Cancer Immunology:
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Understanding the role of immune cells in tumour progression: It is now well established that immune system has a pivotal role in cancer progression. Different immune cells, receptors, checkpoint inhibitors along with other stromal cells control the proliferation of clone of cancers cells. Presently our group is working to understand the cross talk between immune cells: Monocyte /Macrophage and breast cancer cells. Group also looking for soluble markers for breast cancer.
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Investigation of the role of immune checkpoints in Breast Cancer: TIM-3 immune checkpoint blockade, tested in a murine breast cancer model, unexpectedly accelerated tumor growth and liver metastasis. Despite increased CD8⁺ T-cell infiltration, TIM-3 inhibition activated PI3K/Akt-mTORC, EMT, and c-MYC signaling, suppressed autophagy and apoptosis, and promoted tumor proliferation and stemness, highlighting context-dependent adverse effects of TIM-3 targeting.
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Figure: Mechanistic model explaining blockade of TIM3 leads to immunosuppressive tumor microenvironment and promotes cancer cell proliferation, stemness and EMT.
Dolui B, Majumdar B, Bandyopadhyay A, Desai KV, Basu A. TIM-3 inhibition enhances breast tumor progression and metastasis: A paradoxical immune checkpoint response. J Biol Chem. Published online December 22, 2025. doi:10.1016/j.jbc.2025.111096.
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Discovery of the Surface Localization of Toll -like Receptor 3 in Cancer Cell: It has been known for long time that Innate immune receptor -TLR3, locating inside the endosomal compartment of the cells, promote apoptosis. Accordingly, ligands of TLR3 had been used as adjuvant therapy in several clinical trials. Group first time discovered that TLR3 also present on cell surface apart from endosomal compartment and induce cellular proliferation instead of apoptosis.
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Discovery of cell surface mediated MyD88 -TLR3 signalling cascade: It has been known earlier that TLR3 use TRIF mediated signalling pathway to induce apoptosis. Very recently group has discovered that when TLR3 is present on the surface of the cancer cell cells, uses different signaling pathway involving MyD88 - NFkB mediated signalling cascade to influence cellular proliferation.
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Clinical relevance of TLR2, TRR4 and TLR 9 in cervical and breast cancer: Group is pio showed the diagnostic and prognostic importance of TLR2 and TLR9 in breast and cervical cancer. It has already been showed the role of different proteases in epithelial to mesenchymal transition (EMT) for breast cancer metastasis. Accordingly, our group has reported that TLR 4 expresses in non-immune ductal epithelial cells of the breast cancer and can be responsible for the cellular invasiveness (Published several papers in reputed journals)
Figure: Schematic diagram showing mechanism of MyD88 adopter-mediated surface TLR3 signaling. The diagram illustrating how TLR3 ligand polyinosinic:polycytidylic acid [poly(I:C)] induces the recruitment of the MyD88 complex and activation of downstream signaling cascade. Downstream activation of IRAK-1, TAK1, TRAF6, and TAB1 enables translocation of NF-κB, p65 to the nucleus to induce the secretion of proinflammatory cytokine IL-6 that induces cell proliferation via cyclin D1
Singh A, Devkar R, Basu A. Myeloid Differentiation Primary Response 88-Cyclin D1 Signaling in Breast Cancer Cells Regulates Toll-Like Receptor 3-Mediated Cell Proliferation. Front Oncol. 2020;10:1780. Published 2020 Sep 18. doi:10.3389/fonc.2020.01780