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.
Oncogene (2005) 24, 7125-7126. doi:10.1038/sj.onc.1208885; published online 4 July 2005.
MeSH terms
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Amino Acid Substitution
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Autoantigens
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Cell Cycle Proteins / chemistry
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Cell Cycle Proteins / genetics*
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Chromosomes, Human, Pair 8
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Chromosomes, Human, Pair 9
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Enzyme Activation / genetics
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Humans
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Janus Kinase 2
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Leukemia / genetics
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
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Oncogene Proteins, Fusion / genetics
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Phenylalanine / metabolism
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Protein Structure, Tertiary
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Protein-Tyrosine Kinases / chemistry
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Protein-Tyrosine Kinases / genetics*
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Proto-Oncogene Proteins / chemistry
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Proto-Oncogene Proteins / genetics*
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Translocation, Genetic
Substances
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Autoantigens
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Cell Cycle Proteins
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Oncogene Proteins, Fusion
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PCM1 protein, human
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Proto-Oncogene Proteins
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Phenylalanine
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Protein-Tyrosine Kinases
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JAK2 protein, human
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Janus Kinase 2