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10.1038/s41467-018-04572-3 http://scihub22266oqcxt.onion/10.1038/s41467-018-04572-3 C6048166!6048166!30013058     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       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30013058|t=2018. In vivo screening identifies GATAD2B as a metastasis driver in KRAS-driven lung cancer |pdf=|usr=}}{{30013058}} gab.com Text In vivo screening identifies GATAD2B as a metastasis driver in KRAS-driven lung cancer JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30013058 #FOAvip Genetic aberrations driving pro-oncogenic and pro-metastatic activity remain an elusive target in the quest of precision oncology. To identify such drivers, we use an animal model of KRAS-mutant lung adenocarcinoma to perform an in vivo functional screen of 217 genetic aberrations selected from lung cancer genomics datasets. We identify 28 genes whose expression promoted tumor metastasis to the lung in mice. We employ two tools for examining the KRAS-dependence of genes identified from our screen: 1) a human lung cell model containing a regulatable mutant KRAS allele and 2) a lentiviral system permitting co-expression of DNA-barcoded cDNAs with Cre recombinase to activate a mutant KRAS allele in the lungs of mice. Mechanistic evaluation of one gene, GATAD2B, illuminates its role as a dual activity gene, promoting both pro-tumorigenic and pro-metastatic activities in KRAS-mutant lung cancer through interaction with c-MYC and hyperactivation of the c-MYC pathway. Twit Text FOAVip In vivo screening identifies GATAD2B as a metastasis driver in KRAS-driven lung cancer ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30013058 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30013058 #FOAvip English Wikipedia <ref>{{Cite pmid|30013058}}</ref> In vivo screening identifies GATAD2B as a metastasis driver in KRAS-driven lung cancer #MMPMID30013058 Grzeskowiak CL; Kundu ST; Mo X; Ivanov AA; Zagorodna O; Lu H; Chapple RH; Tsang YH; Moreno D; Mosqueda M; Eterovic K; Fradette JJ; Ahmad S; Chen F; Chong Z; Chen K; Creighton CJ; Fu H; Mills GB; Gibbons DL; Scott KL Nat Commun 2018[]; 9 (ä): ä PMID30013058show ga Genetic aberrations driving pro-oncogenic and pro-metastatic activity remain an elusive target in the quest of precision oncology. To identify such drivers, we use an animal model of KRAS-mutant lung adenocarcinoma to perform an in vivo functional screen of 217 genetic aberrations selected from lung cancer genomics datasets. We identify 28 genes whose expression promoted tumor metastasis to the lung in mice. We employ two tools for examining the KRAS-dependence of genes identified from our screen: 1) a human lung cell model containing a regulatable mutant KRAS allele and 2) a lentiviral system permitting co-expression of DNA-barcoded cDNAs with Cre recombinase to activate a mutant KRAS allele in the lungs of mice. Mechanistic evaluation of one gene, GATAD2B, illuminates its role as a dual activity gene, promoting both pro-tumorigenic and pro-metastatic activities in KRAS-mutant lung cancer through interaction with c-MYC and hyperactivation of the c-MYC pathway. äIn vivo screening identifies GATAD2B as a metastasis driver in KRAS-dr(epmc).pdf DeepDyve Pubget Overpricing