The expression level of BAALC-associated microRNA miR-3151 is an independent prognostic factor in younger patients with cytogenetic intermediate-risk acute myeloid leukemia

M. Díaz-Beyá, S. Brunet, J. Nomdedéu, A. Cordeiro, M. Tormo, L. Escoda, J. M. Ribera, M. Arnan, I. Heras, D. Gallardo, J. Bargay, M. P. Queipo De Llano, O. Salamero, J. M. Martí, A. Sampol, C. Pedro, M. Hoyos, M. Pratcorona, J. J. Castellano, M. NomdedeuR. M. Risueño, J. Sierra, M. Monzó, A. Navarro, J. Esteve

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12 Citations (Scopus)

Abstract

Acute myeloid leukemia (AML) is a heterogeneous disease whose prognosis is mainly related to the biological risk conferred by cytogenetics and molecular profiling. In elderly patients (≥60 years) with normal karyotype AML miR-3151 have been identified as a prognostic factor. However, miR-3151 prognostic value has not been examined in younger AML patients. In the present work, we have studied miR-3151 alone and in combination with BAALC, its host gene, in a cohort of 181 younger intermediate-risk AML (IR-AML) patients. Patients with higher expression of miR-3151 had shorter overall survival (P=0.0025), shorter leukemia-free survival (P=0.026) and higher cumulative incidence of relapse (P=0.082). Moreover, in the multivariate analysis miR-3151 emerged as independent prognostic marker in both the overall series and within the unfavorable molecular prognostic category. Interestingly, the combined determination of both miR-3151 and BAALC improved this prognostic stratification, with patients with low levels of both parameters showing a better outcome compared with those patients harboring increased levels of one or both markers (P=0.003). In addition, we studied the microRNA expression profile associated with miR-3151 identifying a six-microRNA signature. In conclusion, the analysis of miR-3151 and BAALC expression may well contribute to an improved prognostic stratification of younger patients with IR-AML.
Original languageEnglish
Pages (from-to)e352
JournalBlood Cancer Journal
Volume5
DOIs
Publication statusPublished - 2 Oct 2015

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