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Single case sample of a Non-Hodgkin lymphoma

ABSTRACT: Our study provides evidence that JAK2, PDL1 and PDL2 are recurrently affected by structural and numerical aberrations in lymphoid neoplasms. The study highlights the role of PDL1/PDL2 in lymphoma progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46005 | GEO | 2013/04/13

SECONDARY ACCESSION(S): PRJNA196910

REPOSITORIES: GEO

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Single case sample of a Non-Hodgkin lymphoma

Project description:Our study provides evidence that JAK2, PDL1 and PDL2 are recurrently affected by structural and numerical aberrations in lymphoid neoplasms. The study highlights the role of PDL1/PDL2 in lymphoma progression. single case analysis

2013-04-13 | E-GEOD-46005 | biostudies-arrayexpress

PD-1 induced proliferating T cells exhibit a distinct transcriptional signature

Project description:Analysis of primary human CD4+ T cells stained with the proliferation tracker CFSE and stimulated with anti-CD3, anti-CD28, and PDL1 or PDL2 for 5 days. Cells were sorted at the end of stimulation based on number of proliferative doublings prior to RNA isolation. Results provide insight into the PD-1 response pathway in CD4+ T cells that are proliferating or non-proliferating following stimulation.

2021-10-20 | GSE159774 | GEO

Oncostatin M effects in IMR90 cells

Project description:The JAK2 mutation V617F is detectable in a majority of patients with Ph-negative myeloproliferative neoplasms (MPN). Enforced expression of JAK2 V617F in mice induces myeloproliferation and bone marrow (BM) fibrosis suggesting a causal role for the JAK2 mutant in the pathogenesis of MPN. However, little is known about mechanisms and effector molecules contributing to JAK2 V617F-induced myeloproliferation and fibrosis. Here we show that JAK2 V617F promotes expression of oncostatin M (OSM) in neoplastic myeloid cells. Correspondingly, OSM was found to be overexpressed in the BM and elevated in the serum of patients with JAK2 V617F+ MPN. In addition, OSM secreted by JAK2 V617F+ cells stimulated growth of fibroblasts and microvascular endothelial cells and induced the production of angiogenic and profibrogenic cytokines (HGF, VEGF, and SDF-1) in BM fibroblasts. All effects of MPN cell-derived OSM were blocked by a neutralizing anti-OSM antibody, whereas the production of OSM in MPN cells was effectively suppressed by a pharmacologic JAK2 inhibitor or RNAi-mediated knockdown of JAK2. In summary, JAK2 V617F-mediated upregulation of OSM may contribute to fibrosis, neoangiogenesis, and the cytokine storm observed in JAK2 V617F+ MPN, suggesting that OSM could serve as a novel therapeutic target molecule in these neoplasms. IMR90 cells were treated with a single dose of rh Oncostatin M (10ng/ml).

2013-01-29 | E-GEOD-29655 | biostudies-arrayexpress

Talarmain2022- Model of JAK2/TET2/HOXA9 in myeloproliferative neoplasms

Project description:Model describing how HOXA9 may control the evolution of myeloproliferative neoplasms by integrating the orders of JAK2 and TET2 mutation

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Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predispose to myeloproliferative neoplasms

Project description:Genome-wide association study of JAK2 V617F negative myeloproliferative neoplasms consisting of 524 cases at stage 1

2015-02-20 | E-MTAB-3340 | biostudies-arrayexpress

Iron-dependent switch in MPN-phenotype

Project description:Iron is a modifier of the phenotypes of JAK2-mutant myeloproliferative neoplasms

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Oncostatin M effects in IMR90 cells

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RNA Sequencing Analysis of Wild Type and Non-phosphorylatable CARM1 mutation knock-in HEL cells

Project description:CARM1 is essential for the development and maintenance of myeloid neoplasms. We found that non-phosphorylatable CARM1 mutation impairs cell cycle progression, induces apoptosis, and downregulates stemness in JAK2-mutant cell lines, suggesting that CARM1 phosphorylation is required for maximal proliferation of myeloid neoplasms.

2024-04-03 | GSE174432 | GEO

Mus musculus

Project description:PDL2+, PDL2- and LPS treated PDL2- WT bone-marrow derived murine DCs

| PRJNA219317 | ENA

Identification of potential new therapeutic approaches for JAK2 V617F mutant patients

Project description:Myelofibrosis is often associated with the myeloproliferative neoplasms and expression of oncogenic JAK2 mutants. Patients with myelofibrosis have diminished quality of life due to systemic symptoms arising from fibrotic changes in the bone marrow. The introduction of the JAK2 inhibitor, ruxolitinib, has been of benefit in the treatment of myelofibrosis patients however, it is not curative and there is still a requirement for new targeted therapies to eradicate the cells at the heart of myelofibrosis pathology. Repurposing drugs bypasses many of the hurdles present in drug development, such as toxicity and pharmacodynamic profiling. To this end we undertook a re-analysis of our pre-existing proteomic data sets to identify perturbed biochemical pathways and their associated drugs/inhibitors to potentially target the cells driving myelofibrosis. This approach identified CBL0137 as a candidate for targeting JAK2 mutant driven malignancies. We therefore assessed CBL0137 as a new agent to extinguish JAK2 mutant primitive cells and show its ability to preferentially target cells from MF patients compared to healthy control cells. Further we define its mechanistic action in primary haemopoietic progenitor cells and demonstrate its ability to reduce splenomegaly and reticulocyte number in a transgenic murine model of myeloproliferative neoplasms.

2022-08-11 | E-MTAB-11653 | biostudies-arrayexpress

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