Methylation profiles of PMF with and without progression to myelofibrosis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE152519 | GEO | 2021/02/08
REPOSITORIES: GEO
Similar Datasets
Project description:Methylation profiles of PMF with and without progression to myelofibrosis
| PRJNA639574 | ENA
Project description:Primary myelofibrosis (PMF) together with polycythemia vera (PV) and essential thrombocythemia (ET) belongs to the classic Philadelphia-negative myeloproliferative neoplasms (MPNs). PV and ET can evolve to secondary myelofibrosis (SMF) giving rise to post-PV (PPV) and post-ET (PET) myelofibrosis (MF). PMF and SMF patients are currently managed in the same way and prediction of survival is based on the same prognostic models, even if it has been demonstrated that they can’t accurately distinguish different risk categories in SMF. In the last few years interest grew concerning the ability of gene expression profiling (GEP) to provide valuable prognostic information for clinical decision making. To construct a molecular signature that can predict survival according to gene expression we studied GEP of granulocytes from 114 MF patients, including 35 prefibrotic/early PMF (Pre-PMF), 37 overt PMF (Overt-PMF), 26 PET and 16 PPV, using microarray platform.
2021-03-09 | GSE159514 | GEO
Project description:Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm whose severity and treatment complexity is attributed to the presence of bone marrow (BM) fibrosis and alterations of stroma impairing the production of normal blood cells. Despite the recently discovered mutations including the JAK2V617F mutation in about half of patients, the primitive event responsible for the clonal proliferation is still unknown. In the highly inflammatory context of PMF, the presence of fibrosis associated with a neoangiogenesis and an osteosclerosis concomitant to the myeloproliferation and to the increase number of circulating hematopoietic progenitors suggests that the crosstalk between hematopoietic and stromal cells is deregulated in the PMF BM microenvironment. Within these niches, Mesenchymal Stromal Cells (BM-MSC) play a supportive role in the production of growth factors and extracellular matrix which regulate the proliferation, differentiation, adhesion and migration of hematopoietic progenitors. A transcriptome analysis of BM-MSC in PMF patients will help to characterize their molecular alterations and to understand their involvement in the hematopoietic progenitor deregulation that features PMF. Primary Myelofibrosis, mesenchymal stroma cells, bone marrow, myeloproliferative disorders Transcriptome analysis was performed on BM-MSC amplified in vitro after 3 to 5 passages. Agilent Whole Human Genome Oligo Microarrays were used to compare expression profiling of BM-MSC from PMF patients and healthy donors.
2015-01-10 | E-GEOD-44426 | biostudies-arrayexpress
Project description:Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm whose severity and treatment complexity is attributed to the presence of bone marrow (BM) fibrosis and alterations of stroma impairing the production of normal blood cells. Despite the recently discovered mutations including the JAK2V617F mutation in about half of patients, the primitive event responsible for the clonal proliferation is still unknown. In the highly inflammatory context of PMF, the presence of fibrosis associated with a neo-osteogenesis and an osteosclerosis concomitant to the myeloproliferation and to the increase number of circulating hematopoietic progenitors suggests that the crosstalk between hematopoietic cells and the osteoblastic niche is deregulated in the PMF BM microenvironment. Osteoblastic niche is well known to be an important support to regulate hematopoietic stem cell functions in bone marrow. A transcriptome analysis of bone marrow mesenchymal stem cells (BM-MSC) induced in vitro to differentiate in osteoblasts will help to understand the role of these cells in pathophysiology of PMF. Transcriptome analysis was performed on BM-MSC at J0 and J21 of in vitro osteoblastic differentiation. Agilent Whole Human Genome Oligo Microarrays were used to compare expression profiling of BM-MSCs from PMF patients and healthy donors before and after osteoblastic differentiation. Primary Myelofibrosis, mesenchymal stroma cells, bone marrow, myeloproliferative disorders
2015-01-10 | E-GEOD-46021 | biostudies-arrayexpress
Project description:Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm whose severity and treatment complexity is attributed to the presence of bone marrow (BM) fibrosis and alterations of stroma impairing the production of normal blood cells. Despite the recently discovered mutations including the JAK2V617F mutation in about half of patients, the primitive event responsible for the clonal proliferation is still unknown. In the highly inflammatory context of PMF, the presence of fibrosis associated with a neoangiogenesis and an osteosclerosis concomitant to the myeloproliferation and to the increase number of circulating hematopoietic progenitors suggests that the crosstalk between hematopoietic and stromal cells is deregulated in the PMF BM microenvironment. Within these niches, Mesenchymal Stromal Cells (BM-MSC) play a supportive role in the production of growth factors and extracellular matrix which regulate the proliferation, differentiation, adhesion and migration of hematopoietic progenitors. A transcriptome analysis of BM-MSC in PMF patients will help to characterize their molecular alterations and to understand their involvement in the hematopoietic progenitor deregulation that features PMF. Primary Myelofibrosis, mesenchymal stroma cells, bone marrow, myeloproliferative disorders
2015-01-10 | GSE44426 | GEO
Project description:Microarrays were used to assess gene expression in patients with ET, PV, and PMF before and after treatment with IFNalpha2 in a paired design.
2018-06-15 | GSE57793 | GEO
Project description:Microarrays were used to assess gene expression in patients with ET, PV, and PMF before treatment with IFNalpha2.
2017-02-09 | GSE61629 | GEO
Project description:We used microarrays to assess gene expression in patients with ET, PV, and PMF compared to control subjects
2012-01-10 | GSE26049 | GEO
Project description:We performed single cell DNA sequencing by means of Tapestri platform on a mix of Peripheral Blood Mononuclear Cells (PBMCs) and CD34+ hematopoietic stem/progenitor cells (HSPCs) from a primary myelofibrosis (PMF). The main purpose of this project was to reconstruct the clonal composition of the neoplastic population by analyzing the mutational profile at the single-cell level.
2024-10-15 | GSE251689 | GEO
Project description:Primary mielofibrosis (PMF) is a rare chronic myeloproliferative disorder characterized by the accumulation of abnormal megakaryocytes (Mks) in the bone marrow (BM), variable degrees of BM fibrosis, osteosclerosis and angiogenesis, immature myeloid and erythroid cells, and tear-drop erythrocytes in the peripheral blood (PB), and extramedullary hematopoiesis. The identification of the JAK2V617F mutation represented a seminal discovery in the field of Philadelphia-chromosome–negative chronic myeloproliferative neoplasms (MPNs), providing clues to the pathogenesis, prompting a revision of the diagnostic criteria, and culminating in the development of clinical trials with JAK2 (and JAK1) inhibitors. The JAK2V617F mutation occurs in almost all patients with polycythemia vera (PV) and in 50%-70% of those with essential thrombocythemia (ET) and primary myelofibrosis (PMF). Soon after the identification of the JAK2V617F mutation, mutations in JAK2 exon 12 were described in rare patients with JAK2V617F-negative PV and mutations in MPL were reported in 5%-10% of ET or PMF subjects. The complexity of the molecular pathogenesis of MPNs is reinforced by discovery of additional mutations in TET2, ASXL1, CBL, IDH1/IDH2, EZH2 and IKZF1. These mutations are detected in a minority of patients at different phases of the disorder, including leukemic transformation, and are variably associated each other and with JAK2 or MPL mutations. In order to better characterize biological differences between mutated and wild-type PMF cell populations we performed a gene expression profiling on 9 samples carrying at least one mutation in ASXL1, SRSF2 or EZH2 genes and 11 wild-type samples using the Affymetrix GeneChip technology. After data preprocessing and filtering a supervised analysis approach was used to define a gene expression signature for mutated samples. PMF samples carrying at least one mutation in ASXL1, SRSF2 or EZH2 genes exhibit a specific molecular signature as compared with WT samples. Gene expression profile (GEP) of CD34+ cells from 20 PMF patients (1 replicate for each sample). In particular, GEP was performed on 9 samples carrying at least one mutation in ASXL1, SRSF2 or EZH2 genes and 11 wild-type samples.
2013-07-23 | E-GEOD-41812 | biostudies-arrayexpress