Hacker Hanna
Pancreatic cancer remains one of the most lethal malignancies, with a five-year survival rate that continues to be dismally low despite advances in medical research and treatment modalities. This is largely due to its aggressive nature, late-stage diagnosis, and resistance to conventional therapies. The complexity of pancreatic cancer lies in its unique tumor microenvironment, which fosters immune evasion and promotes tumor progression. Recent research has turned its focus toward targeting the tumor immune milieu and molecular pathways as a promising strategy to improve patient outcomes. This approach aims to dismantle the intricate network of immune suppressive cells and signaling cascades that contribute to treatment resistance and tumor growth. The Tumor Immune Microenvironment (TIME) in pancreatic cancer is characterized by an abundance of immunosuppressive cells, including regulatory T cells (Tregs), Myeloid-Derived Suppressor Cells (MDSCs), and Tumor-Associated Macrophages (TAMs). These cellular components work in concert to inhibit cytotoxic T cell responses, thereby creating a permissive environment for tumor growth. One of the major challenges in pancreatic cancer immunotherapy is the exclusion of effector T cells from the tumor site, which limits the effectiveness of immune checkpoint inhibitors (ICIs) that have shown success in other malignancies.
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Journal of Genetics and DNA Research received 3 citations as per Google Scholar report