title: [Chemokines in chronic myeloid leukemia].
abstract: Several tyrosine kinase inhibitors have been developed to target the BCR-ABL fusion gene, a pathognomonic genetic change in chronic myeloid leukemia (CML), and have dramatically improved the outcomes of CML patients. BCR-ABL-expressing CML cells compete with normal hematopoietic cells over the limited space in the bone marrow to proliferate. Moreover, CML cells can gain resistance to tyrosine kinase inhibitors by utilizing bone marrow microenvironments. Thus, in order to develop a novel treatment strategy for CML, it is necessary to elucidate the cellular and molecular basis underlying the interactions between CML and normal hematopoietic cells. Herein, we discuss the roles of chemokines, particularly CXCL12 and CCL3, in reconstruction processes of bone marrow microenvironments by CML cells and the possibility of novel treatment modalities against CML, based on targeting these chemokines.
authors.affiliation: Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University.
authors.forename: Naofumi
authors.initials: N
authors.lastname: Mukaida
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Baba
mesh_terms: D001853:Bone Marrow / Q000378:metabolism; D060833:Cellular Microenvironment; D018925:Chemokines / Q000378:metabolism*; D016044:Fusion Proteins, bcr-abl / Q000378:metabolism; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000378:metabolism*
chemical_list: D018925:Chemokines; D016044:Fusion Proteins, bcr-abl