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10.1016/j.celrep.2018.03.052 http://scihub22266oqcxt.onion/10.1016/j.celrep.2018.03.052 C6055527!6055527!29617666     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2018 ; 23 (1): 270-281.e3 Nephropedia Template TP {{tp|p=29617666|t=2018. Systematic Analysis of Splice-Site-Creating Mutations in Cancer |pdf=|usr=}}{{29617666}} gab.com Text Systematic Analysis of Splice-Site-Creating Mutations in Cancer JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29617666 #FOAvip 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. Twit Text FOAVip Systematic Analysis of Splice-Site-Creating Mutations in Cancer ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29617666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29617666 #FOAvip English Wikipedia <ref>{{Cite pmid|29617666}}</ref> Systematic Analysis of Splice-Site-Creating Mutations in Cancer #MMPMID29617666 Jayasinghe RG; Cao S; Gao Q; Wendl MC; Vo NS; Reynolds SM; Zhao Y; Climente-González H; Chai S; Wang F; Varghese R; Huang M; Liang WW; Wyczalkowski MA; Sengupta S; Li Z; Payne SH; Fenyö D; Miner JH; Walter MJ; Vincent B; Eyras E; Chen K; Shmulevich I; Chen F; Ding L Cell Rep 2018[Apr]; 23 (1): 270-281.e3 PMID29617666show ga 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. äSystematic Analysis of Splice-Site-Creating Mutations in Cancer (epmc).pdf DeepDyve Pubget Overpricing