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TARGETING THE METABOLIC SIGNALING NETWORK FOR IMMUNE CELL LONGEVITY AND FUNCTION IN ORAL CANCER THERAPY
Author(s) -
Allevato Michael
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.696.3
Subject(s) - immune system , cancer , immunity , cancer research , immunology , t cell , cancer cell , cell , medicine , biology , genetics
Oral squamous cell carcinoma (OSCC), which includes cancer of the oral cavity and oropharynx, is a significant health issue. Despite aggressive multimodality therapies, OSCC has a poor five year survival rate (60%), which results in ~300,000 deaths each year worldwide1. OSCC is associated with human papillomavirus (HPV) infection, and abusive intake of tobacco and alcohol 2–3. OSCC evades the immune recognition and anti‐tumor immune response, by exploiting the immune system's regulatory immune suppressive mechanisms 2–3. A key mechanism of tumor immune suppression has been depicted as T‐cell exhaustion 4–7. In this case, T‐cell's effector function is restrained due to the activation of checkpoints, such as PD‐1 by its ligand PD‐L1, expressed on cancers cells, T‐cells, natural killer cells and macrophages 4–7. Immune checkpoint inhibitors have demonstrated revolutionary restoration of T‐cell mediated anti‐tumor immunity in OSCC 4–7. Despite this success, the overall response rate of these immune therapies in OSCC is only ~20 percent 4–7. New therapeutic options to prevent and treat OSCC are urgently needed. The unrestrained growth of cancer cells and the effector function of immune cells are often supported by the same metabolic pathway, namely aerobic glycolysis8. We believe that by taking advantage of the unique metabolic requirement of tumor cells and the cancer‐fighting immune cells, we can discover new insights into how such a relationship regulates anti‐tumor immunity. Our aim is to elucidate the role of immune and cancer cell metabolic properties in regulating the efficacy of the anti‐tumor response. Targeting both the metabolic signaling pathways of the OSCC tumor cells and tumor infiltrating immune cells has the potential to achieve cancer remission by both halting OSCC progression and enhancing the longevity of the anti‐tumor immune response. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .