Influence of IDH on FLT3 -ITD status in newly diagnosed AML

Internal tandem duplication (ITD) mutations of the FMS-like Tyrosine Kinase (FLT3) gene are among the most frequently encountered mutations in adult acute myeloid leukemia (AML), occurring in 21-34% of de novo AML, with a higher frequency in younger patients and those with diploid cytogenetics.1, 2, 3, 4 FLT3-ITD mutations confer higher risk disease, particularly in younger patients, where FLT3-ITD is associated with shorter remission durations and high relapse rates after conventional induction therapy.5 Importantly however, the prognostic impact of FLT3-ITD is influenced by, and must be interpreted in the context of, concurrent mutations in other recurrently identified genes, including NPM1 and DNMT3A.5, 6, 7 Isocitrate dehydrogenase (IDH) mutations represent another class of frequently occurring molecular aberrations in AML, with IDH1 and IDH2 mutations noted in 6–16% and 8–19% of AML cases, respectively.8, 9 The prognostic relevance of IDH mutations remains a matter of debate, and appears to differ by the specific IDH mutation and by co-occurring mutations in other myeloid-associated genes.6, 10