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10.1093/carcin/bgw016 http://scihub22266oqcxt.onion/10.1093/carcin/bgw016 C5006212!5006212 !26905589     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26905589 &cmd=llinks): Failed to open stream: HTTP request failed! 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Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma |pdf=|usr=}}{{26905589 }} gab.com Text Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma JO: Carcinogenesis http://www.kidney.de/pget.php?&tw=1&pmid=26905589 #FOAvip Hepatocellular carcinoma (HCC) is a heterogeneous disease in which tumor subtypes can be identified based on the presence of adult liver progenitor cells. Having previously identified the mTOR pathway as critical to progenitor cell proliferation in a model of liver injury, we investigated the temporal activation of mTOR signaling in a rat model of hepatic carcinogenesis. The model employed chemical carcinogens and partial hepatectomy to induce progenitor marker-positive HCC. Immunohistochemical staining for phosphorylated ribosomal protein S6 indicated robust mTOR complex 1 (mTORC1) activity in early preneoplastic lesions that peaked during the first week and waned over the subsequent 10 days. Continuous administration of rapamycin by subcutaneous pellet for 70 days markedly reduced the development of focal lesions, but resulted in activation of the PI3K signaling pathway. To test the hypothesis that early mTORC1 activation was critical to the development and progression of preneoplastic foci, we limited rapamycin administration to the 3-week period at the start of the protocol. Focal lesion burden was reduced to a degree indistinguishable from that seen with continuous administration. Short-term rapamycin did not result in the activation of PI3K or mTORC2 pathways. Microarray analysis revealed a persistent effect of short-term mTORC1 inhibition on gene expression that resulted in a genetic signature reminiscent of normal liver. We conclude that mTORC1 activation during the early stages of hepatic carcinogenesis may be critical due to the development of preneoplastic focal lesions in progenitor marker-positive HCC. mTORC1 inhibition may represent an effective chemopreventive strategy for this form of liver cancer. Twit Text FOAVip Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma ????Carcinogenesis http://www.kidney.de/pget.php?&tw=1&pmid=26905589 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26905589 #FOAvip English Wikipedia <ref>{{Cite pmid|26905589 }}</ref> Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma #MMPMID26905589 Francois-Vaughan H ; Adebayo AO ; Brilliant KE ; Parry NMA ; Gruppuso PA ; Sanders JA Carcinogenesis 2016[Apr]; 37 (4 ): 408-419 PMID26905589 show ga Hepatocellular carcinoma (HCC) is a heterogeneous disease in which tumor subtypes can be identified based on the presence of adult liver progenitor cells. Having previously identified the mTOR pathway as critical to progenitor cell proliferation in a model of liver injury, we investigated the temporal activation of mTOR signaling in a rat model of hepatic carcinogenesis. The model employed chemical carcinogens and partial hepatectomy to induce progenitor marker-positive HCC. Immunohistochemical staining for phosphorylated ribosomal protein S6 indicated robust mTOR complex 1 (mTORC1) activity in early preneoplastic lesions that peaked during the first week and waned over the subsequent 10 days. Continuous administration of rapamycin by subcutaneous pellet for 70 days markedly reduced the development of focal lesions, but resulted in activation of the PI3K signaling pathway. To test the hypothesis that early mTORC1 activation was critical to the development and progression of preneoplastic foci, we limited rapamycin administration to the 3-week period at the start of the protocol. Focal lesion burden was reduced to a degree indistinguishable from that seen with continuous administration. Short-term rapamycin did not result in the activation of PI3K or mTORC2 pathways. Microarray analysis revealed a persistent effect of short-term mTORC1 inhibition on gene expression that resulted in a genetic signature reminiscent of normal liver. We conclude that mTORC1 activation during the early stages of hepatic carcinogenesis may be critical due to the development of preneoplastic focal lesions in progenitor marker-positive HCC. mTORC1 inhibition may represent an effective chemopreventive strategy for this form of liver cancer. |*Gene Expression [MESH] |Animals [MESH] |Carcinoma, Hepatocellular/*surgery [MESH] |Disease Progression [MESH] |Liver Neoplasms/*surgery [MESH] |Male [MESH] |Rats [MESH] |Rats, Inbred F344 [MESH]Persistent effect of mTOR inhibition on preneoplastic foci progression(epmc).pdf DeepDyve Pubget Overpricing