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PubMed · 16007127

JAK the trigger.

François-Xavier Mahon
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Abstract

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.

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Amino Acid SubstitutionAutoantigensCell Cycle ProteinsChromosomes, Human, Pair 8Chromosomes, Human, Pair 9Enzyme ActivationHumansJanus Kinase 2LeukemiaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveOncogene Proteins, FusionPhenylalanineProtein Structure, TertiaryProtein-Tyrosine KinasesProto-Oncogene ProteinsTranslocation, GeneticCommentJournal Article

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François-Xavier Mahon. 2005-11-03. JAK the trigger.. https://doi.org/10.1038/sj.onc.1208885

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