ReviewLeukemia2008
Aberrant signal transduction pathways in myeloproliferative neoplasms.
Review in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 70 citations in OpenAlex.
- Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice.Nature communications · 2026Article
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- Modelling Cancer in Drosophila: Exploration to Personalised Medicine.Advances in experimental medicine and biology · 2025Review
- 2022 Cannon lecture: an ode to signal transduction: how the growth hormone pathway revealed insight into height, malignancy, and obesity.American journal of physiology. Endocrinology and metabolism · 2023Review
- TGF-β signaling in myeloproliferative neoplasms contributes to myelofibrosis without disrupting the hematopoietic niche.The Journal of clinical investigation · 2022Article
- HMGA Proteins in Hematological Malignancies.Cancers · 2020Review
- Review
- Genetic alterations of 9p24 in lymphomas and their impact for cancer (immuno-)therapy.Virchows Archiv : an international journal of pathology · 2019Article
- Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors.Frontiers in oncology · 2019Article
- Article
- Identification of functionally primitive and immunophenotypically distinct subpopulations in secondary acute myeloid leukemia by mass cytometry.Cytometry. Part B, Clinical cytometry · 2019Article
- Role of TGF-β1/miR-382-5p/SOD2 axis in the induction of oxidative stress in CD34+ cells from primary myelofibrosis.Molecular oncology · 2018Article
- Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells.Journal of visualized experiments : JoVE · 2018Article
- Article
- JAK2 inhibition has different therapeutic effects according to myeloproliferative neoplasm development in mice.Journal of cellular and molecular medicine · 2015Article
- Origins of the Vertebrate Erythro/Megakaryocytic System.BioMed research international · 2015Review
- Eliminative signaling by Janus kinases: role in the downregulation of associated receptors.Journal of cellular biochemistry · 2014Review
- Molecular pathways: Jak/STAT pathway: mutations, inhibitors, and resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Review
- Cooperative effects of Janus and Aurora kinase inhibition by CEP701 in cells expressing Jak2V617F.Journal of cellular and molecular medicine · 2013Article
- A novel, highly sensitive and rapid allele-specific loop-mediated amplification assay for the detection of the JAK2V617F mutation in chronic myeloproliferative neoplasms.Haematologica · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BCR-ABL-negative myeloproliferative neoplasms (MPNs), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF), entered the spotlight in 2005 when the unique somatic acquired JAK2 V617F mutation was described in >95% of PV and in 50% of ET and PMF patients. For the very rare PV patients who do not harbor the JAK2 V617F mutation, exon 12 JAK2 mutants were discovered also to result in activated forms of JAK2. A minority of ET and PMF patients harbor mutations that constitutively activate the thrombopoietin receptor (TpoR). In bone marrow reconstitution models based on retroviral transduction, the phenotype induced by JAK2 V617F is less severe and different from the rapid fatal myelofibrosis induced by TpoR W515L. The reasons for these differences are unknown. Exactly by which mechanism(s) one acquired somatic mutation, JAK2 V617F, can promote three different diseases remains a mystery, although gene dosage and host genetic variation might have important functions. We review the recent progress made in deciphering signaling anomalies in PV, ET and PMF, with an emphasis on the relationship between JAK2 V617F and cytokine receptor signaling and on cross-talk with several other signaling pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.