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These results offer the rationale for a strategy to monitor MRD in CLL patients. ""After their initial identification in high-grade gliomas, acquired heterozygous mutations in the NADPH-dependent isocitrate dehydrogenase (IDH) 1 and 2 genes (IDH1, IDH2) were recently described in patients with de novo acute myeloid leukaemia (AML) (Mardis et?al, 2009) and leukaemic transformation of JAK2 mutation positive myeloproliferative neoplasms (Green & Beer, 2010). These mutations lead to the substitution of arginines in the catalytic site of IDH1/2 resulting in neomorphic enzyme activity with accumulation of 2-hydroxyglutarate https://www.selleckchem.com/products/VX-770.html (Dang et?al, 2009; Gross et?al, 2010; Ward et?al, 2010). To determine the frequency and pathogenetic impact of these mutations in patients with therapy-related AML (t-AML) or secondary AML https://www.selleck.cn/products/Verteporfin(Visudyne).html (sAML) evolved from myelodysplastic syndromes (MDS), we performed a mutational analysis of the affected arginine residues in the IDH1 and IDH2 genes in 101 individuals with these disorders. Demographic and clinical characteristics of this cohort are presented in Table?S1. At t-AML and sAML diagnosis, DNA was isolated from diagnostic peripheral blood or bone marrow samples after Ficoll enrichment, yielding >90% blast cells for direct sequencing. In patients with MDS DNA was directly isolated from bone marrow biopsy specimens without further enrichment. This study was approved by the institutional https://www.selleckchem.com/products/ch5424802.html review board of the Medical University of Graz, Austria, and patients provided informed consent in accordance with the declaration of Helsinki. We identified one IDH1 (R132H) and three IDH2 mutations (2�� R140Q and R172K) in 73 patients with t-AML. Thus, the frequencies of mutated IDH1 and IDH2 samples in this t-AML cohort were lower than previously reported for de novo AML (1��4% vs. 8��5%, P?