Literature DB >> 22262141

Successful treatment of a chronic-phase T-315I-mutated chronic myelogenous leukemia patient with a combination of imatinib and interferon-alfa.

Hidehiro Itonaga1, Hideki Tsushima, Tomoko Hata, Emi Matsuo, Daisuke Imanishi, Yoshitaka Imaizumi, Yasuhisa Kawaguchi, Takuya Fukushima, Yuko Doi, Sayaka Mori, Shimeru Kamihira, Masao Tomonaga, Yasushi Miyazaki.   

Abstract

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 (IFNα) 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/IFNα combination therapy for CML patients bearing the T315I BCR-ABL mutation.

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Year:  2012        PMID: 22262141     DOI: 10.1007/s12185-012-1005-1

Source DB:  PubMed          Journal:  Int J Hematol        ISSN: 0925-5710            Impact factor:   2.490


  24 in total

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3.  C/EBPβ is a critical mediator of IFN-α-induced exhaustion of chronic myeloid leukemia stem cells.

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7.  Enlarged memory T-cell pool and enhanced Th1-type responses in chronic myeloid leukemia patients who have successfully discontinued IFN-α monotherapy.

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8.  Interferon-α Revisited: Individualized Treatment Management Eased the Selective Pressure of Tyrosine Kinase Inhibitors on BCR-ABL1 Mutations Resulting in a Molecular Response in High-Risk CML Patients.

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