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A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.

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N Engl J Med2003PMID 12660384stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (5)

How each link was made (MeSH, dictionary, registry reference, curation…) and whether it has been validated. Candidate links are not counted in entity statistics.

Validated 5

Curated evidence

Evidence citing this paper (2)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
12660384
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–2 of 2 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
PDGFRA Fusion1
ImatinibMyeloid/Lymphoid Neoplasms with Eosinophilia and Tyrosine Kinase Gene FusionsALIASPredictiveASupports Sensitivity Response3accepted
EID1445

Of eleven patients prospectively accrued with hypereosinophilic syndrome, nine had favorable responses to imatinib that lasted >3 months post-treatment. Of these nine patients, five were found to have… (full text at CIViC)

PMID 12660384 · Cools et al., 2003 · Open in CIViC

civic
PDGFRA Fusion + PDGFRA T674I1
ImatinibMyeloid/Lymphoid Neoplasms with Eosinophilia and Tyrosine Kinase Gene FusionsALIASPredictiveCSupports Resistance2accepted
EID1446

A patient treated with imatinib for a FIP1L1-PDGFRA mutation relapsed during treatment. A T674I mutation in the PDGFRA split kinase domain was hypothesized to confer resistance, due to the strong evid… (full text at CIViC)

PMID 12660384 · Cools et al., 2003 · Open in CIViC

civic