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10.1016/j.cell.2015.02.038 http://scihub22266oqcxt.onion/10.1016/j.cell.2015.02.038 C4380877!4380877!25748654     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2015 ; 160 (6): 1246-60 Nephropedia Template TP {{tp|p=25748654|t=2015. Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis |pdf=|usr=}}{{25748654}} gab.com Text Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=25748654 #FOAvip Genetic screens are powerful tools for identifying genes responsible for diverse phenotypes. Here we describe a genome-wide CRISPR-Cas9-mediated loss-of-function screen in tumor growth and metastasis. We mutagenized a non-metastatic mouse cancer cell line using a genome-scale library with 67,405 single guide RNAs (sgRNAs). The mutant cell pool rapidly generates metastases when transplanted into immunocompromised mice. Enriched sgRNAs in lung metastases and late stage primary tumors were found to target a small set of genes, suggesting specific loss-of-function mutations drive tumor growth and metastasis. Individual sgRNAs and a small pool of 624 sgRNAs targeting the top scoring genes from the primary screen dramatically accelerate metastasis. In all of these experiments, the effect of mutations on primary tumor growth positively correlates with the development of metastases. Our study demonstrates Cas9-based screening as a robust method to systematically assay gene phenotypes in cancer evolution in vivo. Twit Text FOAVip Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=25748654 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25748654 #FOAvip English Wikipedia <ref>{{Cite pmid|25748654}}</ref> Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis #MMPMID25748654 Chen S; Sanjana NE; Zheng K; Shalem O; Lee K; Shi X; Scott DA; Song J; Pan JQ; Weissleder R; Lee H; Zhang F; Sharp PA Cell 2015[Mar]; 160 (6): 1246-60 PMID25748654show ga Genetic screens are powerful tools for identifying genes responsible for diverse phenotypes. Here we describe a genome-wide CRISPR-Cas9-mediated loss-of-function screen in tumor growth and metastasis. We mutagenized a non-metastatic mouse cancer cell line using a genome-scale library with 67,405 single guide RNAs (sgRNAs). The mutant cell pool rapidly generates metastases when transplanted into immunocompromised mice. Enriched sgRNAs in lung metastases and late stage primary tumors were found to target a small set of genes, suggesting specific loss-of-function mutations drive tumor growth and metastasis. Individual sgRNAs and a small pool of 624 sgRNAs targeting the top scoring genes from the primary screen dramatically accelerate metastasis. In all of these experiments, the effect of mutations on primary tumor growth positively correlates with the development of metastases. Our study demonstrates Cas9-based screening as a robust method to systematically assay gene phenotypes in cancer evolution in vivo. äGenome-wide CRISPR screen in a mouse model of tumor growth and metasta(epmc).pdf DeepDyve Pubget Overpricing