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10.1038/nature15251 http://scihub22266oqcxt.onion/10.1038/nature15251 C4568559!4568559!26331536     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2015 ; 525 (7568): 206-11 Nephropedia Template TP {{tp|p=26331536|t=2015. Prevalent p53 mutants co-opt chromatin pathways to drive cancer growth |pdf=|usr=}}{{26331536}} gab.com Text Prevalent p53 mutants co-opt chromatin pathways to drive cancer growth JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=26331536 #FOAvip TP53 is the most frequently mutated gene among all human cancers. Prevalent p53 missense mutations abrogate its tumor suppressive function and lead to ?gain-of-function? (GOF) that promotes cancer. Here we show that p53 GOF mutants bind to and upregulate chromatin regulatory genes, including the methyltransferases KMT2A (MLL1) and KMT2D (MLL2), and acetyltransferase KAT6A (MOZ or MYST3), resulting in genome-wide increases of histone methylation and acetylation. Analysis of The Cancer Genome Atlas shows specific upregulation of MLL1, MLL2, and MOZ in p53 GOF patient-derived tumors, but not in p53 wildtype or p53 null tumors. Cancer cell proliferation is dramatically lowered by genetic knockdown of MLL1, or by pharmacological inhibition of the MLL1 methyltransferase complex. Our study reveals a novel chromatin mechanism underlying the progression of tumors with GOF p53, and suggests new possibilities for designing combinatorial chromatin-based therapies for treating individual cancers driven by prevalent GOF p53 mutations. Twit Text FOAVip Prevalent p53 mutants co-opt chromatin pathways to drive cancer growth ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=26331536 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26331536 #FOAvip English Wikipedia <ref>{{Cite pmid|26331536}}</ref> Prevalent p53 mutants co-opt chromatin pathways to drive cancer growth #MMPMID26331536 Zhu J; Sammons MA; Donahue G; Dou Z; Vedadi M; Getlik M; Barsyte-Lovejoy D; Al-Awar R; Katona BW; Shilatifard A; Huang J; Hua X; Arrowsmith CH; Berger SL Nature 2015[Sep]; 525 (7568): 206-11 PMID26331536show ga TP53 is the most frequently mutated gene among all human cancers. Prevalent p53 missense mutations abrogate its tumor suppressive function and lead to ?gain-of-function? (GOF) that promotes cancer. Here we show that p53 GOF mutants bind to and upregulate chromatin regulatory genes, including the methyltransferases KMT2A (MLL1) and KMT2D (MLL2), and acetyltransferase KAT6A (MOZ or MYST3), resulting in genome-wide increases of histone methylation and acetylation. Analysis of The Cancer Genome Atlas shows specific upregulation of MLL1, MLL2, and MOZ in p53 GOF patient-derived tumors, but not in p53 wildtype or p53 null tumors. Cancer cell proliferation is dramatically lowered by genetic knockdown of MLL1, or by pharmacological inhibition of the MLL1 methyltransferase complex. Our study reveals a novel chromatin mechanism underlying the progression of tumors with GOF p53, and suggests new possibilities for designing combinatorial chromatin-based therapies for treating individual cancers driven by prevalent GOF p53 mutations. äPrevalent p53 mutants co-opt chromatin pathways to drive cancer growth(epmc).pdf DeepDyve Pubget Overpricing