Published: 8 March 2016
Author(s): Grzegorz Helbig
Issue: March 2016
Section: Letter to the Editor

The high efficacy of tyrosine kinase inhibitor, imatinib mesylate (IM), is well-documented in patients with hypereosinophilic syndromes (HES) and detectable rearrangements of platelet-derived growth factor receptor α or β (PDGFRA/B) [1]. Most of these IM responders were found to possess an interstitial deletion in chromosome 4q12 leading to constitutively active tyrosine kinase, FIP1L1-PDGFRA (F/P) [2]. In contrast, the place of IM in the treatment of unmutated HES remains to be elucidated. Of note is, that IM was found to be ineffective in most HES patients with unknown or negative PDGFRA rearrangement.


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