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10.1097/CCO.0b013e32834d816a http://scihub22266oqcxt.onion/10.1097/CCO.0b013e32834d816a C4612588!4612588!22080945     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Oncol 2012 ; 24 (1): 83-9 Nephropedia Template TP {{tp|p=22080945|t=2012. Altered cancer cell metabolism in gliomas with mutant IDH1 or IDH2 |pdf=|usr=}}{{22080945}} gab.com Text Altered cancer cell metabolism in gliomas with mutant IDH1 or IDH2 JO: Curr Opin Oncol http://www.kidney.de/pget.php?&tw=1&pmid=22080945 #FOAvip Purpose of review: IDH1/2 mutations occur in up to 70% of low-grade gliomas and secondary glioblastomas. Mutation of these enzymes reduces the wildtype function of the enzyme (conversion of isocitrate to ?-ketoglutarate) while conferring a new enzymatic function, the production of d-2-hydroxyglutarate (d-2-HG) from ?-ketoglutarate (?-KG). However, it is unclear how these enzymatic changes contribute to tumorigenesis. Here, we discuss the recent studies that demonstrate how IDH1/2 mutation may alter the metabolism and epigenome of gliomas, how these changes may contribute to tumor formation, and opportunities they might provide for molecular targeting. Recent findings: Metabolomic studies of IDH1/2 mutant cells have revealed alterations in glutamine, fatty acid, and citrate synthesis pathways. Additionally, d-2-HG produced by IDH1/2 mutant cells can competitively inhibit ?-KG-dependent enzymes, including histone demethylases and DNA hydroxylases, potentially leading to a distinct epigenetic phenotype. Alterations in metabolism and DNA methylation present possible mechanisms of tumorigenesis. Summary: Recent attempts to improve outcomes for glioma patients have resulted in incremental gains. Studies of IDH1/2 mutations have provided mechanistic insights into tumorigenesis and potential avenues for therapeutic intervention. Further study of IDH1/2 mutations might allow for improved therapeutic strategies. Twit Text FOAVip Altered cancer cell metabolism in gliomas with mutant IDH1 or IDH2 ????Curr Opin Oncol http://www.kidney.de/pget.php?&tw=1&pmid=22080945 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22080945 #FOAvip English Wikipedia <ref>{{Cite pmid|22080945}}</ref> Altered cancer cell metabolism in gliomas with mutant IDH1 or IDH2 #MMPMID22080945 Borodovsky A; Seltzer MJ; Riggins GJ Curr Opin Oncol 2012[Jan]; 24 (1): 83-9 PMID22080945show ga Purpose of review: IDH1/2 mutations occur in up to 70% of low-grade gliomas and secondary glioblastomas. Mutation of these enzymes reduces the wildtype function of the enzyme (conversion of isocitrate to ?-ketoglutarate) while conferring a new enzymatic function, the production of d-2-hydroxyglutarate (d-2-HG) from ?-ketoglutarate (?-KG). However, it is unclear how these enzymatic changes contribute to tumorigenesis. Here, we discuss the recent studies that demonstrate how IDH1/2 mutation may alter the metabolism and epigenome of gliomas, how these changes may contribute to tumor formation, and opportunities they might provide for molecular targeting. Recent findings: Metabolomic studies of IDH1/2 mutant cells have revealed alterations in glutamine, fatty acid, and citrate synthesis pathways. Additionally, d-2-HG produced by IDH1/2 mutant cells can competitively inhibit ?-KG-dependent enzymes, including histone demethylases and DNA hydroxylases, potentially leading to a distinct epigenetic phenotype. Alterations in metabolism and DNA methylation present possible mechanisms of tumorigenesis. Summary: Recent attempts to improve outcomes for glioma patients have resulted in incremental gains. Studies of IDH1/2 mutations have provided mechanistic insights into tumorigenesis and potential avenues for therapeutic intervention. Further study of IDH1/2 mutations might allow for improved therapeutic strategies. äAltered cancer cell metabolism in gliomas with mutant IDH1 or IDH2 (epmc).pdf DeepDyve Pubget Overpricing