000125471 001__ 125471
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000125471 0247_ $$2doi$$a10.1038/leu.2015.317
000125471 0247_ $$2pmid$$apmid:26582645
000125471 0247_ $$2ISSN$$a0887-6924
000125471 0247_ $$2ISSN$$a1476-5551
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000125471 1001_ $$0P:(DE-HGF)0$$aBalss, J.$$b0$$eFirst author
000125471 245__ $$aPretreatment d-2-hydroxyglutarate serum levels negatively impact on outcome in IDH1-mutated acute myeloid leukemia.
000125471 260__ $$aBasingstoke$$bNature Publ. Group$$c2016
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000125471 520__ $$aMutations in isocitrate dehydrogenases (IDHs) 1 and 2 frequently occur in acute myeloid leukemia (AML) and result in the production of the oncometabolite d-2-hydroxyglutarate (D2HG). D2HG has been shown to promote leukemogenesis even in the absence of mutated IDH, but the prognostic significance of pretreatment serum D2HG levels in patients with IDH-mutated AML is unclear. We measured D2HG serum levels in 84 patients with IDH-mutated AML treated in the prospective, randomized multicenter AML2003 trial of the German Study Alliance Leukemia. Multivariate Cox regression showed D2HG levels to negatively impact on event-free survival (EFS) as a continuous variable in the entire IDH(mut) cohort (P=0.04), with no effect on overall survival (OS). In a subgroup analysis, the negative impact of D2HG on EFS was found to be restricted to patients with mutations in IDH1 (P=0.003), adjusted for age, leukocyte count, serum lactate dehydrogenase and European LeukemiaNet risk score. We thus conclude that pretreatment D2HG serum levels may yield prognostic information in patients with IDH1-mutated, but not in IDH2-mutated AML, possibly due to different subcellular localizations of IDH1 and IDH2.
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000125471 650_7 $$2NLM Chemicals$$aBiomarkers, Tumor
000125471 650_7 $$2NLM Chemicals$$aGlutarates
000125471 650_7 $$02889-31-8$$2NLM Chemicals$$aalpha-hydroxyglutarate
000125471 650_7 $$0EC 1.1.1.41$$2NLM Chemicals$$aIsocitrate Dehydrogenase
000125471 650_7 $$0EC 1.1.1.42.$$2NLM Chemicals$$aIDH1 protein, human
000125471 7001_ $$aThiede, C.$$b1
000125471 7001_ $$0P:(DE-He78)c741dc7f974390ad4310349f29aac40b$$aBochtler, T.$$b2$$udkfz
000125471 7001_ $$aOkun, J. G.$$b3
000125471 7001_ $$0P:(DE-He78)609d3f1c1420bf59b2332eeab889cb74$$aSaadati, M.$$b4$$udkfz
000125471 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, A.$$b5$$udkfz
000125471 7001_ $$0P:(DE-He78)f2efee17b6ca2f790176a2c036912536$$aPusch, Stefan$$b6$$udkfz
000125471 7001_ $$aEhninger, G.$$b7
000125471 7001_ $$aSchaich, M.$$b8
000125471 7001_ $$0P:(DE-HGF)0$$aHo, A. D.$$b9
000125471 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, A.$$b10$$udkfz
000125471 7001_ $$0P:(DE-He78)493c5fbf69f1b20df6f048712f3ad4a0$$aKrämer, A.$$b11$$udkfz
000125471 7001_ $$0P:(DE-He78)42b6114cd48e033299b2b6ef4bf56cc6$$aHeilig, Christoph$$b12$$eLast author$$udkfz
000125471 773__ $$0PERI:(DE-600)2008023-2$$a10.1038/leu.2015.317$$gVol. 30, no. 4, p. 782 - 788$$n4$$p782 - 788$$tLeukemia$$v30$$x1476-5551$$y2016
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