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10.1158/1541-7786.MCR-15-0130 http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-15-0130 C4573363!4573363!26078295     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cancer+Res 2015 ; 13 (9): 1306-15 Nephropedia Template TP {{tp|p=26078295|t=2015. Patient mutation directed shRNA screen uncovers novel bladder tumor growth suppressors |pdf=|usr=}}{{26078295}} gab.com Text Patient mutation directed shRNA screen uncovers novel bladder tumor growth suppressors JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26078295 #FOAvip Next generation sequencing (NGS) of human bladder cancer has revealed many gene alterations compared with normal tissue, with most being predicted to be ?loss of function?. However, given the high number of alterations, evaluating the functional impact of each is impractical. Here we develop and use a high-throughput, in vivo strategy to determine which alterations are loss of function in tumor growth suppressors. Genes reported as altered by NGS in bladder cancer patients were bioinformatically processed by MutationTaster and MutationAssessor, with 283 predicted as loss of function. A shRNA lentiviral library targeting these genes was transduced into T24 cells, a non-tumorigenic human bladder cancer cell line, followed by injection into mice. Tumors that arose were sequenced and the dominant shRNA constructs were found to target IQGAP1, SAMD9L, PCIF1, MED1 and KATNAL1 genes. In vitro validation experiments revealed that shRNA molecules directed at IQGAP1 showed the most profound increase in anchorage-independent growth of T24 cells. The clinical relevance of IQGAP1 as a tumor growth suppressor is supported by the finding that its expression is lower in bladder cancer compared with benign patient urothelium in multiple independent datasets. Lower IQGAP1 protein expression associated with higher tumor grade and decreased patient survival. Finally, depletion of IQGAP1 leads to increased TGFBR2 with TGF? signaling, explaining in part how reduced IQGAP1 promotes tumor growth. These findings suggest IQGAP1 is a bladder tumor growth suppressor that works via modulating TGF? signaling and is a potentially clinically useful biomarker.Implications: This study used gene mutation information from patient-derived bladder tumor specimens to inform the development of a screen used to identify novel tumor growth suppressors. This included identification of the protein IQGAP1 as a potent bladder cancer growth suppressor. Twit Text FOAVip Patient mutation directed shRNA screen uncovers novel bladder tumor growth suppressors ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26078295 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26078295 #FOAvip English Wikipedia <ref>{{Cite pmid|26078295}}</ref> Patient mutation directed shRNA screen uncovers novel bladder tumor growth suppressors #MMPMID26078295 Hensel J; Duex JE; Owens C; Dancik GM; Edwards MG; Frierson HF; Theodorescu D Mol Cancer Res 2015[Sep]; 13 (9): 1306-15 PMID26078295show ga Next generation sequencing (NGS) of human bladder cancer has revealed many gene alterations compared with normal tissue, with most being predicted to be ?loss of function?. However, given the high number of alterations, evaluating the functional impact of each is impractical. Here we develop and use a high-throughput, in vivo strategy to determine which alterations are loss of function in tumor growth suppressors. Genes reported as altered by NGS in bladder cancer patients were bioinformatically processed by MutationTaster and MutationAssessor, with 283 predicted as loss of function. A shRNA lentiviral library targeting these genes was transduced into T24 cells, a non-tumorigenic human bladder cancer cell line, followed by injection into mice. Tumors that arose were sequenced and the dominant shRNA constructs were found to target IQGAP1, SAMD9L, PCIF1, MED1 and KATNAL1 genes. In vitro validation experiments revealed that shRNA molecules directed at IQGAP1 showed the most profound increase in anchorage-independent growth of T24 cells. The clinical relevance of IQGAP1 as a tumor growth suppressor is supported by the finding that its expression is lower in bladder cancer compared with benign patient urothelium in multiple independent datasets. Lower IQGAP1 protein expression associated with higher tumor grade and decreased patient survival. Finally, depletion of IQGAP1 leads to increased TGFBR2 with TGF? signaling, explaining in part how reduced IQGAP1 promotes tumor growth. These findings suggest IQGAP1 is a bladder tumor growth suppressor that works via modulating TGF? signaling and is a potentially clinically useful biomarker.Implications: This study used gene mutation information from patient-derived bladder tumor specimens to inform the development of a screen used to identify novel tumor growth suppressors. This included identification of the protein IQGAP1 as a potent bladder cancer growth suppressor. äPatient mutation directed shRNA screen uncovers novel bladder tumor gr(epmc).pdf DeepDyve Pubget Overpricing