Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance.
Blood, 2005/8/01;106(3):899-902.
Alcalay M[1], Tiacci E, Bergomas R, Bigerna B, Venturini E, Minardi SP, Meani N, Diverio D, Bernard L, Tizzoni L, Volorio S, Luzi L, Colombo E, Lo Coco F, Mecucci C, Falini B, Pelicci PG
Affiliations
PMID: 15831697
Impact factor: 25.476
Abstract
Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal. These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, FLT3 mutations, and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 without major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM. Unsupervised clustering clearly separated NPMc+ from NPMc- AMLs, regardless of the presence of FLT3 mutations or non-major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity. The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem-cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor.
MeSH terms
Acute Disease; Cell Lineage; Cytoplasm; DNA Mutational Analysis; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Hematopoietic Stem Cells; Leukemia, Myeloid; Neoplasm Proteins; Nuclear Proteins; Nucleophosmin; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Up-Regulation; fms-Like Tyrosine Kinase 3
More resources
EndNote: Download