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10.1158/1940-6207.CAPR-13-0444-T http://scihub22266oqcxt.onion/10.1158/1940-6207.CAPR-13-0444-T C4082466!4082466!24778325     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24778325&cmd=llinks): Failed to open stream: HTTP request failed! 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Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/?-catenin signaling pathway |pdf=|usr=}}{{24778325}} gab.com Text Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/ -catenin signaling pathway JO: Cancer Prev Res (Phila) http://www.kidney.de/pget.php?&tw=1&pmid=24778325 #FOAvip Although alcohol effects within the liver have been extensively studied, the complex mechanisms by which alcohol causes liver cancer are not well understood. It has been suggested that ethanol (EtOH) metabolism promotes tumor growth by increasing hepatocyte proliferation. In this study, we developed a mouse model of tumor promotion by chronic EtOH consumption in which EtOH feeding began 46 days post-injection of the chemical carcinogen diethylnitrosamine (DEN) and continued for 16 weeks. With a final EtOH concentration of 28% of total calories, we observed a significant increase in the total number of preneoplastic foci and liver tumors per mouse in the EtOH+DEN group compared to corresponding pair-fed (PF)+DEN and chow+DEN control groups. We also observed a 4-fold increase in hepatocyte proliferation (p<0.05) and increased cytoplasmic staining of active-?-catenin in non-tumor liver sections from EtOH+DEN mice compared to PF+DEN controls. In a rat model of alcohol-induced liver disease, we found increased hepatocyte proliferation (p<0.05); depletion of retinol and retinoic acid stores (p<0.05); increased expression of cytosolic and nuclear expression of ?-catenin (p<0.05) and phosphorylated-glycogen synthase kinase 3 ? (p-GSK3?, p<0.05; significant up-regulation in Wnt7a mRNA expression; and increased expression of several ?-catenin targets, including, glutamine synthetase (GS), cyclin D1, Wnt1 inducible signaling pathway protein (WISP1), and matrix metalloproteinase-7 (MMP7), p<0.05. These data suggest that chronic EtOH consumption activates the Wnt/?-catenin signaling pathways to increase hepatocyte proliferation, thus promoting tumorigenesis following an initiating insult to the liver. Twit Text FOAVip Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/ -catenin signaling pathway ????Cancer Prev Res (Phila) http://www.kidney.de/pget.php?&tw=1&pmid=24778325 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24778325 #FOAvip English Wikipedia <ref>{{Cite pmid|24778325}}</ref> Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/?-catenin signaling pathway #MMPMID24778325 Mercer KE; Hennings L; Sharma N; Lai K; Cleves MA; Wynne RA; Badger TM; Ronis MJ Cancer Prev Res (Phila) 2014[Jul]; 7 (7): 675-85 PMID24778325show ga Although alcohol effects within the liver have been extensively studied, the complex mechanisms by which alcohol causes liver cancer are not well understood. It has been suggested that ethanol (EtOH) metabolism promotes tumor growth by increasing hepatocyte proliferation. In this study, we developed a mouse model of tumor promotion by chronic EtOH consumption in which EtOH feeding began 46 days post-injection of the chemical carcinogen diethylnitrosamine (DEN) and continued for 16 weeks. With a final EtOH concentration of 28% of total calories, we observed a significant increase in the total number of preneoplastic foci and liver tumors per mouse in the EtOH+DEN group compared to corresponding pair-fed (PF)+DEN and chow+DEN control groups. We also observed a 4-fold increase in hepatocyte proliferation (p<0.05) and increased cytoplasmic staining of active-?-catenin in non-tumor liver sections from EtOH+DEN mice compared to PF+DEN controls. In a rat model of alcohol-induced liver disease, we found increased hepatocyte proliferation (p<0.05); depletion of retinol and retinoic acid stores (p<0.05); increased expression of cytosolic and nuclear expression of ?-catenin (p<0.05) and phosphorylated-glycogen synthase kinase 3 ? (p-GSK3?, p<0.05; significant up-regulation in Wnt7a mRNA expression; and increased expression of several ?-catenin targets, including, glutamine synthetase (GS), cyclin D1, Wnt1 inducible signaling pathway protein (WISP1), and matrix metalloproteinase-7 (MMP7), p<0.05. These data suggest that chronic EtOH consumption activates the Wnt/?-catenin signaling pathways to increase hepatocyte proliferation, thus promoting tumorigenesis following an initiating insult to the liver. äAlcohol consumption promotes diethylnitrosamine-induced hepatocarcinog(epmc).pdf DeepDyve Pubget Overpricing