期刊
CELL
卷 171, 期 6, 页码 1272-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2017.09.050
关键词
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资金
- NSF [2015205295]
- Ramon y Cajal Fellowship [RYC-2015-18544]
- NIH [DP5-OD017937, K99/R00CA191152, U24 CA184427]
- Fred Luddy Family Foundation [U54CA209891]
MHC-I molecules expose the intracellular protein content on the cell surface, allowing T cells to detect foreign or mutated peptides. The combination of six MHC-I alleles each individual carries defines the sub-peptidome that can be effectively presented. We applied this concept to human cancer, hypothesizing that oncogenic mutations could arise in gaps in personal MHC-I presentation. To validate this hypothesis, we developed and applied a residuecentric patient presentation score to 9,176 cancer patients across 1,018 recurrent oncogenic mutations. We found that patient MHC-I genotype-based scores could predict which mutations were more likely to emerge in their tumor. Accordingly, poor presentation of a mutation across patients was correlated with higher frequency among tumors. These results support that MHC-I genotype-restricted immunoediting during tumor formation shapes the landscape of oncogenic mutations observed in clinically diagnosed tumors and paves the way for predicting personal cancer susceptibilities from knowledge of MHC-I genotype.
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