MicroRNA expression in cytogenetically normal acute myeloid leukemia

N Engl J Med. 2008 May 1;358(18):1919-28. doi: 10.1056/NEJMoa074256.

Abstract

Background: A role of microRNAs in cancer has recently been recognized. However, little is known about the role of microRNAs in acute myeloid leukemia (AML).

Methods: Using microRNA expression profiling, we studied samples of leukemia cells from adults under the age of 60 years who had cytogenetically normal AML and high-risk molecular features--that is, an internal tandem duplication in the fms-related tyrosine kinase 3 gene (FLT3-ITD), a wild-type nucleophosmin (NPM1), or both. A microRNA signature that was associated with event-free survival was derived from a training group of 64 patients and tested in a validation group of 55 patients. For the latter, a microRNA compound covariate predictor (called a microRNA summary value) was computed on the basis of weighted levels of the microRNAs forming the outcome signature.

Results: Of 305 microRNA probes, 12 (including 5 representing microRNA-181 family members) were associated with event-free survival in the training group (P<0.005). In the validation group, the microRNA summary value was inversely associated with event-free survival (P=0.03). In multivariable analysis, the microRNA summary value remained associated with event-free survival (P=0.04) after adjustment for the allelic ratio of FLT3-ITD to wild-type FLT3 and for the white-cell count. Using results of gene-expression microarray analysis, we found that expression levels of the microRNA-181 family were inversely correlated with expression levels of predicted target genes encoding proteins involved in pathways of innate immunity mediated by toll-like receptors and interleukin-1beta.

Conclusions: A microRNA signature in molecularly defined, high-risk, cytogenetically normal AML is associated with the clinical outcome and with target genes encoding proteins involved in specific innate-immunity pathways.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Analysis of Variance
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Leukemic / genetics
  • Gene Expression*
  • Genetic Markers
  • Genetic Predisposition to Disease
  • Humans
  • Kaplan-Meier Estimate
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / pathology
  • MicroRNAs / metabolism*
  • Middle Aged
  • Mutation
  • Nuclear Proteins / genetics
  • Nucleophosmin
  • Oligonucleotide Array Sequence Analysis
  • Prognosis
  • Proportional Hazards Models
  • RNA Probes
  • RNA, Neoplasm / metabolism*
  • Trans-Activators / genetics
  • Trans-Activators / metabolism
  • Transcriptional Regulator ERG
  • fms-Like Tyrosine Kinase 3 / genetics

Substances

  • DNA-Binding Proteins
  • ERG protein, human
  • Genetic Markers
  • MicroRNAs
  • NPM1 protein, human
  • Nuclear Proteins
  • RNA Probes
  • RNA, Neoplasm
  • Trans-Activators
  • Transcriptional Regulator ERG
  • Nucleophosmin
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3