Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia

Blood

Volumn 109, Issue 11, 2007, Pages 4635-4640

  Jovanovic, Jelena V ^a   Score, Joannah ^b   Waghorn, Katherine ^b   Cilloni, Daniela ^c   Gottardi, Enrico ^c   Metzgeroth, Georgia ^d   Erben, Philipp ^d   Popp, Helena ^d   Walz, Christoph ^d   Hochhaus, Andreas ^d   Roche Lestienne, Catherine ^e   Preudhomme, Claude ^e   Solomon, Ellen ^a   Apperley, Jane ^f   Rondoni, Michela ^g   Ottaviani, Emanuela ^g   Martinelli, Giovanni ^g   Brito Babapulle, Finella ^h   Saglio, Giuseppe ^c   Hehlmann, Rüdiger ^d   Cross, Nicholas C P ^b   Reiter, Andreas ^d   Grimwade, David ^a,i   more..

^a KING'S COLLEGE LONDON   (United Kingdom)

^b UNIVERSITY OF SOUTHAMPTON   (United Kingdom)

^c UNIVERSITY OF TURIN   (Italy)

^d UNIVERSITY OF HEIDELBERG   (Germany)

^e LILLE UNIVERSITY HOSPITAL   (France)

^f IMPERIAL COLLEGE LONDON   (United Kingdom)

^g UNIVERSITY OF BOLOGNA   (Italy)

^h EALING HOSPITAL   (United Kingdom)

ⁱ GUY S HOSPITAL   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

IMATINIB; PLATELET DERIVED GROWTH FACTOR ALPHA RECEPTOR;

ARTICLE; CONTROLLED STUDY; DRUG WITHDRAWAL; EOSINOPHILIC LEUKEMIA; GENE EXPRESSION; GENE FUSION; GENE INDUCTION; GENETIC TRANSCRIPTION; HUMAN; HYPEREOSINOPHILIA; MAJOR CLINICAL STUDY; PATIENT MONITORING; PREVALENCE; PRIORITY JOURNAL; REAL TIME POLYMERASE CHAIN REACTION; SCREENING; SENSITIVITY ANALYSIS;

EID: 34249732053     PISSN: 00064971     EISSN: 00064971     Source Type: Journal    
DOI: 10.1182/blood-2006-10-050054     Document Type: Article

References (28)

1. Cools J, DeAngelo 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. Vandenberghe P, Wlodarska I, Michaux L, et al. Clinical and molecular features of FIP1L1-PDFGRA (+) chronic eosinophilic leukemias. Leukemia. 2004;18:734-742.
3. Roche-Lestienne C, Lepers S, Soenen-Cornu V, et al. Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics. Leukemia. 2005;19:792-798.
4. Pardanani A, Ketterling RP, Li CY, et al. FIP1L1-PDGFRA in eosinophilic disorders: prevalence in routine clinical practice, longterm experience with imatinib therapy, and a critical review of the literature. Leuk Res. 2006;30:965-970.
5. Pardanani A, Brockman SR, Paternoster SF, et al. FIP1L1-PDGFRA fusion: prevalence and clinicopathologic correlates in 89 consecutive patients with moderate to severe eosinophilia. Blood. 2004;104:3038-3045.
6. Bacher U, Reiter A, Haferlach T, et al. A combination of cytomorphology, cytogenetic analysis, fluorescence in situ hybridization and reverse transcriptase polymerase chain reaction for establishing clonality in cases of persisting hypereosinophilia. Haematologica. 2006;91:817-820.
7. Gotlib J, Cools J, Malone JM 3rd, Schrier SL, Gilliland DG, Coutre SE. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood. 2004;103:2879-2891.
8. Walz C, Cilloni D, Soverini S, et al. Molecular heterogeneity of the FIP1L1-PDGFRA fusion gene in chronic eosinophilic leukaemia (CEL) and systemic mastocytosis with eosinophilia (SME): a study of 43 cases [abstract]. Blood. 2004;104:667a. Abstract 2428.
9. Score J, Curtis C, Waghorn K, et al. Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia. Leukemia. 2006;20:827-832.
10. Pardanani A, Ketterling RP, Brockman SR, et al. CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy. Blood. 2003;102:3093-3096.
11. La Starza R, Specchia G, Cuneo A, et al. The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases. Haematologica. 2005;90:596-601.
12. Gabert J, Beillard E, van der Velden VH, et al. Standardization and quality control studies of 'real-time' quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia - a Europe Against Cancer program. Leukemia. 2003;17:2318-2357.
13. Reiter A, Saussele S, Grimwade D, et al. Genomic anatomy of the specific reciprocal translocation t(15;17) in acute promyelocytic leukemia. Genes Chromosomes Cancer. 2003;36:175-188.
14. Flora R, Grimwade D. Real-time quantitative RTPCR to detect fusion gene transcripts associated with AML. Methods Mol Med. 2004;91:151-173.
15. Beillard E, Pallisgaard N, van der Velden VH, et al. Evaluation of candidate control genes for diagnosis and residual disease detection in leukemic patients using 'real-time' quantitative reverse-transcriptase polymerase chain reaction (RQPCR) - a Europe Against Cancer program. Leukemia. 2003;17:2474-2486.
16. Pallisgaard N, Clausen N, Schroder H, Hokland P. Rapid and sensitive minimal residual disease detection in acute leukemia by quantitative realtime RT-PCR exemplified by t(12;21) TEL-AML1 fusion transcript. Genes Chromosomes Cancer. 1999;26:355-365.
17. Bain B, Pierre R, Imbert M, Vardiman JW, Brunning RD, Flandrin G. Chronic eosinophilic leukemia and the hypereosinophilic syndrome. In: Jaffe ES, Harris NL, Stein H, Vardiman JW, eds. World Health Organization Classification of Tumours: Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. Lyon, France: IARC Press; 2001:29-31.
18. Griffin JH, Leung J, Bruner RJ, Caligiuri MA, Briesewitz R. Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndrome. Proc Natl Acad Sci U S A. 2003;100:7830-7835.
19. Cools J, Quentmeier H, Huntly BJ, et al. The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. Blood. 2004;103:2802-2805.
20. Chung KF, Hew M, Score J, et al. Cough and hypereosinophilia due to FIP1L1-PDGFRA fusion gene with tyrosine kinase activity. Eur Resp J. 2006;27:230-232.
21. 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.
22. Klion AD, Robyn J, Akin C, et al. Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome. Blood. 2004;103:473-478.
23. Hughes TP, Kaeda J, Branford S, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003;349:1423-1432.
24. Hughes T, Deininger M, Hochhaus A, et al. Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. Blood. 2006;108:28-37.
25. von Bubnoff N, Sandherr M, Schlimok G, Andreesen R, Peschel C, Duyster J. Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent 5 eosinophilia. Leukemia. 2005;19:286-287.
26. von Bubnoff N, Gorantla SP, Thone S, Peschel C, Duyster J. The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). Blood. 2006;107:4970-4971.
27. Lierman E, Folens C, Stover EH, et al. Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. Blood. 2006;108:1374-1376.
28. Graham SM, Jorgensen HG, Allan E, et al. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood. 2002;99:319-325.