A subset of cells called leukemia stem cells (LSCs) possess limitless self-renewal and are responsible for maintenance of leukemia. Selective eradication of LSCs could offer significant therapeutic benefit and there is great interest in identifying the signaling pathways that control their development. Here, LSCs were studied in mouse models of acute myelogenous leukemia (AML) induced either by co-expression of the Hoxa9 and Meis1a oncogenes or the fusion oncoprotein MLL-AF9. We show that the Wnt/β-catenin signaling pathway is required for self-renewal of LSCs derived from either hematopoietic stem cells (HSC) or more differentiated granulocyte macrophage progenitors (GMP). Since the Wnt/β-catenin pathway is normally active in HSCs, but not in GMP, reactivation of β-catenin signaling is required for transformation of progenitor cells by certain oncogenes. β-catenin is not absolutely required for self-renewal of adult HSCs, thus targeting the Wnt/β-catenin pathway may represent a new therapeutic opportunity in AML.
Solid metal microneedles are capable of increasing transdermal insulin delivery and lowering blood glucose levels by as much as 80% in diabetic hairless rats in vivo.
Highlights d A comprehensive proteomic analyses of localized prostate cancers d Integration of all levels of the central dogma (DNA / RNA / protein) d ETS fusions have divergent effects on transcriptome and proteome d Combining genomics and proteomics improves biomarker performance
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