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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

ABSTRACT: TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

PROVIDER: PRJNA851020 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19753192.fastq.gz	Fastqsanger.gz
	SRR19753193.fastq.gz	Fastqsanger.gz
	SRR19753194.fastq.gz	Fastqsanger.gz
	SRR19753195.fastq.gz	Fastqsanger.gz

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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

Project description:TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

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Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Project description:Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation. These studies show that a ubiquitin ligase-substrate pair can orchestrate the molecular program of HSC differentitiation Gene expression profiles from WT and Tet2-/- sorted LSK and myeloid progenitors (CMP and GMP) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Mouse 430 2.0) and key targets were validated by chromatin immunoprecipitation experiments.

2011-07-01 | E-GEOD-27816 | biostudies-arrayexpress

TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 2]

Project description:To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

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TET2 deficiency maintains leukemia stem cell self-renewal and subverts tumor immunity [model 1]

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Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

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Id1 maintains embryonic stem cell self-renewal by upregulation of Nanog and repression of Brachyury expression

Project description:Understanding the mechanism by which embryonic stem (ES) cells self-renew is critical for the realization of their therapeutic potential. Previously it had been shown that in combination with LIF, Id proteins were sufficient to maintain mouse ES cells in a self-renewing state. Here we investigate the requirement for Id1 in maintaing ES cell self-renewal and blocking differentiation. We find that Id1-/- ES cells have a propensity to differentiate and a decreased capacity to self-renew. Chronic or acute loss of Id1 leads to a down-regulation of Nanog, a critical regulator of self-renewal. In addition, in the absence of Id1, ES cells express elevated levels of Brachyury, a marker of mesendoderm differentiation. We find that loss of both Nanog and Id1 is required for the up-regulation of Brachyury, and Id1 maintains Nanog expression by blocking the expression of Zeb1, a repressor of Nanog transcription. These results identify Id1 as an important factor in the maintenance of ES cell self-renewal and suggest a plausible mechanism for its control of lineage commitment. Wild type and Id1-/- ES cells were grown on gelatin under normal self-renewing conditions (in the presence of serum and LIF).

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TET2 deficiency subverts tumor immunity [model 3]

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Transcriptional and epigenetic reprogramming mediated by chronic IL1β exposure drives self-renewal ability and myeloid priming in TET2 deficient stem and progenitor cells [10x_scRNAseq]

Project description:Clonal hematopoiesis (CH) increases risk for the development of hematological malignancy and cardiovascular disease. IL1β is elevated in patients with CH and its inhibition mitigates cardiovascular risk in murine models with Tet2 loss-of-function. How IL1β alters population dynamics of hematopoietic cells upon Tet2 deletion (Tet2-KO) is not well understood. We demonstrated IL1β expands Tet2-KO neutrophils, monocytes/macrophages, and long-term hematopoietic stem cells with reduced lymphopoiesis. IL1β promotes myeloid bias over other lineages coinciding with failure to demethylate lineage associated enhancer and transcription factor binding sites in Tet2-KO HSPCs. IL1β enhanced self-renewal ability of Tet2-KO HSPCs by upregulating genes associated with self-renewal potential and by failure to demethylate binding sites of transcription factors promoting differentiation. IL1β-mediated premalignant phenotype is reversed by IL1β antagonist anakinra or deletion of the Il1 receptor, in vivo. Our results demonstrated that targeting IL-1 signaling could be an efficient early intervention strategy in preleukemic disorders.

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