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ZFX controls the propagation and cell-of-origin characteristics of acute leukemia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE43022 | GEO | 2014/01/30

SECONDARY ACCESSION(S): PRJNA184063

REPOSITORIES: GEO

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ZFX controls the propagation and cell-of-origin characteristics of acute leukemia

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-30 | E-GEOD-43022 | biostudies-arrayexpress

ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.

Project description:Tumor-propagating cells in acute leukemia maintain a stem/progenitor-like immature phenotype and proliferative capacity. Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) originate from different lineages through distinct oncogenic events such as MLL fusions and Notch signaling, respectively. We found that Zfx, a transcription factor that controls hematopoietic stem cell self-renewal, controls the initiation and maintenance of AML caused by MLL-AF9 fusion and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx prevents differentiation and activates gene sets characteristic of immature cells of the respective lineages. In addition, endogenous Zfx contributes to gene induction and transformation by Myc overexpression in myeloid progenitors. Key Zfx target genes include the mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescues the propagation of Zfx-deficient AML. These results show that distinct leukemia types maintain their undifferentiated phenotype and self-renewal by exploiting a common stem-cell-related genetic regulator.

| S-EPMC3936793 | biostudies-literature