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Previous Volume 348:2687 June 26, 2003 Number 26 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: In some patients with idiopathic hypereosinophilic syndrome, Cools et al. (March 27 issue)¹ detected a FIP1L1-PDGFRA fusion gene that was associated with a dramatic response to imatinib mesylate. Along with the recent description of the "lymphocytic variant" of the hypereosinophilic syndrome,² their observation will provide clinicians with cornerstones for tailoring the management of this heterogeneous disease according to the underlying pathogenic mechanisms.

In their discussion, Cools et al. state that the hypereosinophilic syndrome is a myeloproliferative syndrome, thereby ignoring the involvement of interleukin-5–producing T cells in the pathogenesis of hypereosinophilia in approximately one fourth of patients with . . . [Full Text of this Article]

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• Fukushima, K., Matsumura, I., Ezoe, S., Tokunaga, M., Yasumi, M., Satoh, Y., Shibayama, H., Tanaka, H., Iwama, A., Kanakura, Y. (2009). FIP1L1-PDGFR{alpha} Imposes Eosinophil Lineage Commitment on Hematopoietic Stem/Progenitor Cells. J. Biol. Chem. 284: 7719-7732 [Abstract] [Full Text]