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Year : 2019  |  Volume : 44  |  Issue : 1  |  Page : 48-53

CD34 expression and FLT3 mutation are independent poor prognostic factors in normal karyotype acute myeloid leukemia

Haematology Unit, Internal Medicine Department, Zagazig University Hospitals, Zagazig, Egypt

Correspondence Address:
Ahmed Y Amer
24 Furness Avenue, Blackpool FY3 7QQ, UK
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ejh.ejh_51_18

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Background The prognostic impact of CD34 expression on malignant myeloid leukemia blast cells is still under debate. FLT3 mutation is a well-known poor prognostic factor in acute myeloid leukemia (AML). The aim of the study was to assess CD34 expression in this subgroup of AML patients to detect the association of CD34 expression with FLT3-internal tandem duplication (ITD) mutation and its impact on the outcome. Patients and methods This prospective study, carried out at Zagazig University Hospitals, included 33 de-novo AML patients with a normal karyotype. CD 34 expression was detected by flow cytometry using FITC florescent monoclonal antibody and it was considered positive if a cutoff level of 10% expression was exceeded. FLT3-ITD mutation was detected by PCR. Results CD34 was positive in 20 cases while 13 cases were negative. Twenty-one cases were FLT3-ITD wild type while 12 cases were mutated. FLT3 mutation was significantly linked to CD34 reactivity (P=0.048). CD34-positive cases were associated with a significantly less complete remission (CR) achievement rate (33 and 80% in CD34-positive and CD34 negative, respectively, P=0.03). Those with positive CD34 had significantly lower overall survival compared with CD34-negative cases. Multivariate cox regression survival analysis showed that positive CD34 was a predictor of poor survival and higher risk of mortality (HR=1.3 and P=0.027, confidence interval, 1.1–2.9). Conclusion CD34 expression is a poor prognostic biomarker in normal karyotype AML. It is associated with and further worsens the poor prognosis in FLT3-mutated cases. Its role in different subgroups of AML layered by different genetic aberrations needs further study.

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