Five-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid Leukemia

The constitutively active BCR-ABL tyrosine kinase is the cause of chronic myeloid leukemia. Imatinib is the first small synthetic molecular inhibitor of the BCR-ABL tyrosine kinase with clinical activity in chronic-phase myeloid leukemia. This 5-year follow-up of patients with the disease who began...

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Published inThe New England journal of medicine Vol. 355; no. 23; pp. 2408 - 2417
Main Authors Druker, Brian J, Guilhot, François, O'Brien, Stephen G, Gathmann, Insa, Kantarjian, Hagop, Gattermann, Norbert, Deininger, Michael W.N, Silver, Richard T, Goldman, John M, Stone, Richard M, Cervantes, Francisco, Hochhaus, Andreas, Powell, Bayard L, Gabrilove, Janice L, Rousselot, Philippe, Reiffers, Josy, Cornelissen, Jan J, Hughes, Timothy, Agis, Hermine, Fischer, Thomas, Verhoef, Gregor, Shepherd, John, Saglio, Giuseppe, Gratwohl, Alois, Nielsen, Johan L, Radich, Jerald P, Simonsson, Bengt, Taylor, Kerry, Baccarani, Michele, So, Charlene, Letvak, Laurie, Larson, Richard A
Format Journal Article
LanguageEnglish
Published Boston, MA Massachusetts Medical Society 07.12.2006
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Summary:The constitutively active BCR-ABL tyrosine kinase is the cause of chronic myeloid leukemia. Imatinib is the first small synthetic molecular inhibitor of the BCR-ABL tyrosine kinase with clinical activity in chronic-phase myeloid leukemia. This 5-year follow-up of patients with the disease who began continuous treatment with imatinib reports that the drug can induce durable hematologic and cytogenetic responses in a high proportion of patients. This 5-year follow-up of patients with chronic myeloid leukemia who began continuous treatment with imatinib reports that the drug can induce durable hematologic and cytogenetic responses in a high proportion of patients. Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the expansion of a clone of hematopoietic cells that carries the Philadelphia chromosome (Ph). 1 The Ph chromosome results from a reciprocal translocation between the long arms of chromosomes 9 and 22, t(9;22)(q34;q11). 2 The molecular consequence of this translocation is a novel fusion gene, BCR-ABL, which encodes a constitutively active protein, tyrosine kinase. 3 – 5 Imatinib (Gleevec, Novartis; formerly called STI571) is a relatively specific inhibitor of the BCR-ABL tyrosine kinase and has efficacy in CML. 6 – 11 Before the availability of imatinib, interferon alfa plus cytarabine was considered standard therapy for patients . . .
ISSN:0028-4793
1533-4406
1533-4406
DOI:10.1056/NEJMoa062867