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10.1007/s10014-016-0265-5 http://scihub22266oqcxt.onion/10.1007/s10014-016-0265-5 C5488809!5488809!27295313     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       Brain+Tumor+Pathol 2016 ; 33 (3): 161-8 Nephropedia Template TP {{tp|p=27295313|t=2016. Cancer metabolism as a central driving force of glioma pathogenesis |pdf=|usr=}}{{27295313}} gab.com Text Cancer metabolism as a central driving force of glioma pathogenesis JO: Brain Tumor Pathol http://www.kidney.de/pget.php?&tw=1&pmid=27295313 #FOAvip The recent identification of distinct genetic and epigenetic features in each glioma entity is leading to a multilayered, integrated diagnostic approach combining histologic features with molecular genetic information. Somatic mutations in isocitrate dehydrogenase (IDH) and receptor tyrosine kinase (RTK) pathways are key oncogenic events in diffuse gliomas, including lower grade (grade II and III) gliomas (LGG) and the highly lethal brain tumor glioblastoma (GBM) respectively, where they reprogram the epigenome, transcriptome and metabolome to drive tumor growth. However, the mechanisms by which these genetic aberrations are translated into the aggressive nature of gliomas through metabolic reprogramming have just begun to be unraveled. The intricate interactions between the oncogenic signaling and cancer metabolism have also been recently demonstrated. Here we describe a set of recent discoveries on cancer metabolism driven by IDH mutation and mutations in RTK pathways, highlighting the integration of genetic mutations, metabolic reprogramming and epigenetic shifts, potentially providing new therapeutic opportunities. Twit Text FOAVip Cancer metabolism as a central driving force of glioma pathogenesis ????Brain Tumor Pathol http://www.kidney.de/pget.php?&tw=1&pmid=27295313 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27295313 #FOAvip English Wikipedia <ref>{{Cite pmid|27295313}}</ref> Cancer metabolism as a central driving force of glioma pathogenesis #MMPMID27295313 Masui K; Cavenee WK; Mischel PS Brain Tumor Pathol 2016[Jul]; 33 (3): 161-8 PMID27295313show ga The recent identification of distinct genetic and epigenetic features in each glioma entity is leading to a multilayered, integrated diagnostic approach combining histologic features with molecular genetic information. Somatic mutations in isocitrate dehydrogenase (IDH) and receptor tyrosine kinase (RTK) pathways are key oncogenic events in diffuse gliomas, including lower grade (grade II and III) gliomas (LGG) and the highly lethal brain tumor glioblastoma (GBM) respectively, where they reprogram the epigenome, transcriptome and metabolome to drive tumor growth. However, the mechanisms by which these genetic aberrations are translated into the aggressive nature of gliomas through metabolic reprogramming have just begun to be unraveled. The intricate interactions between the oncogenic signaling and cancer metabolism have also been recently demonstrated. Here we describe a set of recent discoveries on cancer metabolism driven by IDH mutation and mutations in RTK pathways, highlighting the integration of genetic mutations, metabolic reprogramming and epigenetic shifts, potentially providing new therapeutic opportunities. äCancer metabolism as a central driving force of glioma pathogenesis (epmc).pdf DeepDyve Pubget Overpricing