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

@article{Cools2003ATK,
  title={A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.},
  author={Jan Cools and Daniel J. Deangelo and Jason Gotlib and Elizabeth H Stover and Robert D. Legare and Jorges Cortes and Jeffrey L. Kutok and Jennifer Hayes Clark and Ilene Galinsky and James D Griffin and Nicholas C P Cross and Ayalew Tefferi and James Malone and Rafeul Alam and Stanley L. Schrier and Janet Schmid and Michal G. Rose and Peter Vandenberghe and Gregor E. G. Verhoef and Marc A. B. Boogaerts and Iwona Wlodarska and Hagop M. Kantarjian and Peter Marynen and Steven E. Coutr{\'e} and Richard C. Stone and Dwight Gary Gilliland},
  journal={The New England journal of medicine},
  year={2003},
  volume={348 13},
  pages={
          1201-14
        }
}
BACKGROUND Idiopathic hypereosinophilic syndrome involves a prolonged state of eosinophilia associated with organ dysfunction. It is of unknown cause. Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause. METHODS We treated 11 patients with the hypereosinophilic syndrome with imatinib and identified the molecular… CONTINUE READING
BETA

Citations

Publications citing this paper.
SHOWING 1-10 OF 631 CITATIONS, ESTIMATED 51% COVERAGE

1,255 Citations

050100'01'04'08'12'16
Citations per Year
Semantic Scholar estimates that this publication has 1,255 citations based on the available data.

See our FAQ for additional information.

Similar Papers

Loading similar papers…