A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.
By J. Cools, D. DeAngelo, J. Gotlib, E. Stover, R. Legare, J. Cortes, J. Kutok, Jennifer Hayes Clark, I. Galinsky, J. Griffin and 16 more. New England Journal of Medicine, 2003
1,745 citations recorded by the source corpus.
Subfields: Infectious Diseases, Rheumatology, Surgery
View Paper: https://www.semanticscholar.org/paper/47db8e8a9af3d8bbd5d604bd61711423bf7af561
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In Rheumatology
Citations in the corpus
- Clinical Pharmacokinetics of Imatinib (2005, background): “[4] Bcr-Abl tyrosine kinase activity also tinib, such as FIP1L1-PDGFRα associated with affects integrin function, impairing cell-cell contact hypereosinophilic syndrome[18] and COL1A1/ and resulting in decreased sensitivity of CML pro-”
- Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain (2005, background): “These results differ from those of acquired resistance mutation in CML [10], GIST [15,27], and HES [16].”
- MPLW515L Is a Novel Somatic Activating Mutation in Myelofibrosis with Myeloid Metaplasia (2006, methodology): “For cell-proliferation assays, 32D cells stably expressing FIP1L1-PDGFRA [16] and MPLW515L were grown in RPMI/ 10% FBS and then incubated with appropriate concentrations of JAK Inhibitor I (Calbiochem, San Diego, California, United States) for 72 hours.”
- Eosinophils: Biological Properties and Role in Health and Disease (2008, background): “Thus, eosinophilic patients with FIP1-L1-PDGFRA-positive disease are now treated with Gleevec as first-line therapy (Gleich et al. 2002).”
- Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. (2005, methodology): “, 1994) and patients with the FIP1L1-PDGFRA fusion and HES (Cools et al., 2003).”