Genomics

Dataset Information

240

BCL6 is required for the initiation and maintenance of chronic myeloid leukemia


ABSTRACT: We identified the BCL6 protooncogene as a critical downstream effector of FoxO3A in self-renewal signaling of CML-initiating cells. BCL6 represses Arf and p53 in CML cells and is required for leukemia stem cell maintenance, colony formation and initiation of leukemia in transplant recipients. Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia-initiation in xenotransplanted mouse recipients. These findings identify peptide-inhibition of BCL6 as a novel strategy to eradicate leukemia-initiating cells in CML. Identification of BCL6 binding sites in human CML cell line JURL-MK1

OTHER RELATED OMICS DATASETS IN: E-GEOD-20987

ORGANISM(S): Homo sapiens  

SUBMITTER: Markus Müschen   Katerina Hatzi  Christian Hurtz 

PROVIDER: E-GEOD-26085 | ArrayExpress | 2011-09-15

SECONDARY ACCESSION(S): GSE26085SRP004887PRJNA135225

REPOSITORIES: GEO, ArrayExpress, ENA

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Publications


Chronic myeloid leukemia (CML) is induced by the oncogenic BCR-ABL1 tyrosine kinase and can be effectively treated for many years with tyrosine kinase inhibitors (TKIs). However, unless CML patients receive life-long TKI treatment, leukemia will eventually recur; this is attributed to the failure of TKI treatment to eradicate leukemia-initiating cells (LICs). Recent work demonstrated that FoxO factors are critical for maintenance of CML-initiating cells; however, the mechanism of FoxO-dependent  ...[more]

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