Rationale for Immune checkpoint therapy in triple-negative breast cancer Sample Clauses

Rationale for Immune checkpoint therapy in triple-negative breast cancer. The use of immune checkpoint therapy has recently joined the other modalities of therapy as one of the pillars of modern cancer treatment. The development of agents that target immune checkpoints has dramatically altered treatment in many difficult to treat cancers such as lung cancers, melanoma, specific subpopulations of colorectal cancer, bladder cancer, chemo- refractory Hodgkin's disease, and others. Immune surveillance in controlling outgrowth of neoplastic transformation has been recognized for decades (Disis 2010). Accumulating evidence shows a correlation between tumor-infiltrating lymphocytes (TILs) in cancer tissue and favorable prognosis in various malignancies (Dong 2002; Xxxxxx 2002; Xxxxx 2003; Francisco 2010; Xxxxxxxx 2007). The magnitude of lymphocytic infiltration is not the only factor modulating disease progression as the phenotype of the lymphocytic infiltrate may be most important (Xxxxxxx 2016). In particular, the presence of CD8+ T-cells and the ratio of the CD8+ effector T- cells/FoxP3+ regulatory T-cells seems to correlate with improved prognosis and long-term survival in many solid tumors. In breast cancer there is variation in the incidence and magnitude of TILs. TNBC demonstrates the highest incidence of TILs. CD8+ T-cell infiltrates indicative of type 1immunity were found in 60% of TNBC. There are many factors that may contribute to the magnitude of TILs in TNBC. For example, hormone receptor negative cancers have been shown to have more genomic instability and more chromosomal instability than hormone-receptor- positive tumors (Disis 2015; Xxxxxxxx 2012). A greater number of mutations raise the chance that mutated protein sequences will be expressed and potentially be recognized as novel antigens by the immune system. In addition, PD-L1 is expressed on many cancer and immune cells and in doing so plays an important role in disrupting cancer surveillance and maintaining an immunosuppressive microenvironment. A recent study of 43 breast tumors demonstrated that 89% of PD-L1+ cancers were associated with increased TIL infiltration compared with 24% of PD-L1− tumors. The PD-L1 receptor-ligand interaction is a major pathway hijacked by tumors to suppress immune control. The normal function of PD-1, expressed on the cell surface of activated T-cells under healthy conditions, is to down-modulate unwanted or excessive immune responses, including autoimmune reactions. Xxxxxxxx XX-0 pathway invigorated the immune system, for example by...
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