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• W2078124664 abstract "In 1968, the term hypereosinophilic syndromes (HES) was coined to refer to a spectrum of eosinophil-associated diseases presumed to be caused by an underlying immunological pathology. In the 1990s, the identification of an HES subset with T lymphocyte clonality and production of cytokines, particularly IL-5, validated this concept. Then, in 2002, imatinib mesylate, which was introduced for the treatment of chronic myelogenous leukemia, effectively controlled another subgroup of HES patients. Imatinib's target is a novel constitutively-active kinase. Most imatinib-responsive HES patients show an increased number of bone marrow mast cells and elevated serum tryptase; mast cells, lymphocytes and neutrophils express the novel kinase. This new information critically modifies our view of HES and indicates that several cell lines are altered and likely to contribute to HES pathophysiology." @default.
• W2078124664 created "2016-06-24" @default.
• W2078124664 creator A5080324106 @default.
• W2078124664 creator A5089757484 @default.
• W2078124664 date "2005-12-01" @default.
• W2078124664 modified "2023-09-23" @default.
• W2078124664 title "The hypereosinophilic syndromes: still more heterogeneity" @default.
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• W2078124664 doi "https://doi.org/10.1016/j.coi.2005.09.008" @default.
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