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STAP-1 is Required for Maintenance of Leukemic Stem Cells in Chronic Myeloid Leukemia.

ABSTRACT: STAP-1 is Required for Maintenance of Leukemic Stem Cells in Chronic Myeloid Leukemia.

PROVIDER: PRJNA525992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8695660.fastq.gz	Fastqsanger.gz
	SRR8695659.fastq.gz	Fastqsanger.gz

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STAP-1 is Required for Maintenance of Leukemic Stem Cells in Chronic Myeloid Leukemia.

Project description:The family of signal transduction adapter proteins (STAPs) has been reported to be involved in a variety of intracellular signaling and transcriptional molecules. We originally cloned STAP-2 as a c-fms interacting protein and found the effects on chronic myeloid leukemia (CML) leukemogenesis. STAP-2 binds to BCR-ABL, up-regulates BCR-ABL phosphorylation and activates its downstream molecules. In this study, we evaluated the role of STAP-1, another member of the family, in CML pathogenesis. The expression of human STAP-1 is aberrantly upregulated in CML stem cells (LSCs) in patient bone marrow. Using experimental model mice, we revealed that deletion of STAP-1 prolonged survival of CML mice with the induced apoptosis of LSCs. The impaired phosphorylated status of STAT5 by STAP-1 ablation results in downregulation of anti-apoptotic genes, BCL-2 and BCL-xL. Interestingly, transcriptome analyses indicate that STAP-1 affects several signaling pathways related to BCR-ABL, JAK2 as well as PPARγ. This adaptor protein directly binds not only BCR-ABL, also STAT5 proteins, showing synergistic effects of STAP-1 inhibition on the treatment with BCR-ABL or JAK2 tyrosine kinase inhibitor. It is known that the inhibition of BCR-ABL alone cannot eliminate CML LSCs. Our results have identified STAP-1 as a regulator of CML LSCs and support the evidence as a novel therapeutic target for CML cure.

2020-07-15 | GSE127984 | GEO

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program II

Project description:We report that IKZF2 is required for maintaining chromatin accessibility in leukemic stem cells in myeloid leukemia. RNA seq and ATAC-seq were performed to investigate the changes in chromatin accessibility of differentially expressed genes in leukemic stem cells when IKZF2 was absent. We found that IKZF2 maintains open accessibility in self-renewal transcription factor motifs such as HOXA9 sites whereas motifs of differentiation transcription factors including C/EBPs are kept closed.

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IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program I

2017-12-21 | GSE108367 | GEO

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

Project description: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

2011-09-15 | E-GEOD-26085 | biostudies-arrayexpress

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program

Project description:IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program

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Bacterial translocation is required for pre-leukemic myeloproliferation in Tet2 deficient mice

Project description:Ten-Eleven-translocation (Tet2) encodes an epigenetic modifier enzyme and is mutated somatically during age-associated clonal hematopoiesis of indeterminate potential (CHIP) as well as in myeloid malignancies 1-7. Tet2 deficiency leads to increased hematopoietic stem cell (HSC) renewal in human 7 and mouse 8. However, the development of myeloproliferation and myeloid malignancies occurs at late age, and only occasionally in humans 2,6,7,9 and in 50-75% of Tet2 deficient animals 8,10,11, suggesting that undefined triggers are required for pre-leukemic myeloid expansion. Our studies reveal that Tet2 deficient mice can exhibit high levels of plasma IL-6, systemic dissemination of indigenous gut bacteria and increased intestinal permeability that correlate with the development of a pre-leukemic myeloproliferative phenotype. Increased intestinal permeability was linked to a large number of transcriptional changes in the jejunum, especially among genes involved in defense response to bacterium and intestinal barrier function. Strikingly, antibiotic treatment reduced plasma IL-6 levels and both, prevented early myeloid expansion and reversed the pre-leukemic myeloproliferative phenotype in Tet2-/- mice. In summary, we show that Tet2 deficiency promotes intestinal bacterial translocation and subsequent systemic inflammation, and that gut-derived microbial signals are required for the development of pre-leukemic myeloproliferation in a Tet2-deficient host. Our studies suggest that controlling bacterial translocation and bacteria-associated systemic inflammation could decrease the risk of myeloid malignancies significantly in individuals with somatic Tet2 mutations.

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

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IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program I

Project description:IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program I

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IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program II

Project description:IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program II

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Pre-leukemic Cebpa mutant myeloid progenitors

Project description:In this study, we use pre-malignant cells from different Cebpa mutant acute myeloid leukemia (AML) models. We have used conditional KO models (CreLoxP) and isolated hematopoietic cells shortly after induction of recombination, in order to look at pre-leukemic cells, which have acquired the first hit, but not yet undergone full malignant transformation. We have sorted granulocyte-macrophage progenitors (GMPs) and the more immature population pre-granulocyte-macrophages (preGMs) from pre-leukemic mice. We analyzed gene-expression profiles in order to find deregulated genes, which make the cells more prone to undergo transformation.

2013-07-08 | E-GEOD-47813 | biostudies-arrayexpress

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