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10.1172/JCI85610 http://scihub22266oqcxt.onion/10.1172/JCI85610 C5199716!5199716!27893463     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       J+Clin+Invest ä ; 127 (1): 183-98 Nephropedia Template TP {{tp|p=27893463|t=ä. Inhibition of the GAS6/AXL pathway augments the efficacy of chemotherapies |pdf=|usr=}}{{27893463}} gab.com Text Inhibition of the GAS6/AXL pathway augments the efficacy of chemotherapies JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27893463 #FOAvip The AXL receptor and its activating ligand, growth arrest?specific 6 (GAS6), are important drivers of metastasis and therapeutic resistance in human cancers. Given the critical roles that GAS6 and AXL play in refractory disease, this signaling axis represents an attractive target for therapeutic intervention. However, the strong picomolar binding affinity between GAS6 and AXL and the promiscuity of small molecule inhibitors represent important challenges faced by current anti-AXL therapeutics. Here, we have addressed these obstacles by engineering a second-generation, high-affinity AXL decoy receptor with an apparent affinity of 93 femtomolar to GAS6. Our decoy receptor, MYD1-72, profoundly inhibited disease progression in aggressive preclinical models of human cancers and induced cell killing in leukemia cells. When directly compared with the most advanced anti-AXL small molecules in the clinic, MYD1-72 achieved superior antitumor efficacy while displaying no toxicity. Moreover, we uncovered a relationship between AXL and the cellular response to DNA damage whereby abrogation of AXL signaling leads to accumulation of the DNA-damage markers ?H2AX, 53BP1, and RAD51. MYD1-72 exploited this relationship, leading to improvements upon the therapeutic index of current standard-of-care chemotherapies in preclinical models of advanced pancreatic and ovarian cancer. Twit Text FOAVip Inhibition of the GAS6/AXL pathway augments the efficacy of chemotherapies ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27893463 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27893463 #FOAvip English Wikipedia <ref>{{Cite pmid|27893463}}</ref> Inhibition of the GAS6/AXL pathway augments the efficacy of chemotherapies #MMPMID27893463 Kariolis MS; Miao YR; Diep A; Nash SE; Olcina MM; Jiang D; Jones DS; Kapur S; Mathews II; Koong AC; Rankin EB; Cochran JR; Giaccia AJ J Clin Invest ä[]; 127 (1): 183-98 PMID27893463show ga The AXL receptor and its activating ligand, growth arrest?specific 6 (GAS6), are important drivers of metastasis and therapeutic resistance in human cancers. Given the critical roles that GAS6 and AXL play in refractory disease, this signaling axis represents an attractive target for therapeutic intervention. However, the strong picomolar binding affinity between GAS6 and AXL and the promiscuity of small molecule inhibitors represent important challenges faced by current anti-AXL therapeutics. Here, we have addressed these obstacles by engineering a second-generation, high-affinity AXL decoy receptor with an apparent affinity of 93 femtomolar to GAS6. Our decoy receptor, MYD1-72, profoundly inhibited disease progression in aggressive preclinical models of human cancers and induced cell killing in leukemia cells. When directly compared with the most advanced anti-AXL small molecules in the clinic, MYD1-72 achieved superior antitumor efficacy while displaying no toxicity. Moreover, we uncovered a relationship between AXL and the cellular response to DNA damage whereby abrogation of AXL signaling leads to accumulation of the DNA-damage markers ?H2AX, 53BP1, and RAD51. MYD1-72 exploited this relationship, leading to improvements upon the therapeutic index of current standard-of-care chemotherapies in preclinical models of advanced pancreatic and ovarian cancer. äInhibition of the GAS6/AXL pathway augments the efficacy of chemothera(epmc).pdf DeepDyve Pubget Overpricing