Journal
NATURE GENETICS
Volume 51, Issue 12, Pages 1741-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41588-019-0532-6
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Funding
- Wenner-Gren Foundation [SSv2017-005]
- Swedish Cancer Society [CAN 2015/541]
- Knut and Alice Wallenberg Foundation [KAW 2014.0057, KAW 2015.0144]
- Swedish Medical Research Council [2018-02852]
- Swedish Foundation for Strategic Research [RB13-0204]
- EMBO [STF7729]
- Cancer Research UK [C14303/A17197, A21141]
- Formas [2018-02852] Funding Source: Formas
- Swedish Foundation for Strategic Research (SSF) [RB13-0204] Funding Source: Swedish Foundation for Strategic Research (SSF)
- Vinnova [2018-02852] Funding Source: Vinnova
- Swedish Research Council [2018-02852] Funding Source: Swedish Research Council
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Somatic mutations can result in the formation of neoantigens, immunogenic peptides that are presented on the tumor cell surface by HLA molecules. These mutations are expected to be under negative selection pressure, but the extent of the resulting neoantigen depletion remains unclear. On the basis of HLA affinity predictions, we annotated the human genome for its translatability to HLA binding peptides and screened for reduced single nucleotide substitution rates in large genomic data sets from untreated cancers. Apparent neoantigen depletion signals become negligible when taking into consideration trinucleotide-based mutational signatures, owing to lack of power or to efficient immune evasion mechanisms that are active early during tumor evolution.
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