2018 Volume 59 Issue 6 Pages 784-792
Tyrosine kinase inhibitors (TKIs) have markedly improved the prognosis of patients with chronic-phase chronic myeloid leukemia (CML). However, the development of a novel therapeutic strategy that can target and eradicate CML stem cells remains an important requirement to achieve a complete cure for CML because these stem cells cause relapse and drug resistance even in patients receiving TKI treatment. Interferon-α (IFNα) has long been used for the treatment of chronic-phase CML, and its efficacy is now being re-evaluated as a therapeutic option. Some clinical studies have demonstrated the additive efficacy of IFNα in CML patients treated with TKI. However, the mechanism of action is not fully understood. In this review, we introduce our recent findings on the effects of IFNα on CML stem cells via the transcription factor CCAAT/enhancer binding protein β, which regulates stress-induced hematopoiesis.
