This SuperSeries is composed of the SubSeries listed below.
ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.
Specimen part, Cell line, Treatment
View SamplesAcute myeloid leukemia (AML) propagates as a cellular hierarchy which is maintained by a rare subpopulation of self-renewing leukemia-initiating cells (LICs). These LICs phenotypically resemble HSCs and early myeloid progenitors, and they are functionally defined by their ability to reconstitute AML in xenografted mice.
ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.
Cell line, Treatment
View SamplesAcute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that the transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms.
ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.
Specimen part, Cell line
View SamplesControl and Liver Insulin Receptor KO mice (LIRKO) were sacrificed in the non-fasted state. RNA was prepared from liver samples and subjected to expression microarray analysis
Flavin-containing monooxygenase 3 as a potential player in diabetes-associated atherosclerosis.
Specimen part
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