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10.1038/srep44089 http://scihub22266oqcxt.onion/10.1038/srep44089 C5343453!5343453!28276478     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28276478|t=2017. B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers |pdf=|usr=}}{{28276478}} gab.com Text B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28276478 #FOAvip The key signature of cancer genomes is the accumulation of DNA mutations, the most abundant of which is the cytosine-to-thymine (C-to-T) transition that results from cytosine deamination. Analysis of The Cancer Genome Atlas (TCGA) database has demonstrated that this transition is caused mainly by upregulation of the cytosine deaminase APOBEC3B (A3B), but the mechanism has not been completely characterized. We found that B-Myb (encoded by MYBL2) binds the A3B promoter, causing transactivation, and this is responsible for the C-to-T transitions and DNA hypermutation in breast cancer cells. Analysis of TCGA database yielded similar results, supporting that MYBL2 and A3B are upregulated and putatively promote C-to-T transitions in multiple cancer types. Moreover, blockade of EGF receptor with afatinib attenuated B-Myb?A3B signaling, suggesting a clinically relevant means of suppressing mutagenesis. Our results suggest that B-Myb?A3B contributes to DNA damage and could be targeted by inhibiting EGF receptor. Twit Text FOAVip B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28276478 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28276478 #FOAvip English Wikipedia <ref>{{Cite pmid|28276478}}</ref> B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers #MMPMID28276478 Chou WC; Chen WT; Hsiung CN; Hu LY; Yu JC; Hsu HM; Shen CY Sci Rep 2017[]; 7 (ä): ä PMID28276478show ga The key signature of cancer genomes is the accumulation of DNA mutations, the most abundant of which is the cytosine-to-thymine (C-to-T) transition that results from cytosine deamination. Analysis of The Cancer Genome Atlas (TCGA) database has demonstrated that this transition is caused mainly by upregulation of the cytosine deaminase APOBEC3B (A3B), but the mechanism has not been completely characterized. We found that B-Myb (encoded by MYBL2) binds the A3B promoter, causing transactivation, and this is responsible for the C-to-T transitions and DNA hypermutation in breast cancer cells. Analysis of TCGA database yielded similar results, supporting that MYBL2 and A3B are upregulated and putatively promote C-to-T transitions in multiple cancer types. Moreover, blockade of EGF receptor with afatinib attenuated B-Myb?A3B signaling, suggesting a clinically relevant means of suppressing mutagenesis. Our results suggest that B-Myb?A3B contributes to DNA damage and could be targeted by inhibiting EGF receptor. äB-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multi(epmc).pdf DeepDyve Pubget Overpricing