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10.1186/s13578-017-0156-4 http://scihub22266oqcxt.onion/10.1186/s13578-017-0156-4 C5450379!5450379!28572915     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       Cell+Biosci 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28572915|t=2017. APOBEC3B, a molecular driver of mutagenesis in human cancers |pdf=|usr=}}{{28572915}} gab.com Text APOBEC3B, a molecular driver of mutagenesis in human cancers JO: Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=28572915 #FOAvip Human cancers results in large part from the accumulation of multiple mutations. The progression of premalignant cells is an evolutionary process in which mutations provide the fundamental driving force for genetic diversity. The increased mutation rate in premalignant cells allows selection for increased proliferation and survival and ultimately leads to invasion, metastasis, recurrence, and therapeutic resistance. Therefore, it is important to understand the molecular determinants of the mutational processes. Recent genome-wide sequencing data showed that apolipoprotein B mRNA editing catalytic polypeptide-like 3B (APOBEC3B) is a key molecular driver inducing mutations in multiple human cancers. APOBEC3B, a DNA cytosine deaminase, is overexpressed in a wide spectrum of human cancers. Its overexpression and aberrant activation lead to unexpected clusters of mutations in the majority of cancers. This phenomenon of clustered mutations, termed kataegis (from the Greek word for showers), forms unique mutation signatures. In this review, we will discuss the biological function of APOBEC3B, its tumorigenic role in promoting mutational processes in cancer development and the clinical potential to develop novel therapeutics by targeting APOBEC3B. Twit Text FOAVip APOBEC3B, a molecular driver of mutagenesis in human cancers ????Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=28572915 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28572915 #FOAvip English Wikipedia <ref>{{Cite pmid|28572915}}</ref> APOBEC3B, a molecular driver of mutagenesis in human cancers #MMPMID28572915 Zou J; Wang C; Ma X; Wang E; Peng G Cell Biosci 2017[]; 7 (ä): ä PMID28572915show ga Human cancers results in large part from the accumulation of multiple mutations. The progression of premalignant cells is an evolutionary process in which mutations provide the fundamental driving force for genetic diversity. The increased mutation rate in premalignant cells allows selection for increased proliferation and survival and ultimately leads to invasion, metastasis, recurrence, and therapeutic resistance. Therefore, it is important to understand the molecular determinants of the mutational processes. Recent genome-wide sequencing data showed that apolipoprotein B mRNA editing catalytic polypeptide-like 3B (APOBEC3B) is a key molecular driver inducing mutations in multiple human cancers. APOBEC3B, a DNA cytosine deaminase, is overexpressed in a wide spectrum of human cancers. Its overexpression and aberrant activation lead to unexpected clusters of mutations in the majority of cancers. This phenomenon of clustered mutations, termed kataegis (from the Greek word for showers), forms unique mutation signatures. In this review, we will discuss the biological function of APOBEC3B, its tumorigenic role in promoting mutational processes in cancer development and the clinical potential to develop novel therapeutics by targeting APOBEC3B. äAPOBEC3B, a molecular driver of mutagenesis in human cancers (epmc).pdf DeepDyve Pubget Overpricing