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The article discusses the recent approval of a cell therapy called lifileucel for the treatment of melanoma. Lifileucel uses a patient's own tumor-infiltrating T lymphocytes (TILs) to target and treat melanoma. This approval marks a significant advancement in cancer treatment, as it is the first cell therapy to be approved for a solid tumor. Clinical trials have shown that lifileucel has a response rate between 30% and 50%, making it a valuable addition to the treatment options for melanoma patients who do not respond to other therapies. However, there are still challenges to overcome, such as the need for a surgical procedure to isolate TILs and the exclusion of patients with certain conditions. Ongoing research is focused on improving the effectiveness and specificity of T-cell therapies for melanoma. [Extracted from the article]

Human melanomas exhibit relatively high somatic mutation burden compared to other malignancies. These somatic mutations may produce neoantigens that are recognized by the immune system, leading to an antitumor response. By irradiating a parental mouse melanoma cell line carrying three driver mutations with UVB and expanding a single-cell clone, we generated a mutagenized model that exhibits high somatic mutation burden. When inoculated at low cell numbers in immunocompetent C57 BL/6J mice, YUMMER1.7 (Yale University Mouse Melanoma Exposed to Radiation) regresses after a brief period of growth. This regression phenotype is dependent on T cells as YUMMER1.7 tumors grow significantly faster in immunodeficient Rag1−/− mice and C57 BL/6J mice depleted of CD4 and CD8 T cells. Interestingly, regression can be overcome by injecting higher cell numbers of YUMMER1.7, which results in tumors that grow without effective rejection. Mice that have previously rejected YUMMER1.7 tumors develop immunity against higher doses of YUMMER1.7 tumor challenge. In addition, escaping YUMMER1.7 tumors are sensitive to anti- CTLA-4 and anti- PD-1 therapy, establishing a new model for the evaluation of immune checkpoint inhibition and antitumor immune responses. [ABSTRACT FROM AUTHOR]