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Gene expression data of c-kit+ BM cells from Gadd45g-deficient mice with MPN and those from controls

ABSTRACT: Gene expression data of c-kit+ BM cells from Gadd45g-deficient mice with MPN and those from controls

PROVIDER: PRJNA954762 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24144050_1.fastq.gz	Fastqsanger.gz
	SRR24144050_2.fastq.gz	Fastqsanger.gz
	SRR24144051_1.fastq.gz	Fastqsanger.gz
	SRR24144051_2.fastq.gz	Fastqsanger.gz

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Gene expression data of c-kit+ BM cells from Gadd45g-deficient mice with MPN and those from controls

Project description:To elucidate the mechanisms underlying the pathogenic role of Gadd45g deficiency in myeloproliferative neoplasms, we performed RNA sequencing on c-kit+ BM cells from heterozygous Gadd45g knockout mice with MPN and those from Ctrl mice.

2024-01-25 | GSE229495 | GEO

Proteins interact with GADD45g in c-kit+ BM cells of wild-type mice

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Gene expression profiles of human Mesenchymal Stromal Cells (MSC) from JAK2+ myeloproliferative neoplasms (MPN)

Project description:In this study we analyzed the behavior of bone marrow MSC (BM-MSC) from MPN patients with the mutation in JAK2V617F. We initially characterized the biological function and gene expression profile changes in BM-MSC from MPN patients when compared to BM-MSC of healthy donors (HD). Then, we established co-cultures between MSC cell lines (HTERT and HS5) and the UKE-1 MPN cell line, and performed RT-PCR to study if the leukemic cells were able to modify the genes related to hematopoietic support.

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Integrated analysis of transcriptional and chromatin alteration in Jak2V617F and Asxl1-/-Jak2V617F BM c-kit+ cells

Project description:We performed bulk RNA-seq, transposase-accessible chromatin using sequencing (ATAC-Seq) and chromatin immunoprecipitation (ChIP)-seq on Asxl1-/-Jak2VF and Jak2VF BM c-kit+ cells to elucidate the transcriptional and associated epigenetic alterations after Asxl1 deletion. GSEA showed that the upregulated genes in Asxl1-/-Jak2VF were significantly associated with bona fide PcG target genes, as identified by the overlap between H3K27me3 and H2AK119ub1 ChIP-seq experiments . Integrated analysis of RNA-seq and ATAC-seq data showed that there existed a significant increase of chromatin accessibility associated with upregulated genes, and these sites with gained accessibility were enriched with increased levels of H3K4me1 and H3K27ac, histone marks of active enhancers in Asxl1-/-Jak2VF BM c-kit+ cells. Moreover, PcG target gene Egr1 was upregulated in BM c-kit+ cells compared with other three genotypes and considered as key gene for disease phenotypes.

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IL-1β promotes MPN disease initiation by favoring early clonal expansion of JAK2-mutant hematopoietic stem cells

Project description:JAK2-V617F is the most frequent somatic mutation causing myeloproliferative neoplasm (MPN). JAK2-V617F can be found in healthy individuals with clonal hematopoiesis of indeterminate potential (CHIP) with a frequency much higher than the prevalence of MPN. The factors controlling the conversion of JAK2-V617F CHIP to MPN are largely unknown. We hypothesized that IL-1β mediated inflammation can favor this progression. We established an experimental system using bone marrow (BM) transplantations from JAK2-V617F and GFP transgenic (VF;GFP) mice, that were further crossed with IL-1β-/- or IL-1R1-/- mice. To study the role of IL-1β and its receptor on monoclonal evolution of MPN, we performed competitive BM transplantations at high dilutions with only 1-3 hematopoietic stem cells (HSCs) per recipient. Loss of IL-1β in JAK2-mutant HSCs reduced engraftment, restricted clonal expansion, lowered the total numbers of functional HSCs, and decreased the rate of conversion to MPN. Loss of IL-1R1 in the recipients also lowered the conversion to MPN, but did not reduce the frequency of engraftment of JAK2-mutant HSCs. WT recipients transplanted with VF;GFP BM that developed MPN had elevated IL-1β levels and reduced frequencies of mesenchymal stromal cells (MSCs). Interestingly, frequencies of MSCs were also reduced in recipients that did not develop MPN, had only marginally elevated IL-1β levels and displayed low GFP-chimerism resembling CHIP. Anti-IL-1β antibody preserved high frequencies of MSCs in VF;GFP recipients and reduced the rate of engraftment and the conversion to MPN. Our results identify IL-1β as a potential therapeutic target for preventing the transition from JAK2-V617F CHIP to MPN.

2024-01-29 | GSE250507 | GEO

Bisulphite MPN colonies

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Project description:Philadelphia-chromosome negative myeloproliferative neoplasms (MPNs) including polycythemia vera, essential thrombocythemia and primary myelofibrosis show an inherent tendency for transformation into leukemia (MPN-blast phase), which is hypothesized to be accompanied by acquisition of additional genomic lesions. We, therefore, examined chromosomal abnormalities by high-resolution single-nucleotide polymorphism (SNP) array in 88 MPN patients, as well as 71 cases with MPN-blast phase, and correlated these findings with their clinical parameters. Frequent genomic alterations were found in MPN after leukemic transformation with up to 3-fold more genomic changes per sample compared to samples in chronic phase (p<0.001). We identified commonly altered regions involved in disease progression including established targets (ETV6, TP53 and RUNX1), as well as new candidate genes on 7q, 16q, 19p and 21q. Moreover, trisomy 8 or amplification of 8q24 (MYC) was almost exclusively detected in JAK2V617F(-) cases with MPN-blast phase. Remarkably, copy-number neutral-loss of heterozygosity (CNN-LOH) on either 7q or 9p including homozygous JAK2V617F was related to decreased survival after leukemic transformation (p=0.01 and p=0.016, respectively). Our high density SNP-array analysis of MPN genomes in the chronic compared to leukemic stage identified novel target genes and provided prognostic insights associated with the evolution to leukemia. Keywords: SNP-chip To identify oncogenic lesions in MPD, we performed a genome-wide analysis of primary MPD samples using high-density SNP arrays (Affymetrix GeneChip).

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H3K4me3 associated chromatin by CUT&RUN on c-kit+ cells from chimeras

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2023-03-24 | GSE199338 | GEO

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