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10.1038/nature23477 http://scihub22266oqcxt.onion/10.1038/nature23477 C5870757!5870757!28783722     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2017 ; 548 (7669): 537-42 Nephropedia Template TP {{tp|p=28783722|t=2017. Identification of essential genes for cancer immunotherapy |pdf=|usr=}}{{28783722}} gab.com Text Identification of essential genes for cancer immunotherapy JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=28783722 #FOAvip Somatic gene mutations can alter the vulnerability of cancer cells to T cell-based immunotherapies. To mimic loss-of-function mutations involved in resistance to these therapies, we perturbed genes in tumour cells using a genome-scale CRISPR-Cas9 library comprising ~123,000 single guide RNAs, and profiled genes whose loss in tumour cells impaired the effector function of CD8+ T cells (EFT). We correlated these genes with cytolytic activity in ~11,000 patient tumours from The Cancer Genome Atlas. Among the genes validated using different cancer cell lines and antigens, we identified multiple loss-of-function mutations in APLNR, encoding Apelin receptor, in patient tumours refractory to immunotherapy. We show that APLNR interacts with JAK1, modulating interferon-gamma responses in tumours, and its functional loss reduces the efficacy of adoptive cell transfer and checkpoint blockade immunotherapies in murine models. Collectively, our study links the loss of essential genes for EFT with the resistance or non-responsiveness of cancer to immunotherapies. Twit Text FOAVip Identification of essential genes for cancer immunotherapy ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=28783722 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28783722 #FOAvip English Wikipedia <ref>{{Cite pmid|28783722}}</ref> Identification of essential genes for cancer immunotherapy #MMPMID28783722 Patel SJ; Sanjana NE; Kishton RJ; Eidizadeh A; Vodnala SK; Cam M; Gartner JJ; Jia L; Steinberg SM; Yamamoto TN; Merchant AS; Mehta GU; Chichura A; Shalem O; Tran E; Eil R; Sukumar M; Guijarro EP; Day CP; Robbins P; Feldman S; Merlino G; Zhang F; Restifo NP Nature 2017[Aug]; 548 (7669): 537-42 PMID28783722show ga Somatic gene mutations can alter the vulnerability of cancer cells to T cell-based immunotherapies. To mimic loss-of-function mutations involved in resistance to these therapies, we perturbed genes in tumour cells using a genome-scale CRISPR-Cas9 library comprising ~123,000 single guide RNAs, and profiled genes whose loss in tumour cells impaired the effector function of CD8+ T cells (EFT). We correlated these genes with cytolytic activity in ~11,000 patient tumours from The Cancer Genome Atlas. Among the genes validated using different cancer cell lines and antigens, we identified multiple loss-of-function mutations in APLNR, encoding Apelin receptor, in patient tumours refractory to immunotherapy. We show that APLNR interacts with JAK1, modulating interferon-gamma responses in tumours, and its functional loss reduces the efficacy of adoptive cell transfer and checkpoint blockade immunotherapies in murine models. Collectively, our study links the loss of essential genes for EFT with the resistance or non-responsiveness of cancer to immunotherapies. äIdentification of essential genes for cancer immunotherapy (epmc).pdf DeepDyve Pubget Overpricing