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Article

PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.

Cancer cell - 1 May 2003

Cools Jan, Stover Elizabeth H, Boulton Christina L, Gotlib Jason, Legare Robert D, Amaral Sonia M, Curley David P, Duclos Nicole, Rowan Rebecca, Kutok Jeffery L, Lee Benjamin H, Williams Ifor R, Coutre Steven E, Stone Richard M, DeAngelo Daniel J, Marynen Peter, Manley Paul W, Meyer Thomas, Fabbro Doriano, Neuberg Donna, Weisberg Ellen, Griffin James D, Gilliland D Gary

Abstract excerpt

FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec). Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients. However, we observed relapse with resistance to imatinib as consequence of a T674I mutation in FIP1L1-PDGFRalpha, analogous to the imatinib-resistant...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 12781364
DOI: 10.1016/s1535-6108(03)00108-9

Genes

BCR
KIT

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.PMID 12781364Read ↗

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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 SyndromeSemantic proximity Read ↗

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