBT India Alliance and Presidency University, Kolkata at Presidency University, Kolkata on February 23, 2016.
• ‘By monthly’ meeting for "Kolkata Cancer Research Cluster" involving TTCRC/TMC, Presidency University, Bose Institute, NIBMG and TCG Life Sciences (TCGS) at Presidency University, Kolkata on January 27, 2016.
• Seminar by Dr. Shubhankar Chatterjee, Central University of Himachal Pradesh on "Biological significance of microbe-microbe interactions: Metabolomics approach" on January 6, 2016 in weekly departmental colloquium at Presidency University, Kolkata.
• Seminar by Prof. Suman Dhar, Jawaharlal Nehru University, New Delhi on "A Multidisciplinary approach to understand and inhibit DNA replication in human malaria parasite Plasmodium falciparum" on February 3, 2015.
• National symposium on ‘Molecules to Systems’ at Presidency University from January 29 – 31, 2015, Sponsored by DBT-BUILDER program at Presidency University.
• Seminar by Prof. Ranjan Sen, Center for DNA Fingerprinting and Diagnostics, Hyderabad, on "Regulations of Rho-dependent transcription termination in bacteria" on January 16, 2015.

Current Lab Strength:

• Mr. Samaresh Malik (SRF, UGC) (2018 - ) Cleared 5000 Words

Title of the thesis: “Role of Carbonic Anhydrases in Epstein-Barr virus (EBV) induced B-cell lymphomagenesis”

• Mr. Purandar Sarkar, CSIR-SRF (2018 - ) Thesis Submitted.

Title of the thesis: “Microbial Signature Associated with the Development of Prostate and Oral Cancers in Eastern Region of India”

• Mr. Joyanta Biswas, UGC-SRF (2020 - )

Proposed title of the thesis: “Mechanisms of Reactivation of Epstein-Barr virus (EBV) from Latency to Lytic Replication: Role of E2F Transcription Factors”

• Mr. Subhadeep Nag, UGC-SRF (2020 - )

Proposed title of the thesis: “Mechanistic Dissection of DUOX1 as Methylation Driven Tumor Suppressor Gene in Prostate Adenocarcinoma”

• Mr. SK Asif Ali, Project Fellow, DBT Project (2023 - )
• Ms. Nazmin Haque, UGC-SRF (2024 - )

Proposed title of the thesis: “Dissecting the role of Enolase 1 mediated altered metabolic activities in EBV induced B-cell lymphomagenesis”

• PG Dissertation Students: Mr. Ayanabha Bardhan and Ms. Nazifa Ahmed (2024)

Past Lab Members:

• Dr. Shaoni Bhattacharjee, DST-INSPIRE Fellow (2015 - 2020), Currently working as a Postdoctoral Fellow at Institut Pasteur, France
• Title of the thesis: “Understanding the Role of Epstein- Barr virus Essential Nuclear Antigen EBNA3C in Regulating Unfolding Protein Response (UPR)-Autophagy Network”
• Dr. Chandrima Gain (SRF, UGC) (2016 - 2021), Currently working as a Postdoctoral Fellow at University of California, Los Angeles, USA
• Title of the thesis: “Crosstalk between Proteasomal and Lysosomal Protein Degradation Pathway in EBV-Induced B-cell Lymphomas”
• Mr. Subhajit Maity, Research Assistant, DST-SERB Project (2019 - 2021), Currently pursuing PhD program at University of Texas, Dallas, USA
• Mr. Shatadru Ghosh Roy, Research Assistant, Wellcome Trust/DBT IA Project (2015 - 2018). Currently pursuing PhD program at Ben Gurion University of the Negev, Be'er Sheva, Israel.
• Ms. Priyanka Bose, Research Technician, DBT/Wellcome Trust IA Project (2015 - 2018). Currently pursuing PhD program at Ben Gurion University of the Negev, Be'er Sheva, Israel.
• Mr. Shayan Sarkar, MSc, Research Trainee (2018 – 19). Currently pursuing PhD program at Stony Brook University-Cold Spring Harbor Laboratory, USA.
• Ms. Shrea Bural, MSc Life Sciences Dissertation Student (2018 – 19) at Dept. of Life Sciences, Presidency University, Kolkata. Currently pursuing PhD program at Dartmouth College, Hanover, USA.
• Ms. Priyasmita Chakraborty, MSc Life Sciences Dissertation Student (2017 – 18) at Dept. of Life Sciences, Presidency University, Kolkata. Currently pursuing PhD program at Weizmann Institute of Science, Rehovot, Israel.
• Ms. Sryeshi Chandra, Student, BSc, Biological Sciences (2013 – 16). Currently pursuing PhD program at National Brain Research Centre (NBRC), Manesar, Hariyana, India.
• Mr. Syamantak Ghosh, MSc Dissertation Student (2015 – 16) at Dept. of Life Sciences, Presidency University, Kolkata. Currently pursuing PhD program at Indian Institute of Chemical Biology, Kolkata
• Ms. Oindrila Som, MSc Dissertation Student (2015 – 16) at Dept. of Life Sciences, Presidency University, Kolkata.  
• Mr. Shatadru Ghosh Roy, MSc Dissertation Student (2014 – 15) at Dept. of Biological Sciences, Presidency University, Kolkata (College Street Campus). Later joined my lab as a Research Assistant, DBT/Wellcome Trust IA Project (2015 - 2018). Currently pursuing PhD program at Ben Gurion University of the Negev, Be'er Sheva, Israel.
• Ms. Priyanka Bose, MSc Dissertation Student (2014 – 15) at Dept. of Biological Sciences, Presidency University, Kolkata (College Street Campus). Later joined my lab as a Research Technician, DBT/Wellcome Trust IA Project (2015 - 2018). Currently pursuing PhD program at Ben Gurion University of the Negev, Be'er Sheva, Israel.  
• Ms. Arifa Akbar, MSc Biotechnology Dissertation Student (2013 - 14) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus).
• Ms. Koyeli Das, MSc Biotechnology Dissertation Student (2013 - 14) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus).
• Ms. Pratiti Nath, MSc Biotechnology Dissertation Student (2013 - 14) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus).
• Ms. Poulami Tapadar, MSc Biotechnology Dissertation Student (2012 – 13) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus). Currently pursuing PhD program at Dept. of Life Sciences, Presidency University, Kolkata, India.
• Mr. Sayantan Joardar, MSc Biotechnology Dissertation Student (2012 – 13) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus).
• Ms. Wahida Rahman, MSc Biotechnology Dissertation Student (2012 – 13) at Dept. of Biotechnology, Presidency University, Kolkata (College Street Campus). Currently pursuing PhD program at Dept. of Life Sciences, Presidency University, Kolkata, India.

• Society of Biological Chemists (SBC), India
• Indian Virological Society (IVS) 

h-index: 24

A.   Research Articles: 26

1. Malik S, Biswas J, Sarkar P, Nag S, Gain C, Roy SG, Bhattacharya B, Ghosh D, Saha A*. Differential Carbonic Anhydrase Activities Control EBV-Induced B-Cell Transformation and Lytic Cycle Reactivation. PLoS Pathog. 2024; 20(3):e1011998.
2. Banerjee A, Bardhan A, Sarkar P, Datta C, Pal DK, Saha A, Ghosh A. Dysregulation of DNA epigenetic modulators during prostate carcinogenesis in an eastern Indian patient population: Prognostic implications. Pathol Res Pract. 2024; 253:154970.
3. Sarkar P, Malik S, Banerjee A, Datta C, Pal DK, Ghosh A, Saha A*. Differential Microbial Signature Associated With Benign Prostatic Hyperplasia and Prostate Cancer. Front Cell Infect Microbiol. 2022; 12:894777.
4. Gain C, Sarkar A, Bural S, Rakshit M, Banerjee J, Dey A, Biswas N, Kar GK, Saha A*. Identification of two novel thiophene analogues as inducers of autophagy mediated cell death in breast cancer cells. Bioorg Med Chem. 2021; 37:116112.
5. Sarkar P, Malik S, Laha S, Das S, Bunk S, Ray JG, Chatterjee R, Saha A*. Dysbiosis of Oral Microbiota During Oral Squamous Cell Carcinoma Development. Front Oncol. 2021; 11:614448.
6. Gain C, Malik S, Bhattacharjee S, Ghosh A, Robertson ES, Das BB, Saha A*. Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway. PLoS Pathog. 2020; 16(2):e1008105.
7. Zhang S, Pei Y, Lang F, Sun K, Singh RK, Lamplugh ZL, Saha A, Robertson ES. EBNA3C facilitates RASSF1A downregulation through ubiquitin-mediated degradation and promoter hypermethylation to drive B-cell proliferation. PLoS Pathog. 2019; 15(1):e1007514.
8. Bhattacharjee S, Bose P, Patel K, Roy SG, Gain C, Gowda H, Robertson ES, Saha A*. Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival. Cell Death Dis. 2018; 9(6):605.
9. Pei Y, Banerjee S, Sun Z, Jha HC, Saha A, Robertson ES. EBV nuclear antigen 3C mediates regulation of E2F6 to inhibit E2F1 transcription and promote cell proliferation. PloS Pathog. 2016; 12(8):e1005844.
10. Saha A, Jha HC, Upadhyay SK, Robertson ES. (2015). Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection. Proc Natl Acad Sci U S A. 2015; 112(37):E5199-207. 
11. Dzeng RK, Jha HC, Lu J, Saha A, Banerjee S, Robertson ES. Small molecule growth inhibitors of human oncogenic gammaherpesvirus infected B-cells. Mol Oncol. 2015; 9(2):365-76.
12. Jha HC, Aj MP, Saha A, Banerjee S, Lu J, Robertson ES. EBV essential antigen EBNA3C attenuates H2AX expression. J Virol. 2014; 88(7):3776-88.
13. Jha HC, Lu J, Saha A, Cai Q, Banerjee S, Prasad MA, Robertson ES. EBNA3C-mediated regulation of aurora kinase B contributes to Epstein-Barr virus-induced B-cell proliferation through modulation of the activities of the retinoblastoma protein and apoptotic caspases. J Virol. 2013; 87(22):12121-38.
14. Banerjee S, Lu J, Cai Q, Saha A, Jha HC, Dzeng RK, and Robertson ES. The EBV latent antigen 3C inhibits apoptosis through targeted regulation of interferon regulatory factors 4 and 8. Plos Pathog. 2013; 9(5):e1003314.
15. Jha HC, Upadhyay SK, Aj MP, Lu J, Cai Q, Saha A, Robertson ES. H2AX Phosphorylation Is Important for LANA-Mediated Kaposi's Sarcoma-Associated Herpesvirus Episome Persistence. J Virol. 2013; 87(9):5255-69.
16. Saha A, Lu J, Morizur L, Upadhayay SK, AJ Prasad M, Robertson ES. Epstein-Barr virus Nuclear Antigen 3C Blocks E2F1 Induced Apoptotic Pathway in EBV Infected Cells. Plos Pathog. 2012; 8(3): e1002573.
17. Lu J, Verma SC, Cai Q, Saha A, Dzeng R, Robertson ES. Enhanced KSHV latent infection and proliferative capacity during primary infection. Plos Pathog. 2012; 8(1):e1002479.
18. Cai Q, Guo Y, Xiao B, Banerjee S, Saha A, Lu J, Glisovic T, Robertson ES. Epstein-Barr virus Nuclear Antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis. Plos Pathog. 2011; 7(12): e1002418.
19. Saha A, Halder S, Upadhayay SK, Lu J, Kumar P, Murakami M, Cai Q, Robertson ES. EBNA3C Facilitates G1-S Transition by Stabilizing and Enhancing the Function of Cyclin D1. Plos Pathog. 2011; 7(2):e1001275.
20. Saha A, Bamidele A, Murakami M, Robertson ES. EBNA3C Attenuates the Function of p53 through Interaction with the Inhibitor of Growth Family Proteins, 4 and 5. J Virol. 2011; 85(5):2079-88.
21. Xiao B, Verma SC, Cai Q, Kaul R, Lu J, Saha A, Robertson ES. Bub1 and CENP-F can contribute to Kaposi's sarcoma-associated herpesvirus genome persistence by targeting LANA to kinetochores. J Virol. 2010; 84(19):9718-32.
22. Yi F*, Saha A*, Murakami M*, Kumar P, Knight JS, Cai Q, Choudhuri T, Robertson ES. Epstein-Barr virus nuclear antigen 3C targets p53 and modulates its transcriptional and apoptotic activities. Virology 2009; 388(2):236-47.
23. Saha A, Murakami M, Kumar P, Bajaj B, Sims K, Robertson ES. Epstein-Barr virus nuclear antigen 3C augments Mdm2-mediated p53 ubiquitination and degradation by deubiquitinating Mdm2. J Virol. 2009; 83(9):4652-69.
24. Mitra G, Saha A, Gupta TD, Poddar A, Das KP, Das Gupta SK, Bhattacharyya B. Chaperone-Mediated Inhibition of Tubulin Self-Assembly. Proteins. 2007; 67(1):112-20.
25. Sharma A, Saha A, Bhattacharjee S, Majumdar S, Das Gupta SK. Specific and Randomly Derived Immunoactive Peptide Mimotopes of Mycobacterial Antigens. Clin Vaccine Immunol. 2006; 13(10):1143-54.
26. Saha A, Sharma A, Dhar A, Bhattacharyya B, Roy S, Das Gupta SK. Antagonists of Hsp16.3, A Low-Molecular-Weight Mycobacterial Chaperone and Virulence Factor, Derived from Phage-Displayed Peptide Libraries. Appl Environ Microbiol. 2005; 71(11):7334-44.

B.   Reviews: 10

1. Maity S, Saha A*. Therapeutic Potential of Exploiting Autophagy Cascade Against Coronavirus Infection. Front Microbiol. 2021;12:675419.
2. Saha A*, Robertson ES. Epstein-Barr virus: a powerful tool to study B-cell lymphomagenesis . J Virol. 2019; 14;93(13).
3. Ghosh Roy S, Robertson ES, Saha A*. Epigenetic impact on EBV associated B-cell lymphomagenesis. Biomolecules. 2016; 6(4), pii: E46.
4. Bhattacharjee S, Ghosh Roy S, Bose P, Saha A*. Role of EBNA3-family proteins in EBV associated B-cell lymphomagenesis. Front Microbiol. 2016; 7:457.
5. Saha A, Robertson ES. Insights into the Epstein-Barr virus nuclear antigen 3C mediated deregulation of cell-proliferation and apoptosis. Future Microbiol. 2013; 8(3):323-52.
6. Saha A, Robertson ES. Functional Modulation of the Metastatic Suppressor Nm23-H1 by Oncogenic Viruses. FEBS Lett. 2011; 585(20):3174-84.
7. Saha A, Robertson ES. Epstein-Barr virus in B-cell Lymphoma: Pathogenesis and Clinical Outcomes. Clin Cancer Res. 2011; 17(10):3056-63.
8. Saha A*, Kaul R*, Murakami M, Robertson ES. Tumor viruses and cancer biology: modulating signaling pathways for therapeutic intervention. Cancer Biol Ther. 2010; 10(10):961-78. * Equal contribution.
9. Kumar P*, Saha A*, Robertson ES. Epstein-Barr virus Hijacks Cell-Cycle Machinery: EBV can perturb cellular pathways, contributing to the development of cancer. Microbe. 2010; 5: 1-6. * Equal contribution.
10. Kumar P, Murakami M, Kaul R, Saha A, Cai Q and Robertson ES. Deregulation of Cell Cycle Machinery by the Epstein-Barr virus Nuclear Antigen 3C. Future Virology. 2009; 4(1):79-91.

C.   Book Chapters: 3

1. Saha A* and Robertson ES. (2018). Microbiome and Human Malignancies. Robertson ES Ed. Caister-Horizon Press, London England. Book Chapter. 
2. Upadhayay SK, Jha HC, Saha A, Robertson ES. (2012). Lymphocryptoviruses: EBV and Its Role in Human Cancer. Robertson ES Ed. Springer Science+Business Media, LLC, New York, USA. Book Chapter.
3. Sims K, Saha A, and Robertson ES. (2009). Epstein-Barr virus Nuclear Antigen Family 3 in Regulation of Cellular Processes. Robertson ES Ed. Caister-Horizon Press, London England. Book Chapter.

* Corresponding Author.

PubMed Link: https://pubmed.ncbi.nlm.nih.gov/?term=abhik%20saha&sort=date

Google Scholar: https://scholar.google.co.in/citations?user=h4ravHIAAAAJ&hl=en