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- W4361823770 abstract "<div>Abstract<p>Melanoma often recurs after a latency period of several years, presenting a T cell–edited phenotype that reflects a role for CD8<sup>+</sup> T cells in maintaining metastatic latency. Here, we report an investigation of a patient with multiple recurrent lesions, where poorly immunogenic melanoma phenotypes were found to evolve in the presence of autologous tumor antigen–specific CD8<sup>+</sup> T cells. Melanoma cells from two of three late recurrent metastases, developing within a 6-year latency period, lacked HLA class I expression. CD8<sup>+</sup> T cell–resistant, HLA class I–negative tumor cells became clinically apparent 1.5 and 6 years into stage IV disease. Genome profiling by SNP arrays revealed that HLA class I loss in both metastases originated from a shared chromosome 15q alteration and independently acquired focal <i>B2M</i> gene deletions. A third HLA class I haplotype-deficient lesion developed in year 3 of stage IV disease that acquired resistance toward dominant CD8<sup>+</sup> T-cell clonotypes targeting stage III tumor cells. At an early stage, melanoma cells showed a dedifferentiated c-Jun<sup>high</sup>/MITF<sup>low</sup> phenotype, possibly associated with immunosuppression, which contrasted with a c-Jun<sup>low</sup>/MITF<sup>high</sup> phenotype of T cell–edited tumor cells derived from late metastases. In summary, our work shows how tumor recurrences after long-term latency evolve toward T-cell resistance by independent genetic events, as a means for immune escape and immunotherapeutic resistance. <i>Cancer Res; 76(15); 4347–58. ©2016 AACR</i>.</p></div>" @default.
- W4361823770 created "2023-04-05" @default.
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- W4361823770 date "2023-03-31" @default.
- W4361823770 modified "2023-09-26" @default.
- W4361823770 title "Data from Melanoma Lesions Independently Acquire T-cell Resistance during Metastatic Latency" @default.
- W4361823770 doi "https://doi.org/10.1158/0008-5472.c.6508620.v1" @default.
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