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10.1158/1940-6207.CAPR-15-0349 http://scihub22266oqcxt.onion/10.1158/1940-6207.CAPR-15-0349 C4930698!4930698!26883721     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Prev+Res+(Phila) 2016 ; 9 (7): 534-46 Nephropedia Template TP {{tp|p=26883721|t=2016. DNA hypomethylation contributes to genomic instability and intestinal cancer initiation |pdf=|usr=}}{{26883721}} gab.com Text DNA hypomethylation contributes to genomic instability and intestinal cancer initiation JO: Cancer Prev Res (Phila) http://www.kidney.de/pget.php?&tw=1&pmid=26883721 #FOAvip Intestinal cancer is a heterogeneous disease driven by genetic mutations and epigenetic changes. Approximately 80% of sporadic colorectal cancers are initiated by mutation and inactivation of the adenomatous polyposis coli (APC) gene, which results in unrestrained intestinal epithelial growth and formation of adenomas. Aberrant DNA methylation promotes cancer progression by the inactivation of tumor suppressor genes via promoter methylation. Additionally, global DNA hypomethylation is often seen before the formation of adenomas, suggesting it contributes to neoplastic transformation. Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the ApcMin/+ mouse model of intestinal cancer. However, the consequences of intestinal-epithelial specific acute hypomethylation during ApcMin/+ tumor initiation have not been reported.Using temporally controlled intestinal epithelial-specific gene ablation, we show that total loss of Dnmt1 in the ApcMin/+ mouse model of intestinal cancer causes accelerated adenoma initiation. Deletion of Dnmt1 precipitates an acute response characterized by hypomethylation of repetitive elements and genomic instability, which, surprisingly is followed by remethylation with time. Two months post-Dnmt1 ablation, mice display increased macroadenoma load, consistent with a role for Dnmt1 and DNA methylation in maintaining genomic stability. These data suggest that DNA hypomethylation plays a previously unappreciated role in intestinal adenoma initiation. Twit Text FOAVip DNA hypomethylation contributes to genomic instability and intestinal cancer initiation ????Cancer Prev Res (Phila) http://www.kidney.de/pget.php?&tw=1&pmid=26883721 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26883721 #FOAvip English Wikipedia <ref>{{Cite pmid|26883721}}</ref> DNA hypomethylation contributes to genomic instability and intestinal cancer initiation #MMPMID26883721 Sheaffer KL; Elliott EN; Kaestner KH Cancer Prev Res (Phila) 2016[Jul]; 9 (7): 534-46 PMID26883721show ga Intestinal cancer is a heterogeneous disease driven by genetic mutations and epigenetic changes. Approximately 80% of sporadic colorectal cancers are initiated by mutation and inactivation of the adenomatous polyposis coli (APC) gene, which results in unrestrained intestinal epithelial growth and formation of adenomas. Aberrant DNA methylation promotes cancer progression by the inactivation of tumor suppressor genes via promoter methylation. Additionally, global DNA hypomethylation is often seen before the formation of adenomas, suggesting it contributes to neoplastic transformation. Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the ApcMin/+ mouse model of intestinal cancer. However, the consequences of intestinal-epithelial specific acute hypomethylation during ApcMin/+ tumor initiation have not been reported.Using temporally controlled intestinal epithelial-specific gene ablation, we show that total loss of Dnmt1 in the ApcMin/+ mouse model of intestinal cancer causes accelerated adenoma initiation. Deletion of Dnmt1 precipitates an acute response characterized by hypomethylation of repetitive elements and genomic instability, which, surprisingly is followed by remethylation with time. Two months post-Dnmt1 ablation, mice display increased macroadenoma load, consistent with a role for Dnmt1 and DNA methylation in maintaining genomic stability. These data suggest that DNA hypomethylation plays a previously unappreciated role in intestinal adenoma initiation. äDNA hypomethylation contributes to genomic instability and intestinal (epmc).pdf DeepDyve Pubget Overpricing