Molecular and Cellular Mechanisms of Chronic Myelogenous Leukemia

Dear Colleagues,

Chronic myeloid leukemia (CML) is a hematological disorder, characterized by a chromosomal translocation between chromosomes 9 and 22 [t(9;22)], resulting in the BCR/ABL1 oncoprotein being produced.

The current treatment for CML patients in the chronic phase is to keep receiving TKI treatment, inducing a deep molecular response (DMR). Not only imatinib, but also second-generation TKI, nilotinib, and dasatinib have induced a high rate of DMR in CML patients. Such an intensive TKI treatment could induce treatment-free remission (TFR), which occurs in approximately half of all CML patients.  So, CML must be a curable hematological disorder. In this process, the immunological mechanism, including cellular immune function, was considered.

In this Issue, the major role of the BCR/ABL oncoprotein for the development of CML, the mechanism of TKI treatment for CML, and the immunological involvement for TFR will be summarized.

We are looking forward to your contributions.

Dr. Yasuhiro Maeda
Guest Editor

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