The surface molecular signature of leukemic cells is associated with NPM1 mutations and FLT3 -ITD in patients with de novo acute myeloid leukemia

Acta Haematol. 2014;131(3):148-52. doi: 10.1159/000353663. Epub 2013 Oct 31.

Abstract

Certain molecular mutations are associated with signs of cell morphology and differentiation in acute myeloid leukemia (AML). However, only limited data are available for the detailed analysis of such correlations. In this study, AML patients were classified into 4 subsets according to CD34, HLA-DR and CD11c expression levels. Significantly low CD34 antigen expression was observed in nucleophosmin (NPM1)-mutated patients and in those with FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD). No correlations were observed among NPM1 mutations, FLT3-ITD and monocytic morphology in patients without CD34 expression. Both NPM1 mutations and FLT3-ITD were absent in cluster IIb patients (CD34(+)CD11c(-)). The associations among NPM1 mutations, FLT3-ITD and the surface molecular signature of leukemic cells may offer beneficial information about the pathogenesis of AML.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Antigens, CD34 / metabolism
  • CD11c Antigen / metabolism
  • Child
  • Female
  • HLA-DR Antigens / metabolism
  • Humans
  • Immunophenotyping
  • Leukemia, Myeloid, Acute / classification
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / immunology
  • Male
  • Middle Aged
  • Mutation*
  • Nuclear Proteins / genetics*
  • Nucleophosmin
  • Tandem Repeat Sequences
  • Young Adult
  • fms-Like Tyrosine Kinase 3 / genetics*

Substances

  • Antigens, CD34
  • CD11c Antigen
  • HLA-DR Antigens
  • NPM1 protein, human
  • Nuclear Proteins
  • Nucleophosmin
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3