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Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia
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2006 (Engelska)Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 355, nr 23, s. 2408-2417Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND: The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase. For 5 years, we followed patients with CML who received imatinib as initial therapy. METHODS: We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events. RESULTS: The median follow-up was 60 months. Kaplan-Meier estimates of cumulative best rates of complete cytogenetic response among patients receiving imatinib were 69% by 12 months and 87% by 60 months. An estimated 7% of patients progressed to accelerated-phase CML or blast crisis, and the estimated overall survival of patients who received imatinib as initial therapy was 89% at 60 months. Patients who had a complete cytogenetic response or in whom levels of BCR-ABL transcripts had fallen by at least 3 log had a significantly lower risk of disease progression than did patients without a complete cytogenetic response (P<0.001). Grade 3 or 4 adverse events diminished over time, and there was no clinically significant change in the profile of adverse events. CONCLUSIONS: After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients. (ClinicalTrials.gov number, NCT00006343 [ClinicalTrials.gov].)

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2006. Vol. 355, nr 23, s. 2408-2417
Nationell ämneskategori
Medicin och hälsovetenskap
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URN: urn:nbn:se:uu:diva-24928DOI: 10.1056/NEJMoa062867ISI: 000242581400005PubMedID: 17151364OAI: oai:DiVA.org:uu-24928DiVA, id: diva2:52702
Tillgänglig från: 2007-02-15 Skapad: 2007-02-15 Senast uppdaterad: 2017-12-07Bibliografiskt granskad

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