Complete molecular remission of chronic eosinophilic leukemia complicated by CNS disease after targeted therapy with imatinib

被引:24
作者
Frickhofen, N
Märker-Hermann, E
Reiter, A
Walz, C
Jung, B
Bauer, H
Hochhaus, A
机构
[1] Dr Horst Schmidt Kliniken GmbH, Dept Hematol Oncol, D-65199 Wiesbaden, Germany
[2] Dr Horst Schmidt Kliniken GmbH, Dept Rheumatol Clin Immunol Nephrol, D-65199 Wiesbaden, Germany
[3] Heidelberg Univ, Fak Klin Med Mannheim, Med Klin 3, D-6800 Mannheim, Germany
关键词
hypereosinophilic syndrome; enzyme inhibitors; imatinib; therapeutic use; human; drug therapy; genetics;
D O I
10.1007/s00277-004-0845-z
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Many cases of hypereosinophilia, formerly classified as hypereosinophilic syndrome, can now be characterized as chronic eosinophilic leukemia (CEL) based on the demonstration of characteristic genetic markers indicating clonality of hematopoiesis. Here we report on a 33-year-old male patient with central nervous system manifestations of CEL and an excellent response to low-dose imatinib (Glivec). Molecular analysis demonstrated a constitutive activation of the platelet-derived growth factor receptor-alpha (PDGFR-A) as the mechanism of responsiveness to imatinib.
引用
收藏
页码:477 / 480
页数:4
相关论文
共 21 条
[1]   Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta [J].
Apperley, JF ;
Gardembas, M ;
Melo, JV ;
Russell-Jones, R ;
Bain, BJ ;
Baxter, J ;
Chase, A ;
Chessells, JM ;
Colombat, M ;
Dearden, CE ;
Dimitrijevic, S ;
Mahon, FX ;
Marin, D ;
Nikolova, Z ;
Olavarria, E ;
Silberman, S ;
Schultheis, B ;
Cross, NCP ;
Goldman, JM .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (07) :481-487
[2]   Cytogenetic and molecular genetic aspects of eosinophilic leukaemias [J].
Bain, BJ .
BRITISH JOURNAL OF HAEMATOLOGY, 2003, 122 (02) :173-179
[3]   HYPEREOSINOPHILIC SYNDROME - ANALYSIS OF 14 CASES WITH REVIEW OF LITERATURE [J].
CHUSID, MJ ;
DALE, DC ;
WEST, BC ;
WOLFF, SM .
MEDICINE, 1975, 54 (01) :1-27
[4]   A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome [J].
Cools, J ;
DeAngelo, DJ ;
Gotlib, J ;
Stover, EH ;
Legare, RD ;
Cortes, J ;
Kutok, J ;
Clark, J ;
Galinsky, I ;
Griffin, JD ;
Cross, NCP ;
Tefferi, A ;
Malone, J ;
Alam, R ;
Schrier, SL ;
Schmid, J ;
Rose, M ;
Vandenberghe, P ;
Verhoef, G ;
Boogaerts, M ;
Wlodarska, I ;
Kantarjian, H ;
Marynen, P ;
Coutre, SE ;
Stone, R ;
Gilliland, DG .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (13) :1201-1214
[5]   Efficacy of imatinib mesylate in the treatment of idiopathic hypereosinophilic syndrome [J].
Cortes, J ;
Ault, P ;
Koller, C ;
Thomas, D ;
Ferrajoli, A ;
Wierda, W ;
Rios, MB ;
Letvak, L ;
Kaled, ES ;
Kantarjian, H .
BLOOD, 2003, 101 (12) :4714-4716
[6]  
COUTANT G, 1993, ANN MED INTERNE, V144, P243
[7]   MINIMAL RESIDUAL DISEASE AFTER BONE-MARROW TRANSPLANT FOR CHRONIC MYELOID-LEUKEMIA DETECTED BY THE POLYMERASE CHAIN-REACTION [J].
CROSS, NCP ;
LIN, F ;
BUNGEY, J ;
GOLDMAN, JM .
LEUKEMIA & LYMPHOMA, 1993, 11 :39-43
[8]  
CROSS NCP, 1994, LEUKEMIA, V8, P186
[9]   Tyrosine kinase fusion genes in chronic myeloproliferative diseases [J].
Cross, NCP ;
Reiter, A .
LEUKEMIA, 2002, 16 (07) :1207-1212
[10]  
EstevaLorenzo FJ, 1996, AM J HEMATOL, V51, P164, DOI 10.1002/(SICI)1096-8652(199602)51:2<164::AID-AJH12>3.0.CO