ArrayExpress Uploader01266WTtestwild-typeM4eWTtestwild-typeM4internal tandem duplication (ITD)testwild-typeM4internal tandem duplication (ITD)testwild-typeM4internal tandem duplication (ITD)testwild-typeM4WTtestwild-typeM2WTtestwild-typeM2WTtestwild-typeM0WTtestwild-typeM1internal tandem duplication (ITD)testwild-typeM1internal tandem duplication (ITD)testwild-typeM5ainternal tandem duplication (ITD)/D835 mutationtestmutatedM5binternal tandem duplication (ITD)testmutatedM5bWTtestmutatedM4internal tandem duplication (ITD)testmutatedM4WTtestmutatedM1WTtestmutatedM0WTtestmutatedM5bWTtestmutatedM5bWTtestmutatedM5bWTtestmutatedM5binternal tandem duplication (ITD)testmutatedM5binternal tandem duplication (ITD)testmutatedM5bWTtestmutatedM5ainternal tandem duplication (ITD)testmutatedM5ainternal tandem duplication (ITD)testmutatedM5ainternal tandem duplication (ITD)testmutatedM5WTtestmutatedM4internal tandem duplication (ITD)/D835 mutationtestmutatedM4internal tandem duplication (ITD)testmutatedM4internal tandem duplication (ITD)testmutatedM4internal tandem duplication (ITD)testmutatedM4D835 mutationtestmutatedM4WTtestmutatedM2WTtestmutatedM2internal tandem duplication (ITD)testmutatedM2D835 mutationtestmutatedM2WTtestmutatedM1internal tandem duplication (ITD)testmutatedM1internal tandem duplication (ITD)trainingwild-typeM2internal tandem duplication (ITD)trainingwild-typeM5aWTtrainingwild-typeM4WTtrainingwild-typeM4WTtrainingwild-typeM2WTtrainingwild-typeM1WTtrainingwild-typeM1WTtrainingwild-typeM1WTtrainingwild-typeM0internal tandem duplication (ITD)trainingwild-typeM0WTtrainingmutatedM5bD835 mutationtrainingmutatedM5bD835 mutationtrainingmutatedM5bWTtrainingmutatedM5aWTtrainingmutatedM5aWTtrainingmutatedM5aWTtrainingmutatedM4WTtrainingmutatedM4internal tandem duplication (ITD)trainingmutatedM4internal tandem duplication (ITD)trainingmutatedM4WTtrainingmutatedM2WTtrainingmutatedM2WTtrainingmutatedM2WTtrainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2internal tandem duplication (ITD)trainingmutatedM2WTtrainingmutatedM1WTtrainingmutatedM1WTtrainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1internal tandem duplication (ITD)trainingmutatedM1arrayexpress_sid3Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of Nucleophosmin (NPMc+...15831697E-GEOD-34860/profile/8773/arrayexpressuploader478cellcell phenotypestem celltyrosineDec.12, 2014Falsegene-expression-profiling-in-acute-myeloid-leukemiE-GEOD-34860_A-AFFY-33Gene expression profiling in acute myeloid leukemia with mutated NPMJun.18, 2014Approximately 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, Fms-like tyrosine kinase (FLT3) mutations and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 with non-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. 78 de novo AMLs, negative for AML-associated chromosomal translocations at the cytogenetic and/or molecular level.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-34860humanhttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-34860/samples/