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Interactions between cancer cells and tumor associated host immune cells initiate and maintain tumor immune tolerance which eventually predominates and mitigates the effective host immune response. The nature of the interactions between cancer cells and immune cells, and the molecular mechanisms underlying tumor immune tolerance is poorly understood. As part of its tumor promoting effects, TFG-b has a broad influence on the immune system through cross-talk with several immunomodulatory signaling pathways including toll-like receptors (TLRs) signaling. TLRs recognize non-self pathogen associated molecular patterns to trigger innate immuric responses. In addition, TLRs can also recognize several endogenous danger associated molecules including heat shock proteins, double stranded DNA, and components of extracellular matrix. Tumor microenvironments are rich in such molecules that can potentially trigger anti-tumor immune responses. Our group is interested in investigating potential TGF-b mediated mechanisms which help tumor cells to circumvent TLR-mediated anti-tumor responses and identify molecular targets that mediate these mechanisms for prevention and treatment of lung cancer.



1. Will cover the role of TGF-b signaling in cancer and fibrosis

2. Current strategies of targeting TGF-b signaling and their drawbacks

3. Some potential new strategies that we are testing

Presentation: 48 minutes