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• W2924003728 abstract "A central role for immunotherapy in the management of head and neck cancer is emerging as a result of the elevated inflammatory state of its microenvironment. Head and neck cancer hijacks numerous molecular and cellular immunomodulatory pathways to evade recognition and eradication by host immunity. To date, only transient responses to single-agent immune checkpoint blockade have been observed in head and neck cancer or durable response only in a minority of patient subsets. Combination treatment strategies targeting multiple immunologic pathways in conjunction with traditional approaches such as radiation or surgery may induce more robust and durable responses to immunotherapy in head and neck cancer. Head and neck cancer is disfiguring and deadly, and contemporary treatment has fallen short in terms of morbidity and mortality. The rich immune infiltrate within these tumors designates them as prime candidates for immunotherapy and success with these drugs has been documented for recurrent and metastatic head and neck cancer. Still, single-agent immunotherapy has generated either only transient responses or durable response in only a minority subset of patients. Mapping the immune escape mechanisms enacted by head and neck cancer within the tumor microenvironment allows for rational design of strategies to overcome this tolerance. We outline the immune pathway derangements within the head and neck cancer microenvironment and discuss combination treatment strategies to overcome the limitations of immunologic monotherapy. Head and neck cancer is disfiguring and deadly, and contemporary treatment has fallen short in terms of morbidity and mortality. The rich immune infiltrate within these tumors designates them as prime candidates for immunotherapy and success with these drugs has been documented for recurrent and metastatic head and neck cancer. Still, single-agent immunotherapy has generated either only transient responses or durable response in only a minority subset of patients. Mapping the immune escape mechanisms enacted by head and neck cancer within the tumor microenvironment allows for rational design of strategies to overcome this tolerance. We outline the immune pathway derangements within the head and neck cancer microenvironment and discuss combination treatment strategies to overcome the limitations of immunologic monotherapy. a treatment strategy in which tumor-specific T cells are expanded ex vivo and then returned to the patient to kill tumor cells and generate long-lasting memory. a cell that processes a protein antigen and presents it to T cells in the context of MHC molecules. nonmalignant stromal cells within the tumor microenvironment with a largely tumor-supporting phenotype. recombinant T cell receptor designed to recognize tumor antigen and rapidly generate tumor-targeted T cells. classic immune checkpoint molecule which competes with CD28 for CD80/86 binding and causes immunosuppression; target of the monoclonal antibodies ipilimumab and tremelimumab. a subset of APCs that are uniquely suited for antigen presentation. the gene complex encoding the MHC. HLAs DP, DM, DO, DQ, and DR encode MHC class II. sexually transmitted virus with many subtypes, type 16 and 18 were recently associated with increasing rates of oropharyngeal cancer. molecules expressed on the surface of APCs that function to present extracellular antigen to target cells. They play a prominent role in presentation of tumor neoantigen to immune cells. an immature subset of heterogeneous myeloid cells with potent immunosuppressive properties. cytotoxic immune cell of the innate immune system, the effector arm of antibody-dependent cell-mediated cytotoxicity. protein product expressed by tumor cells that is distinct from any host protein and serves as a unique target for the adaptive immune response to cancer. classic immune checkpoint molecule which binds with PD-L1/L2, causing immunosuppression via reduced TCR signaling, reduced cytokine production, reduced target cell lysis, altered lymphocyte motility, and metabolic reprogramming, in addition to inducing differentiation to Tregs; target of the monoclonal antibodies nivolumab and pembrolizumab. reappearance of a previously treated cancer at the primary site, locoregional draining lymph nodes, or distant end-organs that requires new treatment. subset of T cells with potent immunosuppressive properties, characterized by FoxP3 and CD25 expression. class of immune cells present in the microenvironment with variable antitumor (M1) or tumor-promoting (M2) phenotype. surface molecule on T cells responsible for recognizing antigen in the context of MHC. lymphocytes that have migrated into the TME. the physical milieu in which a tumor exists, including tumor cells, blood vessels, immune cells, stromal cells, extracellular matrix, and signaling molecules." @default.
• W2924003728 created "2019-04-01" @default.
• W2924003728 creator A5000113361 @default.
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• W2924003728 creator A5084155127 @default.
• W2924003728 date "2019-04-01" @default.
• W2924003728 modified "2023-10-18" @default.
• W2924003728 title "Immune Evasion by Head and Neck Cancer: Foundations for Combination Therapy" @default.
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