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10.1158/1078-0432.CCR-13-0275 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-13-0275 C4155001!4155001!24958807     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24958807.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Cancer+Res 2014 ; 20 (17): 4442-8 Nephropedia Template TP {{tp|p=24958807|t=2014. Molecular Pathways: Targeting ETS Gene Fusions in Cancer |pdf=|usr=}}{{24958807}} gab.com Text Molecular Pathways: Targeting ETS Gene Fusions in Cancer JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24958807 #FOAvip Rearrangements, or gene fusions, involving the ETS family of transcription factors are common driving events in both prostate cancer and Ewing?s sarcoma. These rearrangements result in pathogenic expression of the ETS genes, and trigger activation of transcriptional programs enriched for invasion and other oncogenic features. While ETS gene fusions represent intriguing therapeutic targets, transcription factors, such as those comprising the ETS family, have been notoriously difficult to target. Recently, preclinical studies have demonstrated an association between ETS gene fusions and components of the DNA damage response pathway, such as poly (ADP)-ribose polymerase 1 (PARP1), the catalytic subunit of DNA protein kinase (DNA-PK), and histone deactylase 1 (HDAC1), and have suggested that ETS fusions may confer sensitivity to inhibitors of these DNA repair proteins. In this review, we discuss the role of ETS fusions in cancer, the preclinical rationale for targeting ETS fusions with inhibitors of PARP1, DNAPK, and HDAC1, as well as ongoing clinical trials targeting ETS gene fusions. Twit Text FOAVip Molecular Pathways: Targeting ETS Gene Fusions in Cancer ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24958807 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24958807 #FOAvip English Wikipedia <ref>{{Cite pmid|24958807}}</ref> Molecular Pathways: Targeting ETS Gene Fusions in Cancer #MMPMID24958807 Feng FY; Brenner JC; Hussain M; Chinnaiyan AM Clin Cancer Res 2014[Sep]; 20 (17): 4442-8 PMID24958807show ga Rearrangements, or gene fusions, involving the ETS family of transcription factors are common driving events in both prostate cancer and Ewing?s sarcoma. These rearrangements result in pathogenic expression of the ETS genes, and trigger activation of transcriptional programs enriched for invasion and other oncogenic features. While ETS gene fusions represent intriguing therapeutic targets, transcription factors, such as those comprising the ETS family, have been notoriously difficult to target. Recently, preclinical studies have demonstrated an association between ETS gene fusions and components of the DNA damage response pathway, such as poly (ADP)-ribose polymerase 1 (PARP1), the catalytic subunit of DNA protein kinase (DNA-PK), and histone deactylase 1 (HDAC1), and have suggested that ETS fusions may confer sensitivity to inhibitors of these DNA repair proteins. In this review, we discuss the role of ETS fusions in cancer, the preclinical rationale for targeting ETS fusions with inhibitors of PARP1, DNAPK, and HDAC1, as well as ongoing clinical trials targeting ETS gene fusions. äMolecular Pathways: Targeting ETS Gene Fusions in Cancer (epmc).pdf DeepDyve Pubget Overpricing