{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hormann A"],"funding":["NCI NIH HHS"],"pagination":["28625-28637"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6033344"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(47)"],"pubmed_abstract":["Genotype specific vulnerabilities of cancer cells constitute a promising strategy for the development of new therapeutics. Deletions of non-essential genes in tumors can generate unique vulnerabilities which could be exploited therapeutically. The <i>MTAP</i> gene is recurrently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene <i>CDKN2A</i>. Recent studies have uncovered an increased dependency of <i>MTAP</i>-deleted cancer cells on the function of a PRMT5 containing complex, including WDR77, PRMT5 and the kinase RIOK1. As RIOK1 kinase activity constitutes a potential therapeutic target, we wanted to test if <i>MTAP</i> deletion confers increased sensitivity to RIOK1 inhibition. Using CRISPR/Cas9-mediated genome engineering we generated analog sens"],"journal":["Oncotarget"],"pubmed_title":["RIOK1 kinase activity is required for cell survival irrespective of <i>MTAP</i> status."],"pmcid":["PMC6033344"],"funding_grant_id":["P01 CA013106","R01 CA174793"],"pubmed_authors":["Ehrenhofer K","Krammer T","Wohrle S","Hopfgartner B","Schweifer N","Reiser C","Bader G","Corcokovic M","Kocher T","Kraut N","Hormann A","Petronczki M","Neumuller RA","Vakoc CR","Shi J","Pearson M"],"additional_accession":[]},"is_claimable":false,"name":"RIOK1 kinase activity is required for cell survival irrespective of <i>MTAP</i> status.","description":"Genotype specific vulnerabilities of cancer cells constitute a promising strategy for the development of new therapeutics. Deletions of non-essential genes in tumors can generate unique vulnerabilities which could be exploited therapeutically. The <i>MTAP</i> gene is recurrently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene <i>CDKN2A</i>. Recent studies have uncovered an increased dependency of <i>MTAP</i>-deleted cancer cells on the function of a PRMT5 containing complex, including WDR77, PRMT5 and the kinase RIOK1. As RIOK1 kinase activity constitutes a potential therapeutic target, we wanted to test if <i>MTAP</i> deletion confers increased sensitivity to RIOK1 inhibition. Using CRISPR/Cas9-mediated genome engineering we generated analog sens","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jun","modification":"2025-04-25T21:18:46.396Z","creation":"2019-03-26T23:45:58Z"},"accession":"S-EPMC6033344","cross_references":{"pubmed":["29983885"],"doi":["10.18632/oncotarget.25586"]}}