The FIP1L1-PDGFRA syndrome: A case of mistaken identity?

Blood

Volumn 104, Issue 10, 2004, Pages 2999-3000

  Apperley, Jane ^a   Bain, Barbara ^a  

^a IMPERIAL COLLEGE LONDON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

IMATINIB; TRYPTASE;

DIFFERENTIAL DIAGNOSIS; DISEASE ASSOCIATION; DISEASE CLASSIFICATION; EOSINOPHILIC LEUKEMIA; FLUORESCENCE IN SITU HYBRIDIZATION; FUSION GENE; HUMAN; HYPEREOSINOPHILIC SYNDROME; IMMUNOHISTOCHEMISTRY; MAST CELL; MEGALOCYTOSIS; PATHOGENESIS; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; REVIEW;

EID: 8644238291     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood-2004-08-3310     Document Type: Review

References (4)

1. Cools J, De Angelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med. 2003;348:1201-1214.
2. Klion AD, Noel P, Akin C, et al. Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness. Blood. 2003;101:4660-4666.
3. Pardanani A, Elliott M, Reeder T, et al. Imatinib for systemic mast-cell disease. Lancet. 2003;362:535-536.
4. Jaffe ES, Harris NL, Stein H, Vardiman JW, eds. World Health Organisation Classification of Tumours: Tumours of Haematopoietic and Lymphoid Tissues. Lyon, France: International Agency for Research on Cancer (IARC) Press; 2001.