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Molecular stratification of patients with normal karyotype acute myeloid leukemia based on initial assessment of FLT3-internal tandem duplication status at first complete remission

Karyotype represents the single most important prognostic determinant for predicting clinical outcomes (i.e. remission rate, relapse and overall survival) in patients with acute myeloid leukemia (AML). Although multiple classifications exist, where three prognostic groups are defined: good, intermediate and poor risk cytogenetics [1–3]. The largest subset of patients with AML (40–50%) presents with normal karyotype (NK-AML), which comprises a clinically and genetically heterogeneous group with an intermediate prognosis [4]. In this group, mutations in genes such as FLT3 (internal tandem duplication [ITD] and tyrosine kinase domain mutation [TKD]), CEBPa and NPM1 impart prognostic information [4]. At present, however, these molecular markers are not routinely assessed in newly diagnosed patients with AML in the community. Because this information may influence future treatment decisions, determination of these molecular markers in patients with NKAML, at the time of hematological recovery (postinduction chemotherapy), may provide valuable clinical information. We describe two patients with NK-AML, where molecular testing was successfully obtained only at the time of hematological recovery. Patients were selected from a total of 75 patients with newly diagnosed AML were evaluated at the Stanford Cancer Center between January and June, 2008. The protocol was approved by the Stanford University Research Compliance Office (protocol no. 14839). The diagnosis of AML was based on morphologic, cytochemical and immunophenotypic review, with classification according to the WHO classification. Five patients were referred to Stanford University after the diagnostic bone marrow had been performed and after initiation of induction chemotherapy. FLT3 and NPM-1 mutation testing was performed by a multiplex PCR assay and capillary electrophoresis at the time of hematological recovery in all five patients, two of whom were found to carry a FLT3-ITD mutation. This assay detects FLT3 juxtamembrane region ITD, D835 mutation and insertions or deletions affecting the nucleolar localisation signal in NPM1 exon 12.