Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1111/cas.13156 http://scihub22266oqcxt.onion/10.1111/cas.13156 C5378267!5378267!28064454     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Sci 2017 ; 108 (3): 296-307 Nephropedia Template TP {{tp|p=28064454|t=2017. Hepatocyte growth factor/MET in cancer progression and biomarker discovery |pdf=|usr=}}{{28064454}} gab.com Text Hepatocyte growth factor/MET in cancer progression and biomarker discovery JO: Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28064454 #FOAvip Signaling driven by hepatocyte growth factor (HGF) and MET receptor facilitates conspicuous biological responses such as epithelial cell migration, 3?D morphogenesis, and survival. The dynamic migration and promotion of cell survival induced by MET activation are bases for invasion?metastasis and resistance, respectively, against targeted drugs in cancers. Recent studies indicated that MET in tumor?derived exosomes facilitates metastatic niche formation and metastasis in malignant melanoma. In lung cancer, gene amplification?induced MET activation and ligand?dependent MET activation in an autocrine/paracrine manner are causes for resistance to epidermal growth factor receptor tyrosine kinase inhibitors and anaplastic lymphoma kinase inhibitors. Hepatocyte growth factor secreted in the tumor microenvironment contributes to the innate and acquired resistance to RAF inhibitors. Changes in serum/plasma HGF, soluble MET (sMET), and phospho?MET have been confirmed to be associated with disease progression, metastasis, therapy response, and survival. Higher serum/plasma HGF levels are associated with therapy resistance and/or metastasis, while lower HGF levels are associated with progression?free survival and overall survival after treatment with targeted drugs in lung cancer, gastric cancer, colon cancer, and malignant melanoma. Urinary sMET levels in patients with bladder cancer are higher than those in patients without bladder cancer and associated with disease progression. Some of the multi?kinase inhibitors that target MET have received regulatory approval, whereas none of the selective HGF?MET inhibitors have shown efficacy in phase III clinical trials. Validation of the HGF?MET pathway as a critical driver in cancer development/progression and utilization of appropriate biomarkers are key to development and approval of HGF?MET inhibitors for clinical use. Twit Text FOAVip Hepatocyte growth factor/MET in cancer progression and biomarker discovery ????Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28064454 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28064454 #FOAvip English Wikipedia <ref>{{Cite pmid|28064454}}</ref> Hepatocyte growth factor/MET in cancer progression and biomarker discovery #MMPMID28064454 Matsumoto K; Umitsu M; De Silva DM; Roy A; Bottaro DP Cancer Sci 2017[Mar]; 108 (3): 296-307 PMID28064454show ga Signaling driven by hepatocyte growth factor (HGF) and MET receptor facilitates conspicuous biological responses such as epithelial cell migration, 3?D morphogenesis, and survival. The dynamic migration and promotion of cell survival induced by MET activation are bases for invasion?metastasis and resistance, respectively, against targeted drugs in cancers. Recent studies indicated that MET in tumor?derived exosomes facilitates metastatic niche formation and metastasis in malignant melanoma. In lung cancer, gene amplification?induced MET activation and ligand?dependent MET activation in an autocrine/paracrine manner are causes for resistance to epidermal growth factor receptor tyrosine kinase inhibitors and anaplastic lymphoma kinase inhibitors. Hepatocyte growth factor secreted in the tumor microenvironment contributes to the innate and acquired resistance to RAF inhibitors. Changes in serum/plasma HGF, soluble MET (sMET), and phospho?MET have been confirmed to be associated with disease progression, metastasis, therapy response, and survival. Higher serum/plasma HGF levels are associated with therapy resistance and/or metastasis, while lower HGF levels are associated with progression?free survival and overall survival after treatment with targeted drugs in lung cancer, gastric cancer, colon cancer, and malignant melanoma. Urinary sMET levels in patients with bladder cancer are higher than those in patients without bladder cancer and associated with disease progression. Some of the multi?kinase inhibitors that target MET have received regulatory approval, whereas none of the selective HGF?MET inhibitors have shown efficacy in phase III clinical trials. Validation of the HGF?MET pathway as a critical driver in cancer development/progression and utilization of appropriate biomarkers are key to development and approval of HGF?MET inhibitors for clinical use. äHepatocyte growth factor/MET in cancer progression and biomarker disco(epmc).pdf DeepDyve Pubget Overpricing