Matthew D. Vesely

TL;DR: Current experimental and human clinical data supporting a cancer immunoediting process that provide the fundamental basis for further study of immunity to cancer and for the rational design of immunotherapies against cancer are discussed.

TL;DR: Tumour-specific mutant proteins are identified as a major class of T-cell rejection antigens following anti-PD-1 and/or anti-CTLA-4 therapy of mice bearing progressively growing sarcomas, and it is shown that therapeutic synthetic long-peptide vaccines incorporating these mutant epitopes induce tumour rejection comparably to checkpoint blockade immunotherapy.

TL;DR: It is demonstrated that the strong immunogenicity of an unedited tumour can be ascribed to expression of highly antigenic mutant proteins and shown that outgrowth of tumour cells that lack these strong antigens via a T-cell-dependent immunoselection process represents one mechanism of cancer immunoediting.

TL;DR: The data confirm the key role that MyD88 plays in promoting tumor development but also demonstrate that inflammation-induced carcinogenesis and cancer immunoediting can indeed occur in the same mouse tumor model.

TL;DR: It is demonstrated that immunoselection by CD8+ T cells of tumor variants lacking strong tumor‐specific antigens represents one mechanism by which cancer cells escape tumor immunity and points toward the future of personalized cancer therapy.