JAK the trigger.
A somatic mutation that leads to activation of the JAK2 tyrosine kinase has recently been identified as a recurrent genetic abnormality in several different myeloproliferative disorders. A translocation generating the constitutively activated fusion protein PCM1-JAK2 has also been recently found in atypical chronic myelogenous leukemia and acute leukemia. This recent spate of independent studies (one of which is published in this issue of Oncogene) establish abnormal JAK2 activation as the underlying defect in a significant number of cases of myeloproliferative disease, and JAK2 as an important new therapeutic target.[1]References
- JAK the trigger. Mahon, F.X. Oncogene (2005) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg