A Tyrosine Kinase Created by Fusion of the <i>PDGFRA</i> and <i>FIP1L1</i> Genes as a Therapeutic Target of Imatinib in Idiopathic Hypereosinophilic Syndrome

Abstract

The hypereosinophilic syndrome may result from a novel fusion tyrosine kinase - FIP1L1-PDGFRalpha - that is a consequence of an interstitial chromosomal deletion. The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib. Our data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.