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10.1016/j.trecan.2015.10.001 http://scihub22266oqcxt.onion/10.1016/j.trecan.2015.10.001 C4743050!4743050!26858988     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26858988&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Trends+Cancer 2015 ; 1 (3): 183-98 Nephropedia Template TP {{tp|p=26858988|t=2015. Targeting RAS-mutant cancers: is ERK the key?|pdf=|usr=}}{{26858988}} gab.com Text Targeting RAS-mutant cancers: is ERK the key JO: Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26858988 #FOAvip The three RAS genes comprise the most frequently mutated oncogene family in cancer. With significant and compelling evidence that continued function of mutant RAS is required for tumor maintenance, it is widely accepted that effective anti-RAS therapy will have a significant impact on cancer growth and patient survival. However, despite more than three decades of intense research and pharmaceutical industry efforts, a clinically effective anti-RAS drug has yet to be developed. With the recent renewed interest in targeting RAS, exciting and promising progress has been made. In this review, we discuss the prospects and challenges of drugging oncogenic RAS. In particular we focus on new inhibitors of RAS effector signaling and the ERK mitogen-activated protein kinase cascade. Twit Text FOAVip Targeting RAS-mutant cancers: is ERK the key ????Trends Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26858988 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26858988 #FOAvip English Wikipedia <ref>{{Cite pmid|26858988}}</ref> Targeting RAS-mutant cancers: is ERK the key? #MMPMID26858988 Ryan MB; Der CJ; Wang-Gillam A; Cox AD Trends Cancer 2015[Nov]; 1 (3): 183-98 PMID26858988show ga The three RAS genes comprise the most frequently mutated oncogene family in cancer. With significant and compelling evidence that continued function of mutant RAS is required for tumor maintenance, it is widely accepted that effective anti-RAS therapy will have a significant impact on cancer growth and patient survival. However, despite more than three decades of intense research and pharmaceutical industry efforts, a clinically effective anti-RAS drug has yet to be developed. With the recent renewed interest in targeting RAS, exciting and promising progress has been made. In this review, we discuss the prospects and challenges of drugging oncogenic RAS. In particular we focus on new inhibitors of RAS effector signaling and the ERK mitogen-activated protein kinase cascade. äTargeting RAS-mutant cancers: is ERK the key?(epmc).pdf DeepDyve Pubget Overpricing