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http://scihub22266oqcxt.onion/ C4466681!4466681!25749049     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2015 ; 6 (9): 7232-43 Nephropedia Template TP {{tp|p=25749049|t=2015. Multiple mechanisms of MYCN dysregulation in Wilms tumour |pdf=|usr=}}{{25749049}} gab.com Text Multiple mechanisms of MYCN dysregulation in Wilms tumour JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25749049 #FOAvip Genomic gain of the proto-oncogene transcription factor gene MYCN is associated with poor prognosis in several childhood cancers. Here we present a comprehensive copy number analysis of MYCN in Wilms tumour (WT), demonstrating that gain of this gene is associated with anaplasia and with poorer relapse-free and overall survival, independent of histology. Using whole exome and gene-specific sequencing, together with methylation and expression profiling, we show that MYCN is targeted by other mechanisms, including a recurrent somatic mutation, P44L, and specific DNA hypomethylation events associated with MYCN overexpression in tumours with high risk histologies. We describe parallel evolution of genomic copy number gain and point mutation of MYCN in the contralateral tumours of a remarkable bilateral case in which independent contralateral mutations of TP53 also evolve over time. We report a second bilateral case in which MYCN gain is a germline aberration. Our results suggest a significant role for MYCN dysregulation in the molecular biology of Wilms tumour. We conclude that MYCN gain is prognostically significant, and suggest that the novel P44L somatic variant is likely to be an activating mutation. Twit Text FOAVip Multiple mechanisms of MYCN dysregulation in Wilms tumour ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25749049 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25749049 #FOAvip English Wikipedia <ref>{{Cite pmid|25749049}}</ref> Multiple mechanisms of MYCN dysregulation in Wilms tumour #MMPMID25749049 Williams RD; Chagtai T; Alcaide-German M; Apps J; Wegert J; Popov S; Vujanic G; van Tinteren H; van den Heuvel-Eibrink MM; Kool M; de Kraker J; Gisselsson D; Graf N; Gessler M; Pritchard-Jones K Oncotarget 2015[Mar]; 6 (9): 7232-43 PMID25749049show ga Genomic gain of the proto-oncogene transcription factor gene MYCN is associated with poor prognosis in several childhood cancers. Here we present a comprehensive copy number analysis of MYCN in Wilms tumour (WT), demonstrating that gain of this gene is associated with anaplasia and with poorer relapse-free and overall survival, independent of histology. Using whole exome and gene-specific sequencing, together with methylation and expression profiling, we show that MYCN is targeted by other mechanisms, including a recurrent somatic mutation, P44L, and specific DNA hypomethylation events associated with MYCN overexpression in tumours with high risk histologies. We describe parallel evolution of genomic copy number gain and point mutation of MYCN in the contralateral tumours of a remarkable bilateral case in which independent contralateral mutations of TP53 also evolve over time. We report a second bilateral case in which MYCN gain is a germline aberration. Our results suggest a significant role for MYCN dysregulation in the molecular biology of Wilms tumour. We conclude that MYCN gain is prognostically significant, and suggest that the novel P44L somatic variant is likely to be an activating mutation. äMultiple mechanisms of MYCN dysregulation in Wilms tumour (epmc).pdf DeepDyve Pubget Overpricing