ReviewLeukemia2008
Genetic complexity of 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 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 89 citations in OpenAlex.
- Trial
- Molecular Studies for the Early Detection of Philadelphia-Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Phenotypic characterization of disease-initiating stem cells in JAK2- or CALR-mutated myeloproliferative neoplasms.American journal of hematology · 2023Article
- The Genetic Basis of Primary Myelofibrosis and Its Clinical Relevance.International journal of molecular sciences · 2020Review
- Progress in elucidation of molecular pathophysiology of myeloproliferative neoplasms and its application to therapeutic decisions.International journal of hematology · 2020Review
- Serum of myeloproliferative neoplasms stimulates hematopoietic stem and progenitor cells.PloS one · 2018Article
- MYC Deregulation in Primary Human Cancers.Genes · 2017Review
- Article
- JAK2 exon 14 skipping in patients with primary myelofibrosis: a minor splice variant modulated by the JAK2-V617F allele burden.PloS one · 2015Article
- Back to biology: new insights on inheritance in myeloproliferative disorders.Current hematologic malignancy reports · 2014Review
- Mast cell activation syndrome as a significant comorbidity in sickle cell disease.The American journal of the medical sciences · 2014Article
- Calreticulin mutation-specific immunostaining in myeloproliferative neoplasms: pathogenetic insight and diagnostic value.Leukemia · 2014Article
- Targeted cancer exome sequencing reveals recurrent mutations in myeloproliferative neoplasms.Leukemia · 2014Article
- Spontaneous regression of essential thrombocythemia with MPL mutation on menopause.International journal of hematology · 2014Article
- Genetic basis of MPN: Beyond JAK2-V617F.Current hematologic malignancy reports · 2013Review
- Utility of hydroxyurea in mast cell activation syndrome.Experimental hematology & oncology · 2013Article
- Genetic and epigenetic alterations of myeloproliferative disorders.International journal of hematology · 2013Review
- Allelic expression imbalance of JAK2 V617F mutation in BCR-ABL negative myeloproliferative neoplasms.PloS one · 2013Article
- Cell biology: a key driver of therapeutic innovation.The Journal of cell biology · 2012Article
- [Bone marrow histology from the clinical point of view].Der Pathologe · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenic mutations in JAK2 and MPL genes have recently been identified in myeloproliferative neoplasms (MPNs). In addition to these mutations, cytogenetic aberrations are frequently present at diagnosis but their role in the pathogenesis remains unclear. Two models of MPN pathogenesis have recently emerged based on either a single-hit or a multi-hit concept. The first model proposes that the acquisition of JAK2 mutations is the disease-initiating event, causing both the onset of disease phenotype and establishment of clonal hematopoiesis. The second model postulates the existence of 'pre-JAK2' mutations that establish clonal hematopoiesis before acquisition of JAK2 mutations and onset of disease phenotype. In this review, the two models have been critically evaluated in the context of the latest findings. At present, neither of the two models can be universally applied to all MPN patients due to their genetic heterogeneity. It is likely that the disease pathogenesis in some patients follows the first, and in other patients, the second model. Thus, the somatic mutations in MPN do not seem to be acquired in a predetermined order as seen in other malignancies, but occur randomly. Furthermore, the role of uniparental disomy in MPN and certain aspects of MPN therapy are discussed.
Indexed as
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What OpenQuestion holds
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.