ArticleOncotarget2016
Crucial factors of the inflammatory microenvironment (IL-1β/TNF-α/TIMP-1) promote the maintenance of the malignant hemopoietic clone of myelofibrosis: an in vitro study.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Tumor necrosis factor alpha is a promising circulating biomarker for the development of obstructive sleep apnea syndrome: a meta-analysis.Oncotarget · 2017Pooled it
- Multi-parametric profiling of plasma-derived extracellular vesicles reveals a disease-associated molecular signature supporting a liquid biopsy approach in myelofibrosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Evaluating inflammatory markers in distinguishing polycythemia Vera from secondary polycythemia: a prospect for novel diagnostic marker.Annals of hematology · 2026Article
- DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications.Current issues in molecular biology · 2025Review
- Red Blood Cell Distribution Width May Predict Drug-Induced Anemia and Prognosis in Patients Affected by Primary/Secondary Myelofibrosis Treated with Ruxolitinib.Oncology and therapy · 2025Article
- Brucellosis complicated by myelofibrosis: report of five cases and review of literature.International journal of clinical and experimental pathology · 2023Article
- Understanding Aberrant Signaling to Elude Therapy Escape Mechanisms in Myeloproliferative Neoplasms.Cancers · 2022Review
- Anti-inflammatory treatment in MPN: targeting TNFR1 and TNFR2 in JAK2-V617F-induced disease.Blood advances · 2021Article
- The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Distinct profile of CD34Journal of experimental & clinical cancer research : CR · 2021Article
- The Role of Inflammation and Inflammasome in Myeloproliferative Disease.Journal of clinical medicine · 2020Review
- The role of circulating monocytes and JAK inhibition in the infectious-driven inflammatory response of myelofibrosis.Oncoimmunology · 2020Article
- Disease-Specific Derangement of Circulating Endocannabinoids andInternational journal of molecular sciences · 2020Article
- Article
- Infliximab therapy together with tyrosine kinase inhibition targets leukemic stem cells in chronic myeloid leukemia.BMC cancer · 2019Article
- Cytokines frequently implicated in myeloproliferative neoplasms.Cytokine: X · 2019Review
- Early Plasma Matrix Metalloproteinase Profiles. A Novel Pathway in Pediatric Acute Respiratory Distress Syndrome.American journal of respiratory and critical care medicine · 2019Article
- Autocrine Tnf signaling favors malignant cells in myelofibrosis in a Tnfr2-dependent fashion.Leukemia · 2018Article
- Cold shock proteins: from cellular mechanisms to pathophysiology and disease.Cell communication and signaling : CCS · 2018Review
- Mobilized Peripheral Blood versus Cord Blood: Insight into the Distinct Role of Proinflammatory Cytokines on Survival, Clonogenic Ability, and Migration of CD34Mediators of inflammation · 2018Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Along with molecular abnormalities (mutations in JAK2, Calreticulin (CALR) and MPL genes), chronic inflammation is the major hallmark of Myelofibrosis (MF). Here, we investigated the in vitro effects of crucial factors of the inflammatory microenvironment (Interleukin (IL)-1β, Tumor Necrosis Factor (TNF)-α, Tissue Inhibitor of Metalloproteinases (TIMP)-1 and ATP) on the functional behaviour of MF-derived circulating CD34+ cells.We found that, regardless mutation status, IL-1β or TNF-α increases the survival of MF-derived CD34+ cells. In addition, along with stimulation of cell cycle progression to the S-phase, IL-1β or TNF-α ± TIMP-1 significantly stimulate(s) the in vitro clonogenic ability of CD34+ cells from JAK2V617 mutated patients. Whereas in the JAK2V617F mutated group, the addition of IL-1β or TNF-α + TIMP-1 decreased the erythroid compartment of the CALR mutated patients. Megakaryocyte progenitors were stimulated by IL-1β (JAK2V617F mutated patients only) and inhibited by TNF-α. IL-1β + TNF-α + C-X-C motif chemokine 12 (CXCL12) ± TIMP-1 highly stimulates the in vitro migration of MF-derived CD34+ cells. Interestingly, after migration toward IL-1β + TNF-α + CXCL12 ± TIMP-1, CD34+ cells from JAK2V617F mutated patients show increased clonogenic ability.Here we demonstrate that the interplay of these inflammatory factors promotes and selects the circulating MF-derived CD34+ cells with higher proliferative activity, clonogenic potential and migration ability. Targeting these micro-environmental interactions may be a clinically relevant approach.
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