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Gene expression profile at single cell level of phenotypic LT-HSCs from single-mutant JAK2 V617F and double mutant JAK2 V617F Dnmt3a-/- mice

ABSTRACT: Gene expression profile at single cell level of phenotypic LT-HSCs from single-mutant JAK2 V617F and double mutant JAK2 V617F Dnmt3a-/- mice

PROVIDER: PRJNA938038 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23597771_1.fastq.gz	Fastqsanger.gz
	SRR23597771_2.fastq.gz	Fastqsanger.gz
	SRR23597772_1.fastq.gz	Fastqsanger.gz
	SRR23597772_2.fastq.gz	Fastqsanger.gz
	SRR23597773_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of phenotypic LT-HSCs from single-mutant JAK2 V617F and double mutant JAK2 V617F;Dnmt3a-/- mice

Project description:We investigated if Dnmt3a loss leads to alterations in JAK2 V617F LT-HSCs heterogenity and expression profile using single-cell RNA sequencing.

2024-03-29 | GSE225918 | GEO

Effects of the treatment with pegIFNa, Azacytidine or pegIFNa+Azacytidine in LT-HSCs from JAK2-V617F MPN mice or JAK2-V617F;Dnmt3a-KO MPN mice.

Project description:Pegylated interferon alpha (pegIFNα) can induce molecular remissions in JAK2-V617F-positive myeloproliferative neoplasms (MPN) patients by targeting long-term hematopoietic stem cells (LT-HSCs). Additional somatic mutations in genes regulating LT-HSC self-renewal, such as DNMT3A, have been reported to have poorer responses to pegIFNα. We investigated if DNMT3A loss leads to alterations in JAK2-V617F LT-HSCs functions conferring resistance to pegIFNα treatment in a mouse model of MPN and in hematopoietic progenitors from MPN patients. Long-term treatment with pegIFNα normalized blood parameters, reduced splenomegaly and JAK2-V617F-chimerism in single-mutant JAK2-V617F (VF) mice. However, pegIFNα in VF;Dnmt3aΔ/Δ (VF;DmΔ/Δ) mice worsened splenomegaly and failed to reduce JAK2-V617F-chimerism. Furthermore, LT-HSCs from VF;DmΔ/Δ mice compared to VF were less prone to accumulate DNA damage and exit dormancy upon pegIFNα treatment. RNA-sequencing showed that IFNα induced stronger upregulation of inflammatory pathways in LT-HSCs from VF;DmΔ/Δ compared to VF mice, indicating that the resistance of VF;DmΔ/Δ LT-HSC was not due to failure in IFNα signaling. Transplantations of bone marrow from pegIFNα treated VF;DmΔ/Δ mice gave rise to more aggressive disease in secondary and tertiary recipients. Liquid cultures of hematopoietic progenitors from MPN patients with JAK2-V617F and DNMT3A mutation showed increased percentages of JAK2-V617F-positive colonies upon IFNα exposure, whereas in patients with JAK2-V617F alone the percentages of JAK2-V617F-positive colonies decreased or remained unchanged. PegIFNα combined with 5-azacytidine only partially overcame resistance in VF;DmΔ/Δ mice. However, this combination strongly decreased the JAK2-mutant allele burden in mice carrying VF mutation only, showing potential to inflict substantial damage preferentially to the JAK2-mutant clone.

2024-03-29 | GSE255253 | GEO

Murine Ba/F3 Cells: Ba/F3 cells expressing wild type JAK2 (WT cells) vs. Ba/F3 cells expressing JAK2 V617F mutant (VF cells)

Project description:Transcriptional profiling of transformed Ba/F3 cells by myeloproliferative neoplasm-associated JAK2 V617F mutant comparing control Ba/F3 cells expressing wild type JAK2.

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Murine Ba/F3 Cells: Ba/F3 cells expressing wild type JAK2 (WT cells) vs. Ba/F3 cells expressing JAK2 V617F mutant (VF cells)

Project description:Transcriptional profiling of transformed Ba/F3 cells by myeloproliferative neoplasm-associated JAK2 V617F mutant comparing control Ba/F3 cells expressing wild type JAK2. Two-condition experiment, WT cells vs. VF cells. One replicate per array.

2013-10-31 | E-GEOD-34239 | biostudies-arrayexpress

Effects of the treatment with pegIFNa, Azacytidine or pegIFNa+Azacytidine in LT-HSCs from JAK2-V617F MPN mice or JAK2-V617F Dnmt3a-KO MPN mice.

Project description:Effects of the treatment with pegIFNa, Azacytidine or pegIFNa+Azacytidine in LT-HSCs from JAK2-V617F MPN mice or JAK2-V617F Dnmt3a-KO MPN mice.

| PRJNA1074267 | ENA

Identification of potential new therapeutic approaches for JAK2 V617F mutant patients

Project description:Identification of potential new therapeutic approaches for JAK2 V617F mutant patients

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Project description:Transcriptomics analysis was performed on FACS purified HSPC subsets from SclCre;V617F mice and WT mice bone marrow. The goal of this study is to identify the molecular signatures that are specific to the mutant JAK2 expressing HSPC subsets. We found that mutant JAK2 activation caused dysregulated expression of large numbers of genes in primitive HSPC subsets. Furthermore, this analysis revealed molecular identity and developmental proximity of HSC CD41+/- cells within the HSPC hierarchy.

2021-03-03 | GSE132570 | GEO

Analysis of mouse T cell transcription profile after co-culture with BaF3 cells with or without the oncogenic point mutation JAK2 V617F

Project description:The activation of PD-1 (Programmed Death receptor-1) on T cells can cause T cell exhaustion and immune tolerance. Some tumors up-regulate the expression of the ligand of PD-1, namely PD-L1 (Programmed Death Receptor-Ligand 1), thus preventing anti-tumor immune response and promoting immune-escape. Previous studies have shown that JAK2 (Janus Kinase 2) signaling can promote PD-L1 expression in Hodgkin Lymphoma. In Myeloproliferative Neoplasms (MPN), JAK2 is frequently characterized by the the presence of the point-mutation V617F, which leads to its constitutive activation and to uncontrolled cell proliferation and survival. Accordingly, tumor cell lines expressing JAK2 V617F express higher levels of PD-L1 as compared to tumor cell lines negative for such mutations. In this experiment, we transfected BaF3 cells with a vector (plasmid for Murine Stem Cell Virus) containing the gene for JAK2 with the point-mutation V617F. As control, we used BaF3 cells transfected with the same vector, but without the gene for JAK2 V617F (empty vector). Both the cell lines (with/without JAK2 V617F) were co-cultured with primary murine T cells. When co-cultured with BaF3 cells expressing JAK2 V617F, T cells upregulated genes connected to senescence pathways, showed increased apoptosis, less cytokine production, and displayed other forms of dysfunction which can be associated with the activation of PD-1.

2018-12-01 | E-MTAB-5028 | biostudies-arrayexpress

Proinflammatory phenotype of iPS cell-derived JAK2 V617F megakaryocytes induces fibrosis in 3D in vitro bone marrow niche

Project description:In this dataset, we determine the global gene expression in human induced pluripotent stem (iPS) cell-derived CD61+ megakaryocytes carrying homozygous JAK2 V617F mutation or the JAK2 wildtype gene.

2024-01-25 | GSE228092 | GEO

AG221 and Ruxolitinib Treatment Effects on LSKs in IDH2-R140Q JAK2-V617F Transplant Recipients

Project description:Transplant recipients of IDH2-R140Q JAK2-V617F expressing bone marrow were treated with AG221 and ruxolitinib monotherapy, combined therapy, or vehicle. LSKs were sorted from terminal samples and sequenced with three WT controls.

2018-02-22 | GSE95771 | GEO

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