International Journal of Clinical Oncology

, Volume 11, Issue 3, pp 176–183

Treatment of chronic myeloid leukemia with imatinib mesylate


DOI: 10.1007/s10147-006-0582-5

Cite this article as:
Ohno, R. Int J Clin Oncol (2006) 11: 176. doi:10.1007/s10147-006-0582-5


Philadelphia (Ph) chromosome is the cytogenetic hallmark of chronic myeloid leukemia (CML). The translocation forms a chimeric gene, bcr-abl, which generates BCR-ABL. This fusion protein constitutively activate ABL tyrosine kinase and causes CML. Imatinib mesylate is a selective tyrosine kinase inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive inhibition at the ATP-binding site of the enzyme, which leads to growth arrest or apoptosis in cells that express BCR-ABL. Imatinib has revolutionized the management of patients with CML, and at a dose of 400 mg daily has become the current standard therapy for newly diagnosed patients with CML even when they have HLA-matched family donors. Although imatinib therapy has only a 5-year history, it is hoped that CML will be cured with this drug and with forthcoming second-generation tyrosine kinase inhibitors as well as by allogeneic stem cell transplantation in patients who have become resistant to these drugs.

Key words

Chronic myeloid leukemia BCR-ABL Imatinib mesylate Allogeneic stem cell transplantation Tyrosine kinase inhibitor 

Copyright information

© The Japan Society of Clinical Oncology 2006

Authors and Affiliations

  1. 1.Aichi Cancer Center and Aichi Syukutoku UniversityNagoyaJapan

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