Cancer Immunology refers to the relationship between immune function and cancer. The immunological mechanisms involved in cancer growth are highly complex and provide numerous potential points for intervention with small molecules, including extracellular enzymes, receptors and intracellular signal transduction pathways.
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Although tumor associated antigens are self-antigens, they can be immunogenic as a result of being mutated or overexpressed. This enables the immune system to raise a response to a tumor. However, cancers can evade this immune response by recruiting immunosuppressive cells, including tumor-associated macrophages (TAMs), regulatory T-cells, myeloid-derived suppressor cells and cancer-associated fibroblasts, all of which aid tumor growth. Therapeutic intervention in this system aims either to promote antitumor immune responses or to block the immunosuppressant tumor microenvironment.
A variety of proteins, known as immune checkpoint molecules, also contribute to the ability of tumors to evade the immune system. Immune checkpoint molecules, such as IDO, TDO, PD-1 and CTLA-4, are co-stimulatory or inhibitory proteins that are important in the maintenance of self-tolerance under normal physiological conditions. They are expressed by immune cells, but their expression can be dysregulated in cancers, altering the activation of T cells and/or natural killer (NK) cells and leading to antitumor immunity. Investigation of immune checkpoints should help elucidate the mechanisms by which tumors can avoid the host's immune system.
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December 3 - 7, 2016
San Francisco, CA,