The surface molecule signature of primary human acute myeloid leukemia (AML) cells is highly associated with NPM1 mutation status

Abstract

ReferencesThe surface molecule signature of primary human acute myeloid leukemia (AML) cells is highly associated with NPM1 mutation status Leukemia (2012) 26, 557-559; doi:10.1038/leu.2011 published online 9 September 2011 Even though human acute myeloid leukemia (AML) is characterized by an expansion of malignant myeloblasts, these immature leukemic cells can show signs of differentiation both by morphological examination and by flow-cytometric analysis of membrane molecules.

The Surface Molecular Signature of Leukemic Cells Is Associated with <b><i>NPM1</i></b> Mutations and <b><i>FLT3</i></b>-ITD in Patients with de novo Acute Myeloid Leukemia

“…1). FLT3 -ITD was reported not to be associated with CD34 expression by Tsykunova et al [7]. Contrarily, as shown previously [6,16,17] and in the present study, significantly low CD34 antigen expression was observed in patients with FLT3 -ITD; no correlation could be observed between FLT3 -ITD and monocytic morphology in those patients without CD34 expression.…”

“…Tsykunova et al [7] have classified AML patients into 4 subsets according to CD34, HLA-DR and CD33 expression levels with the J-Express analysis suite [7]. However, in this study, CD33 expression levels were almost the same in all cluster II patients (CD34 high ); further, we were able to divide patients into 4 subgroups according to CD34, HLA-DR and CD11c expression levels (fig.…”

“…Hence, the combination with other surface markers might be beneficial to subdivide patients with CD34 expression, which may further classify patients with respect to therapeutic response and outcome . From the view of FAB classification, the majority subtypes of AML were those with neutrophil and monocytic lineage-associated aberrant immunophenotype; furthermore, in order to be comparable with a previous study presented by Tsykunova et al [7], a limited number of well-characterized surface membrane molecules were chosen in this study.…”

“…The mutational status of molecular markers NPM1 (n = 259), FLT3- ITD (n = 255), c-kit (n = 227), and CCAAT/enhancer binding protein-α ( CEBPA ; n = 57) were analyzed, and polymerase chain reaction was performed as previously described [11,12,13]. Surface differentiation markers - CD11c (expressed on monocytes), CD13 (monocytes, neutrophils), CD14 (mainly expressed on monocytes and, at lower levels, on neutrophils), CD15 (mainly neutrophils, also monocytes), CD33 (appears on myelomonocytic precursors after CD34), CD34 (immature hematopoietic cells), and human leukocyte antigen DR (HLA-DR) - of the leukemic cells were analyzed by flow cytometry [7]. …”

“…Using bioinformatics analysis, Tsykunova et al [7] described a correlation between the surface molecule signature of primary human AML cells and molecular mutations. They concluded that the most striking observation was the absence of NPM1 mutations among patients with the most immature CD34 + CD33 - AML cell phenotype, which is consistent with the hypothesis that the cell origin of NPM1 mutations is a common myeloid progenitor [7,8]. Herein, we discuss the application of the J-Express 2009 analysis suite to examine 259 consecutive Chinese AML patients.…”