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Chemotherapeutic agents can modulate the phenotype of cancer cells by changing the expression Decitabine of APM, MHC I, ICAM 1, and TAAs, making them more susceptible to immune mediated attack. These agents may also cause immunogenic death of cyst cells, ultimately causing IL 12 mediated activation of DCs, accompanied by antigen presentation and cross presentation to T cells, causing CTLs with more efficient and greater cytotoxic potential. Additionally, cytotoxic agents might have direct effects on the host immune system, including a) modulation of immune regulatory factors such as Tregs and MDSCs, b) induction of leukopenia followed closely by differential HPE of regulatory and effector immune subsets, and d) synergy with vaccine to enhance effector immune responses to multiple TAAs. Recent evidence also implies that certain chemotherapeutic regimens can reduce the tumefaction growth rate in cancer patients when combined with certain cancer vaccines. Detail by Infectious causes of cancer detail evaluations of the synergistic effects of cancer chemotherapy and immunotherapy regimens have previously been published. Many preclinical studies have explored combinations of mature vaccine systems with chemotherapy, some of which have been translated in to the clinic. Cisplatin Plus Vinorelbine Platinum alkylating agents such as oxaliplatin and cisplatin, and platinum Alkylating Agents: Oxaliplatin, Cisplatin, Cisplatin/5 FU are generally used to treat a variety of malignancies, including non-small cell lung cancer and HNSCC. The cytotoxicity of these agents is rendered through DNA crosslinking. Nevertheless, accumulating evidence shows that nontoxic concentrations of the agents can induce immune relevant changes Avagacestat in tumor cells and a few components of the immune system. These alterations may be exploited in a combined chemotherapy/vaccine regime to accomplish effective antitumor immunity. In a single study, cyst cells exposed to oxaliplatin expressed higher levels of MHC I proteins and secreted cytokines in a position to complement DC maturation, resulting in the generation of CTLs with increased cytotoxic potential. Cisplatin has also been shown to modulate tumefaction cell faculties toward a far more immunogenic phenotype. Exposure to non-toxic levels of cisplatin increased expression of practical Fas receptor on murine tumor cells, ultimately causing enhanced CTL mediated lysis. Increased sensitivity to antigenspecific CTLs was also observed in human colon carcinoma cell lines treated with cisplatin, an effect associated with increased expression of ICAM 1 and Fas. Similar have been reported with chemotherapy combinations including cisplatin. In a single study, exposure of HNSCC cell lines to cisplatin plus 5 FU triggered a synergistic boost of ICAM 1. Concurrent coverage of Lewis lung cyst cells to sublethal concentrations of cisplatin plus vinorelbine was demonstrated to modulate expression of survival genes and increase expression of Fas and MHC I molecules, causing enhanced sensitivity to CTL mediated lysis.