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• W2510426677 abstract "In carcinogen-driven cancers, a high mutational burden results in neoepitopes that can be recognized immunologically. Such carcinogen-induced tumors may evade this immune response through immunoediting, whereby tumors adapt to immune pressure and escape T cell-mediated killing. Many tumors lack a high neoepitope burden, and it remains unclear whether immunoediting occurs in such cases. Here, we evaluated T cell immunity in an autochthonous mouse model of pancreatic cancer and found a low mutational burden, absence of predicted neoepitopes derived from tumor mutations, and resistance to checkpoint immunotherapy. Spontaneous tumor progression was identical in the presence or absence of T cells. Moreover, tumors arising in T cell-depleted mice grew unchecked in immune-competent hosts. However, introduction of the neoantigen ovalbumin (OVA) led to tumor rejection and T cell memory, but this did not occur in OVA immune-tolerant mice. Thus, immunoediting does not occur in this mouse model - a likely consequence, not a cause, of absent neoepitopes. Because many human tumors also have a low missense mutational load and minimal neoepitope burden, our findings have clinical implications for the design of immunotherapy for patients with such tumors." @default.
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• W2510426677 date "2016-09-08" @default.
• W2510426677 modified "2023-10-16" @default.
• W2510426677 title "Lack of immunoediting in murine pancreatic cancer reversed with neoantigen" @default.
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• W2510426677 doi "https://doi.org/10.1172/jci.insight.88328" @default.
• W2510426677 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5026128" @default.
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• W2510426677 hasPublicationYear "2016" @default.
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