Advances in the molecular characterization of Philadelphia-negative chronic myeloproliferative disorders
Current Opinion in Oncology, ISSN: 1040-8746, Vol: 19, Issue: 6, Page: 628-634
2007
- 8Citations
- 16Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations8
- Citation Indexes8
- CrossRef6
- Captures16
- Readers16
- 16
Review Description
PURPOSE OF REVIEW: The identification and characterization of somatic disease alleles have greatly improved our understanding of the molecular pathogenesis of myeloproliferative disorders. This review focuses on recent studies investigating the role of activated tyrosine kinase signaling in the Philadelphia chromosome negative myeloproliferative disorders. RECENT FINDINGS: Previously identified tyrosine kinase mutations in chronic myeloid leukemia and other myeloproliferative disorders suggested the possibility that polycythemia vera, essential thrombocythemia and primary myelofibrosis are also caused by activated tyrosine kinases. Recent studies identified an activating mutation in the JAK2 tyrosine kinase (JAK2V617F) in most patients with polycythemia vera and in approximately half of those with essential thrombocythemia and primary myelofibrosis. More recently, activating mutations in the thrombopoietin receptor and in JAK2 exon 12 have been identified in JAK2V617F negative myeloproliferative disorders. SUMMARY: The discovery of activated tyrosine kinases in the majority of patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis has diagnostic and pathogenetic implications. Subsequent studies are needed to elucidate the cause of myeloproliferative disorders without known disease alleles and to determine if inhibition of JAK2 signaling has therapeutic efficacy in the treatment of polycythemia vera, essential thrombocythemia and primary myelofibrosis. © 2007 Lippincott Williams & Wilkins, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34848840612&origin=inward; http://dx.doi.org/10.1097/cco.0b013e3282f0e20c; http://www.ncbi.nlm.nih.gov/pubmed/17906464; https://journals.lww.com/00001622-200711000-00016; http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00001622-200711000-00016; https://dx.doi.org/10.1097/cco.0b013e3282f0e20c; https://insights.ovid.com/crossref?an=00001622-200711000-00016
Ovid Technologies (Wolters Kluwer Health)
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