Abstract
Meeting abstracts Genomic analyses have shown that melanoma patients have hundreds to thousands of non-synonymous mutations including unique tumor associated antigens (TAA) that can be recognized by their immune systems. The efficacy of anti-checkpoint monoclonal antibodies provides further proof
Highlights
Phase III randomized, double-blinded, placebocontrolled multicenter trial of melapuldencil-t: autologous dendritic cells loaded with irradiated autologous tumor cells in gm-csf in patients with metastatic melanoma
Genomic analyses have shown that melanoma patients have hundreds to thousands of non-synonymous mutations including unique tumor associated antigens (TAA) that can be recognized by their immune systems
The efficacy of anti-checkpoint monoclonal antibodies provides further proof that host recognition of TAA exists, but many patients do not benefit from such therapy, perhaps because they lack sufficient TAA recognition
Summary
Genomic analyses have shown that melanoma patients have hundreds to thousands of non-synonymous mutations including unique tumor associated antigens (TAA) that can be recognized by their immune systems. Phase III randomized, double-blinded, placebocontrolled multicenter trial of melapuldencil-t: autologous dendritic cells loaded with irradiated autologous tumor cells (dc-tc) in gm-csf in patients with metastatic melanoma Background Genomic analyses have shown that melanoma patients have hundreds to thousands of non-synonymous mutations including unique tumor associated antigens (TAA) that can be recognized by their immune systems. The best source of TAA may be autologous tumor cells that self-renew and proliferate in tissue culture (patient specific tumor stem cells).
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