Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 95, Issue 2, Pages 209-213Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-012-1005-1
Keywords
Chronic myelogenous leukemia; Imatinib; Interferon; T315I
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Funding
- Grants-in-Aid for Scientific Research [22591065] Funding Source: KAKEN
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The T315I BCR-ABL mutation in chronic myelogenous leukemia (CML) patients is responsible for up to 20% of all clinically observed resistance. This mutation confers resistance not only to imatinib, but also to second-generation BCR-ABL tyrosine kinases, such as nilotinib and dasatinib. A number of strategies have been implemented to overcome this resistance, but allogeneic stem cell transplantation remains the only established therapeutic option for a cure. A 61-year-old male was diagnosed with Philadelphia chromosome-positive chronic-phase CML in 2002. He was initially treated with imatinib and complete cytogenetic response (CCyR) was achieved 12 months later. However, after 18 months, a loss of CCyR was observed and a molecular study at 24 months revealed a T315I mutation of the BCR-ABL gene. At 30 months, imatinib/interferon-alfa (IFN alpha) combination therapy was initiated in an effort to overcome the resistance. Thirty months later, he re-achieved CCyR, and the T315I BCR-ABL mutation disappeared at 51 months. To our knowledge, this is the first case report showing the effectiveness of imatinib/IFN alpha combination therapy for CML patients bearing the T315I BCR-ABL mutation.
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