Logo image
Systematic Analysis of Splice-Site-Creating Mutations in Cancer
Journal article   Open access   Peer reviewed

Systematic Analysis of Splice-Site-Creating Mutations in Cancer

Reyka G Jayasinghe, Song Cao, Qingsong Gao, Michael C Wendl, Nam Sy Vo, Sheila M Reynolds, Yanyan Zhao, Héctor Climente-González, Shengjie Chai, Fang Wang, …
Cell reports (Cambridge), Vol.23(1), pp.270-281.e3
04/03/2018
DOI: 10.1016/j.celrep.2018.03.052
PMCID: PMC6055527
PMID: 29617666
url
https://doi.org/10.1016/j.celrep.2018.03.052View
Published (Version of record) Open Access

Abstract

For the past decade, cancer genomic studies have focused on mutations leading to splice-site disruption, overlooking those having splice-creating potential. Here, we applied a bioinformatic tool, MiSplice, for the large-scale discovery of splice-site-creating mutations (SCMs) across 8,656 TCGA tumors. We report 1,964 originally mis-annotated mutations having clear evidence of creating alternative splice junctions. TP53 and GATA3 have 26 and 18 SCMs, respectively, and ATRX has 5 from lower-grade gliomas. Mutations in 11 genes, including PARP1, BRCA1, and BAP1, were experimentally validated for splice-site-creating function. Notably, we found that neoantigens induced by SCMs are likely several folds more immunogenic compared to missense mutations, exemplified by the recurrent GATA3 SCM. Further, high expression of PD-1 and PD-L1 was observed in tumors with SCMs, suggesting candidates for immune blockade therapy. Our work highlights the importance of integrating DNA and RNA data for understanding the functional and the clinical implications of mutations in human diseases.
Mutation BRCA1 Protein - genetics GATA3 Transcription Factor - genetics HEK293 Cells Humans Neoplasms - genetics Poly (ADP-Ribose) Polymerase-1 - genetics Programmed Cell Death 1 Receptor - genetics RNA Splice Sites Tumor Suppressor Protein p53 - genetics X-linked Nuclear Protein - genetics

Details

Metrics

Logo image