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.
Ph.D Microbiology (Bose Institute, 2007)
M.Sc. Biochemistry (Calcutta University, 2000)
B.Sc. Chemistry (Calcutta University, 1998)
Wellcome Trust/DBT Inida Alliance Fellow (2015)
Ramanujan Fellow (2013)
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). My studies led us to find several ‘peptide inhibitors’ could further be used as lead compounds in future development of anti-TB drugs. 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 Dept. of Microbiology, Perelman School of Medicine at the University of Pennsylvania in April 2007. Dr. Robertson is a renowned virologist and made several important contribution in the field of viral mediated-cancer. As a postdoctoral researcher my broad objective is to explore the role of EBNA3C, one of the essential latent antigens of EBV (Epstein–Barr virus) in the development of virus mediated many B-cell lymphomas, particularly in immuno-compromised individuals. My work has shown that EBNA3C can manipulate two fundamental cellular mechanisms – cell-cycle and apoptosis through deregulating a vast range of cellular oncoproteins and tumor suppressors, including p53, Mdm2, E2F1, Cyclin D1 and pRb. Collectively, my scientific achievements show how a systematic basic research on understanding the pathogenesis of diseases can eventually pave the pathway for translating those findings into therapeutic benefit.
Research / Administrative Experience+
As an independent investigator, I propose to study the pathogenesis of human diseases 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 mechanism(s).
My interest in this fascinating area of research initiates from my postdoctoral work in which I study pathogenesis of Epstein-Barr virus (EBV)-associated human cancers. 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 many B-cell lymphomas, particularly in immunocompromised individuals. This exposure gave me the opportunity to appreciate the intricate nature of a particular tumor virus and to comprehend further that how different tumor viruses develop many sophisticated skills in order to manipulate host cell defense mechanism and promote cancer progression.
Therefore, the broad goal of my research is to uncover the pathogenic mechanisms and to identify multiple components that are altered in several important cellular pathways during virus associated cancer development in humans. I hope that information generated from these studies will be important for designing novel therapies against many human malignancies.
Teaching / Other Experience+
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. I would like to teach in the area of Molecular biology, Protein Engineering, Protein Quality Control, Cell Biology and Virology.
Post Graduate Supervision+
I am interested in supervising postgraduate students in the field of Cancer Biology, particulary in the area of virus mediated oncogenesis.
Current Registered PhD Students:
Shaoni Bhattacharjee, DST-INSPIRE Fellow (2014 - )
Chandrima Gain, UGC Fellow (2017 - )
Shatadru Ghosh Roy, Research Assistant, Wellcome Trust/DBT IA Project (2014 - )
Priyanka Bose, Reseach Technician, Wellcome Trust/DBT IA Project (2014 - )
Society of Biological Chemists, India
The American Society for Microbiology
A. Research Articles:
- Bhattacharjee S, Bose P, Patel K, Roy SG, Gain C, Gowda H, Robertson ES, Saha A*. (2018). Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival. Cell Death Dis. 2018 May 22;9(6):605. * Corresponding Author.
- Pei Y, Banerjee S, Sun Z, Jha HC, Saha A, Robertson ES. (2016). EBV nuclear antigen 3C mediates regulation of E2F6 to inhibit E2F1 transcription and promote cell proliferation. PloS Pathogens, 12(8):e1005844.
- 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, 112(37):E5199-207.
- 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 Feb;9(2):365-76.
- Jha HC, Aj MP, Saha A, Banerjee S, Lu J, Robertson ES. (2014). EBV essential antigen EBNA3C attenuates H2AX expression. J Virol.; 88(7):3776-88.
- Jha HC, Lu J, Saha A, Cai Q, Banerjee S, Prasad MA, Robertson ES. (2013). 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.; 87(22):12121-38.
- Banerjee S, Lu J, Cai Q, Saha A, Jha HC, Dzeng RK, and Robertson ES. (2013). The EBV latent antigen 3C inhibits apoptosis through targeted regulation of interferon regulatory factors 4 and 8. Plos Pathogens, 9(5):e1003314.
- Jha HC, Upadhyay SK, Aj MP, Lu J, Cai Q, Saha A, Robertson ES. (2013). H2AX Phosphorylation Is Important for LANA-Mediated Kaposi's Sarcoma-Associated Herpesvirus Episome Persistence. J Virol, 87(9):5255-69.
- Saha A, Lu J, Morizur L, Upadhayay SK, AJ Prasad M, Robertson ES. (2012). Epstein-Barr virus Nuclear Antigen 3C Blocks E2F1 Induced Apoptotic Pathway in EBV Infected Cells. Plos Pathogens; 8(3): e1002573.
- Lu J, Verma SC, Cai Q, Saha A, Dzeng R, Robertson ES. (2012). Enhanced KSHV latent infection and proliferative capacity during primary infection. Plos Pathogens; 8(1):e1002479.
- Cai Q, Guo Y, Xiao B, Banerjee S, Saha A, Lu J, Glisovic T, Robertson ES. (2011). Epstein-Barr virus Nuclear Antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis. Plos Pathogens; 7(12): e1002418.
- Saha A, Halder S, Upadhayay SK, Lu J, Kumar P, Murakami M, Cai Q, Robertson ES. (2011). EBNA3C Facilitates G1-S Transition by Stabilizing and Enhancing the Function of Cyclin D1. Plos Pathogens; 7(2):e1001275.
- Saha A, Bamidele A, Murakami M, Robertson ES. (2011). EBNA3C Attenuates the Function of p53 through Interaction with the Inhibitor of Growth Family Proteins, 4 and 5. J Virol.; 85(5):2079-88.
- Xiao B, Verma SC, Cai Q, Kaul R, Lu J, Saha A, Robertson ES. (2010). Bub1 and CENP-F can contribute to Kaposi's sarcoma-associated herpesvirus genome persistence by targeting LANA to kinetochores. J Virol.; 84(19):9718-32.
- Yi F*, Saha A*, Murakami M*, Kumar P, Knight JS, Cai Q, Choudhuri T, Robertson ES. (2009). Epstein-Barr virus nuclear antigen 3C targets p53 and modulates its transcriptional and apoptotic activities. Virology; 388(2):236-47. * Equal contribution.
- Saha A, Murakami M, Kumar P, Bajaj B, Sims K, Robertson ES. (2009). Epstein-Barr virus nuclear antigen 3C augments Mdm2-mediated p53 ubiquitination and degradation by deubiquitinating Mdm2. J Virol.; 83(9):4652-69.
- Mitra G, Saha A, Gupta TD, Poddar A, Das KP, Das Gupta SK, Bhattacharyya B. (2007). Chaperone-Mediated Inhibition of Tubulin Self-Assembly. Proteins; 67(1):112-20.
- Sharma A, Saha A, Bhattacharjee S, Majumdar S, Das Gupta SK. (2006). Specific and Randomly Derived Immunoactive Peptide Mimotopes of Mycobacterial Antigens. Clin Vaccine Immunol.; 13(10):1143-54.
- Saha A, Sharma A, Dhar A, Bhattacharyya B, Roy S, Das Gupta SK. (2005). Antagonists of Hsp16.3, A Low-Molecular-Weight Mycobacterial Chaperone and Virulence Factor, Derived from Phage-Displayed Peptide Libraries. Appl Environ Microbiol.; 71(11):7334-44.
- Ghosh Roy S, Robertson ES, Saha A*. (2016). Epigenetic impact on EBV associated B-cell lymphomagenesis. Biomolecules, 6(4), pii: E46. * Co-corresponding Author.
- Bhattacharjee S, Ghosh Roy S, Bose P, Saha A*. (2016). Role of EBNA3-family proteins in EBV associated B-cell lymphomagenesis. Front Microbiol, 7:457. * Corresponding Author.
- Saha A, Robertson ES. (2013). Insights into the Epstein-Barr virus nuclear antigen 3C mediated deregulation of cell-proliferation and apoptosis. Future Microbiol, 8(3):323-52.
- Saha A, Robertson ES. Functional Modulation of the Metastatic Suppressor Nm23-H1 by Oncogenic Viruses. FEBS Lett. 2011; 585(20):3174-84.
- Saha A, Robertson ES. Epstein-Barr virus in B-cell Lymphoma: Pathogenesis and Clinical Outcomes. Clin Cancer Res. 2011; 17(10):3056-63.
- 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.
- 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.
- 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):1-8.
C. Book Chapters:
- Saha A* and Robertson ES. Microbiome and Human Malignancies. Robertson ES Ed. Caister-Horizon Press, London England. 2018. Book Chapter. * Co-orresponding Author.
- Upadhayay SK, Jha HC, Saha A, Robertson ES. Lymphocryptoviruses: EBV and Its Role in Human Cancer. Robertson ES Ed. Springer Science+Business Media, LLC, New York, USA. 2012. Book Chapter.
- Sims K, Saha A, and Robertson ES. Epstein-Barr virus Nuclear Antigen Family 3 in Regulation of Cellular Processes. Robertson ES Ed. Caister-Horizon Press, London England. 2009. Book Chapter.
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