Seiichiro Katagiri

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BACKGROUND The ABL kinase inhibitor imatinib is highly effective in treating most, but not all, patients with chronic myeloid leukemia (CML). This is because residual CML cells are generally present in the bone marrow microenvironment and are refractory to imatinib. Hematopoietic cytokine receptor signaling is mediated by Janus kinases (JAKs) and their(More)
BACKGROUND A subset of patients with chronic myeloid leukemia (CML) can sustain a complete molecular response after discontinuing imatinib mesylate (IM). We focused on microRNAs (miRNAs), with the aim of finding a molecular biomarker to discriminate which patients can safely and successfully discontinue IM use. METHODS To identify miRNAs that showed(More)
Imatinib, a tyrosine kinase inhibitor, has dramatically improved the treatment of chronic myeloid leukemia (CML). Recent evidence has revealed that some patients with CML can safely discontinue imatinib therapy without relapse, particularly after achieving a complete molecular response. This review discusses the possible immunosurveillance predictive(More)
Approximately 40% of chronic myeloid leukemia (CML) patients who discontinue imatinib (IM) therapy maintain undetectable minimal residual disease (UMRD) for more than one year (stopping IM (STOP-IM)). To determine a possible biomarker for STOP-IM CML, we examined plasma miRNA expression in CML patients who were able to discontinue IM. We first screened(More)
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