I teach Immunology and cell biology in undergraduate and post graduate level. I like to give some basic idea of how immunity developes in our body, how the complex interplay between various cells of immune system help us to get rid of enormously diverse pathogens. My goal is to discuss the basic concept of immunoregulation with my students but not to be merely informative.
B.Sc. Physiology (Presidency College, 2003)
M.Sc. Biochemistry (Calcutta University 2005)
Ph.D. Cancer cell signalling and apoptosis (Indian Institute of Chemical Biology, Jadavpur 2012)
I Completed my graduation in physiology honours from Presidency college, calcutta and masters from Department of Biochemistry, Calcutta University. I completed my Ph.D. from Indian institute of Chemical Biology. My doctoral work was on Cancer cell signalling and apoptosis in Chronic Myeloid Leukemia where I have shown how Reactive Oxygen Species (ROS) manipulations leads to activation of cell death in the CML cells which were resistant to Imatinib, a well known drug for the treatment of CML. The work also showed that how a small modification of a compound can activate ROS dependent cell signalling differentially in the same Imatinib resistant cells. Apart from my Ph.D work, I have also ventured on the immunological aspects of cancer and checked the Tgeulatory cell status before and after drug treatment in CML cells. This work made me highly interested in cancer immunology.
As an independent researcher, I have started my work on how ROS signaling influence the cellular response towards TRAIL, one of the prominent cytokines. Apart from this we are also working on Immune suppressor cells like Tumor associated macrophage (TAM) and Myeloid derived suppressor cells (MDSC) in Breast and lung cancer model.
Research / Administrative Experience+
Cancer remains a major challenge for humanity. Each of us has known someone who has suffered from this complex and potentially devastating family of diseases. Experience has taught us that there is not likely to be a simple single cure for cancer. At the same time, because of basic research conducted worldwide, we have nevertheless seen remarkable gains in life expectancies and cure rates for cancer.
We, in our lab, are focused on, preclinical studies on various cancer types, like leukemia, Lung cancer and breast cancer. We deals with the molecular aspects of cencer cell signaling to selectively kill cancer cells. To do this our approach is as follows:
Targeting TRAIL-Apoptosis pathway:
Triggering of tumor cell apoptosis through activation of death receptors is one of the emerging trends in cancer therapies. The tumor necrosis factor related apoptosis-inducing ligand (TRAIL), which acts through Death Receptor 4 and 5 (DR4 and DR5) induces apoptosis in tumor cells, while leaving other normal cells mostly unharmed. However, some cancer cells are resistant to apoptosis induction by TRAIL, and some TRAIL-sensitive cancer cells can become resistant to TRAIL-induced apoptosis after repeated exposure to TRAIL (acquired resistance). Furthermore, tumors are highly heterogeneous for treatment response to TRAIL-induced apoptosis and subpopulations of parental cells exist that are inherently TRAIL resistant. We are identifying the differences in signaling mechanisms between intrinsic and acquired TRAIL resistance in Chronic Myeloid Leukemia (CML) cells. To make it more relevant, we are targeting the TRAIL apoptosis pathway in Imatinib-resistant variant of CML cells as acquired resistance to Imatinib Mesylate, the tyrosine kinase inhibitor, is a major drawback of this well known drug in the treatment of CML patients.
Targeting anti-apoptotic proteins:
Defective cell death mechanisms now recognized as one of the six hallmarks of cancer. Thus, antiapoptotic proteins play central roles in cell death regulation and are capable of regulating diverse cell death mechanisms that encompass apoptosis, necrosis and autophagy. Recent literatures suggest that there might be alteration in IAP proteins and its signalling in the metastasis too. Therefore, we are targeting these IAP proteins to manipulate it in favor of cancer cell death.
Myeloid derived suppressor cells (MDSC) and cancer:
MDSC has emerged recently as one of the key molecule that play a crucial role in immne tolarance in cancer. The frequency of M-MDSCs is negatively correlated with the response to chemotherapy in breast, cervical, prostate and colorectal cancer. Myeloid-derived suppressor cells (MDSC) represent one of the major immunosuppressive populations in cancer patients. They consist of populations of polymorphonuclear (PMN-MDSC), monocytic (M-MDSC), and early precursors. We are crrently focused in investigating the role of MDSC in carcinogenesis and how ROS environment inside tumor regulate them.
Teaching / Other Experience+
cell biology and immunology.
- Cell biology - cell signaling, cancer biology, cancer cell signalling, apoptosis, cell cycle.
- Immunology - innate immunity, Adaptive Immunity, antigen processing and presentation, MHC, T cell & B cell biology, cancer immunology.
I think taking classes is not merely delivering a lecture on a topic. Therefore I encourage my students to critically think on the topic. I am very much satisfied by the way they respond and their questions really reflect their good level of intelligence.
Post Graduate Supervision+
1. Dr. Tamalika Paul
Currently two SRF are working in my lab
1. Rajdeep Roy (CSIR-JRF) SRF
2. Samraj Sinha (CSIR-LS), SRF
3. Neelesh Burman (Project trainee)
4. Kalyan Roy (dissertation student)
5. Anusree Halder (Dissertation Student)
NET JRF position is open in the lab. Interested students are requested to send me emai.
Life member of Indian Association for Cancer Research (IACR)
1. Tapadar P, Pal A, Ghosal N, Kumar B, Biswas N, Pal R. CDH1 Protein Plays a Crucial Role in Regulating TRAIL Resistance in Breast Cancer. Under revision
2. Gain C, Sarkar A, Bural S, Rakshit M, Banerjee J, Dey A, Biswas N, Kar G K, Saha A. Identification of Two Novel Thiophene Analogues as Inducers of Autophagy Mediated Cell Death in Breast Cancer Cells. Bioorganic & Medicinal Chemistry. 2021 May 1; 37: 116112
3. Nipa Nayek N, Das S, Sinha S, Biswas N, Ghosh K. Design and Synthesis of Ferrocene Tethered Pyrazolines and Pyrazoles: Photo-physical Studies, Protein Binding Behavior with Bovine Serum Albumin and Anti-proliferative Activity against MDA-MB-231 Triple Negative Breast Cancer Cells. Applied organometallic Chemistry. 2021 July; 35(7): e6248
4. Paul T, Roy R,Sinha S, Dey Sarkar R, Biswas N. ROS mediated FLIP and XIAP down-regulation involves increased ITCH expression and ERK-Akt crosstalk in Imatinib resistant Chronic Myeloid Leukemia cell line K562. Free Rad Biol & Med. 2021; 166: 265–276
5. Dey Sarkar R, Sinha S, Biswas N. Manipulation of Inflammasome: A Promising Approach Towards Immunotherapy of Lung Cancer. International Reviews of Immunology. 2021; 40(3): 171-182
6. Paul T, Banerjee A, Reddy S V B, Mahato S K, Biswas N. Hydroxychavicol sensitizes imatinib-resistant Chronic Myelogenous Leukemia cells to TRAIL-induced apoptosis by ROS-mediated IAP Downregulation. Anticancer Drugs. 2019 Feb; 30(2): 167-178.
7. Chaudhuri J, Chowdhury AA, Biswas N, Manna A, Chatterjee S, Mukherjee T, Chaudhuri U, Jaisankar P, Bandyopadhyay S. Superoxide activates mTOR-eIF4E-Bax route to induce enhanced apoptosis in leukemic cells. Apoptosis. 2014 Jan; 19(1): 135-48
8. Chowdhury AA, Chaudhuri J, Biswas N, Manna A, Chatterjee S, Mahato S K, Chaudhuri U, Jaisankar J, Bandyopadhyay S. Synergistic apoptosis of CML cells by buthionine sulfoximine and hydroxychavicol correlates with activation of AIF and GSH-ROS-JNK-ERK-iNOS pathway. PLOS One. 2013 Sep; 8(9):e73672. doi: 10.1371/journal.pone.0073672.
9. Bhattacharjya S, Nath S, Ghose J, Maiti G P, Biswas N, Bhattacharyya N P, Bandyopadhyay S, Panda C K and Roychoudhury S. “miR-125b promotes cell death by targeting Spindle Assembly Checkpoint gene MAD1 and modulating mitotic progression”. Cell Death Differ. 2013 Mar; 20(3):430-42.
10. Biswas N, Mahato S K, Chowdhury A A, Chaudhuri J, Manna A, Vinayagam J, Chatterjee S, Jaisankar P, Chaudhuri U, Bandyopadhyay S. “ICB3E induces iNOS expression by ROS-dependent JNK and Erk activation for apoptosis of leukemic cells”. Apoptosis. 2012 Jun; 17(6): 612-26
11. Chakraborty J B*, Mahato S K, Joshi K, Shinde V, Rakshit S, Biswas N* (* equal contribution), Choudhury I M, Mandal L, Ganguly D, Chowdhury A A, Chaudhuri J, Paul K, Pal B C, Vinayagam J, Pal B C, Manna A, Jaisankar P, Chaudhuri U, Konar A, Roy S, Bandyopadhyay S. “Hydroxychavicol, a Piper betle leaf component, induces apoptosis of CML cells by mitochondrial ROS-dependent JNK and eNOS activation and overrides imatinib resistance”. Cancer Sci. 2012 Jan; 103(1):88-99
12. Rakshit S, Mandal L, Pal B C, Bagchi J, Biswas N, Chaudhuri J, Chowdhury A A, Manna A, Chaudhuri U, Konar A, Mukherjee T, Jaisankar P, Bandyopadhyay S. “Involvement of ROS in chlorogenic acid-induced apoptosis of Bcr-Abl+ CML cells”. Biochem Pharmacol. 2010 Dec 1; 80(11):1662-75.
13. Rakshit S, Bagchi J, Mandal L, Paul K, Ganguly D, Bhattacharjee S, Ghosh M, Biswas N, Chaudhuri U, Bandyopadhyay S. “N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide”. Apoptosis. 2009 Mar; 14(3):298-308.
86/1 College Street, Kolkata - 700073,
West Bengal, India
Email: nabendu.biotechnology at presiuniv.ac.in
alternate E-mail: nabendubiswas.81 at gmail.com
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