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Presence of FLT3-ITD and high BAALC expression are independent prognostic markers in childhood acute myeloid leukemia

Author

  • Anna Staffas
  • Meena Kanduri
  • Randi Hovland
  • Richard Rosenquist
  • Hans Beier Ommen
  • Jonas Abrahamsson
  • Erik Forestier
  • Kirsi Jahnukainen
  • Olafur G. Jonsson
  • Bernward Zeller
  • Josefine Palle
  • Gudmar Lonnerholm
  • Henrik Hasle
  • Lars Palmqvist
  • Hans Ehrencrona

Summary, in English

Mutation status of FLT3, NPM1, CEBPA, and WT1 genes and gene expression levels of ERG, MN1, BAALC, FLT3, and WT1 have been identified as possible prognostic markers in acute myeloid leukemia (AML). We have performed a thorough prognostic evaluation of these genetic markers in patients with pediatric AML enrolled in the Nordic Society of Pediatric Hematology and Oncology (NOPHO) 1993 or NOPHO 2004 protocols. Mutation status and expression levels were analyzed in 185 and 149 patients, respectively. Presence of FLT3-internal tandem duplication (ITD) was associated with significantly inferior event-free survival (EFS), whereas presence of an NPM1 mutation in the absence of FLT3-ITD correlated with significantly improved EFS. Furthermore, high levels of ERG and BAALC transcripts were associated with inferior EFS. No significant correlation with survival was seen for mutations in CEBPA and WT1 or with gene expression levels of MN1, FLT3, and WT1. In multivariate analysis, the presence of FLT3-ITD and high BAALC expression were identified as independent prognostic markers of inferior EFS. We conclude that analysis of the mutational status of FLT3 and NPM1 at diagnosis is important for prognostic stratification of patients with pediatric AML and that determination of the BAALC gene expression level can add valuable information. (Blood. 2011;118(22):5905-5913)

Publishing year

2011

Language

English

Pages

5905-5913

Publication/Series

Blood

Volume

118

Issue

22

Document type

Journal article

Publisher

American Society of Hematology

Topic

  • Hematology

Status

Published

ISBN/ISSN/Other

  • ISSN: 1528-0020