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These diseases include polycythemia vera (PV), essential thrombocythenia, atypical chronic myeloid leukemia, idiopathic hypereosinophilic syndrome (HES), agnogenic myeloid metaplasia with myelofibrosis, and others. Receptor tyrosine kinases\u2014the platelet\u2010derived growth factor receptors (PDGFRs) and c\u2010Kit\u2014and their respective ligands have been implicated in the pathogenesis of MPDs. For example, a constitutively activated PDGFR fusion tyrosine kinase (FIP1L1\u2010PDGFRA) was identified in some patients with HES, a disease characterized by sustained overproduction of eosinophils that has been classified by the World Health Organization as a chronic subtype of the MPDs. Imatinib is a selective inhibitor of PDGFRs, c\u2010Kit, Abl and Arg protein\u2010tyrosine kinases, as well as Bcr\u2010Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia. The efficacy of imatinib in treating HES, systemic mast cell disease, chronic myelomonocytic leukemia associated with PDGFR\u03b2 fusion genes, and (to a lesser extent) PV and idiopathic myelofibrosis was reviewed from institutional experience and a review of the literature. In 3 studies that involved 11 patients with PV, 10 patients had reductions in phlebotomy with imatinib. Eight studies of 42 patients with HES indicated that 70% achieved complete hematologic remissions with imatinib. Four studies of 6 patients with MPD indicated responses with imatinib in 5 patients. Insight into the molecular pathogenesis of MPDs will improve the definitions of different disease categories and suggests that signal transduction inhibition is likely to be an increasingly important treatment option in the future. Cancer 2004. \u00a9 2004 American Cancer Society.<\/jats:p>","DOI":"10.1002\/cncr.20211","type":"journal-article","created":{"date-parts":[[2004,4,19]],"date-time":"2004-04-19T19:01:03Z","timestamp":1082401263000},"page":"2064-2078","source":"Crossref","is-referenced-by-count":19,"title":["Beyond chronic myelogenous 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