Fluorescence in situ hybridization analysis of minimal residual disease and the relevance of the der(9) deletion in imatinib-treated patients with chronic myeloid leukemia

Haematologica

Volumn 91, Issue 7, 2006, Pages 994-995

  Calabrese, Giuseppe ^a,b   Fantasia, Donatella ^b   Di Gianfilippo, Rita ^b   Stuppia, Liborio ^a   Di Lorenzo, Roberto ^c   Palka, Giandomenico ^a,b  

^a UNIVERSITY OF CHIETI   (Italy)

^b Servizio di Genetica   (Italy)

^c SPIRITO SANTO HOSPITAL   (Italy)

Author keywords

Chronic myeloid leukemia; der(9) deletion; FISH; Imatinib; Minimal residual disease

Indexed keywords

BCR ABL PROTEIN; IMATINIB;

ARTICLE; CHRONIC MYELOID LEUKEMIA; CLINICAL ARTICLE; CONTROLLED STUDY; CYTOGENETICS; DOSE RESPONSE; FLUORESCENCE IN SITU HYBRIDIZATION; FOLLOW UP; GENE DELETION; GENE IDENTIFICATION; HUMAN;

CHROMOSOME DELETION; CHROMOSOMES, HUMAN, PAIR 9; FOLLOW-UP STUDIES; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; LEUKEMIA, MYELOID, CHRONIC; NEOPLASM, RESIDUAL; PIPERAZINES; PYRIMIDINES;

EID: 33745784556     PISSN: 03906078     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (10)

1. Hochhaus A Minimal residual disease in chronic myeloid leukaemia patients. Best Pract Res Clin Haematol 2002;15:159-78.
2. Kaeda J, Chase A, Goldman JM. Cytogenetic and molecular monitoring of residual disease in chronic myeloid leukemia. Acta Haematol 2002;107:64-75.
3. Kantarjian HM, Talpaz M, Cortes J, O'Brien S, Faderl S, Thomas D, et al. Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571: gleevec) in chronic-phase chronic myelogenous leukemia. Clin Cancer Res 2003;9:160-6.
4. Reinhold U, Hennig E, Leiblein S, Niederwieser D, Deininger MW. FISH for BCR-ABL on interphases of peripheral blood neutrophils but not of unselected white cells correlates with bone marrow cytogenetics in CML patients treated with imatinib. Leukemia 2003;17:1925-9.
5. Lesser ML, Dewald GW, Sison CP, Silver RT. Correlation of three methods of measuring cytogenetic response in chronic myelocytic leukemia. Cancer Genet Cytogenet 2002;137:79-84.
6. Huntly BJ, Guilhot F, Reid AG, Vassiliou G, Hennig E, Franke C, et al. Imatinib improves but may not fully reverse the poor prognosis of patients with CML with derivative chromosome 9 deletions. Blood 2003;102:2205-12.
7. Raanani P, Ben-Bassat I, Gan S, Trakhtenbrot L, Mark Z, Ashur-Fabian O, et al. Assessment of the response to imatinib in chronic myeloid leukemia patients - comparison between the FISH, multiplex and RT-PCR methods. Eur J Haematology 2004;73:243-50.
8. Hughes TP, Kaeda J, Branford S, Rudzki Z, Hochhaus A, Hensley ML, 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;349:1423-32.
9. Hochhaus A. Cytogenetic and molecular mechanisms of resistance to imatinib. Semin Hematol 2003;40 Suppl 2:69-79.
10. Quintas-Cardama A, Kantarjian H, Talpaz M, O'Brien S, Garcia-Manero G, Verstovsek S, et al. Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogeneous leukemia. Blood 2005;105:2281-86.