JAKing up hematopoietic proliferation.

Kevin Shannon; Richard A Van Etten

doi:10.1016/j.ccr.2005.04.002

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JAKing up hematopoietic proliferation.

Kevin Shannon·Richard A Van Etten

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Abstract

Mutations that deregulate proliferation and survival pathways have emerged as a common molecular theme in the pathogenesis of myeloproliferative disorders (MPDs). Three studies now report an amino acid substitution in the JAK2 kinase in most patients with polycythemia vera as well as in some cases of essential thrombocythemia and chronic idiopathic myelofibrosis. Functional analysis demonstrates that this mutation confers erythropoietin-independent growth in vitro, deregulates signaling pathways downstream of JAK2, and causes polycythemia in mice. These results open new avenues for diagnosing and classifying patients with these disorders, and identify a new molecular target for drug discovery.

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Animals Erythropoiesis Humans Janus Kinase 2 Mice Models, Biological Mutation Myeloproliferative Disorders Polycythemia Polycythemia Vera Primary Myelofibrosis Protein-Tyrosine Kinases Proto-Oncogene Proteins Signal Transduction Thrombocythemia, Essential Journal Article

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Kevin Shannon, Richard A Van Etten. 2005. JAKing up hematopoietic proliferation.. https://doi.org/10.1016/j.ccr.2005.04.002

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