ReviewLeukemia2006
Chronic myeloproliferative disorders: a tyrosine kinase tale.
Review in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 71 citations in OpenAlex.
- Monitoring Chronic Myeloid Leukemia: How Molecular Tools May Drive Therapeutic Approaches.Frontiers in oncology · 2019Review
- Rapid and sensitive detection of calreticulin type 1 and 2 mutations by real-time quantitative PCR.Molecular diagnosis & therapy · 2015Article
- Alternative TEL-JAK2 fusions associated with T-cell acute lymphoblastic leukemia and atypical chronic myelogenous leukemia dissected in zebrafish.Haematologica · 2012Article
- Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disorders.Leukemia · 2012Article
- JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation.Cancer cell · 2011Article
- Transcription factor mutations in myelodysplastic/myeloproliferative neoplasms.Haematologica · 2010Article
- Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteria.International journal of hematology · 2010Review
- Cell cycle genes and ovarian cancer susceptibility: a tagSNP analysis.British journal of cancer · 2009Article
- Intrinsic differences between the catalytic properties of the oncogenic NUP214-ABL1 and BCR-ABL1 fusion protein kinases.Leukemia · 2008Article
- Review
- Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia.Leukemia · 2008Review
- Review
- Recurrent chromosomal aberration at 12q15 in chronic idiopathic myelofibrosis with or without JAK2(V617F) mutation.Leukemia · 2007Article
- Hematopoietic stem cell transplants for chronic myeloid leukemia in Europe--impact of cost considerations.Leukemia · 2007Article
- Review
- Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors.Leukemia · 2006Article
- The war on cancer: a report from the front lines.Proceedings (Baylor University. Medical Center) · 2006Article
- Oncogenic kinases of myeloproliferative disorders induce both protein synthesis and G1 activators.Leukemia · 2006Article
- JAK2 V617F in myeloid disorders: molecular diagnostic techniques and their clinical utility: a paper from the 2005 William Beaumont Hospital Symposium on Molecular Pathology.The Journal of molecular diagnostics : JMD · 2006Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloproliferative diseases (CMPDs) are characterized by the abnormal proliferation and survival of one or more myeloid cell types. The archetype of this class of hematological diseases is chronic myeloid leukemia (CML), characterized by the presence of the Philadelphia (Ph) chromosome, the result of t(9;22)(q34;q11), and the associated BCR-ABL1 oncogene. Some of the Ph-negative myeloproliferative diseases are characterized by other chromosomal translocations involving a variety of tyrosine kinase genes, including ABL1, ABL2, PDGFRA, PDGFRB, FGFR1, and JAK2. The majority of Ph-negative CMPDs, however, such as chronic eosinophilic leukemia, polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis are not characterized by the presence of recurrent chromosomal abnormalities. Recent studies have identified the FIP1L1-PDGFRA fusion gene, generated due to a small cryptic deletion on chromosome 4q12, and the activating V617F mutation in JAK2 in a significant fraction of Ph-negative CMPDs. These results show that abnormalities in tyrosine kinase genes are central to the molecular pathogenesis of CMPDs. Genome-wide screenings to identify novel tyrosine kinase abnormalities in CMPDs may contribute to further improvement of the diagnosis and the treatment of these diseases.
Indexed as
Identifiers
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.