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Updated: Mar 21, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
Published on: January 7, 2019
Bosutinib for Chronic Myeloid Leukemia
Massimo Breccia1, Gianni Binotto2
1Department of Cellular Biotechnologies and Hematology, Sapienza University, Via Benevento 6, 00161 Rome, Italy.
Abstract:
In recent years the availability of several tyrosine kinase inhibitors (TKI) in the therapeutic armamentarium for chronic myeloid leukemia has dramatically changed the objectives and expectations of healthcare providers and patients. For many, but not all, patients the forerunner of TKI, imatinib, is still an excellent treatment option. Unfortunately, nearly 30-40% of imatinib-treated patients discontinue therapy in the long-term, because of failure and/or intolerance. Second-generation tyrosine kinase inhibitors are more potent drugs which are suitable for treatment of approximately 50% of patents for whom imatinib is unsuitable, and with high success and rapid responses. Bosutinib, an orally bioavailable Src/Abl tyrosine kinase inhibitor, has proved to be effective in vitro against resistant chronic myeloid leukemia cells that do not harbor the T315I or V299L ABL kinase domain mutations. During clinical development the manageable safety profile of bosutinib have become evident for both simple and more advanced treatment. In this review we summarize preclinical and clinical data for bosutinib and discuss its ideal field of action in comparison with other TKI.
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