[Molecular pathogenesis of chronic myeloid leukemia].
Chronic myeloid leukemia (CML) is a paradigm for neoplasias that are defined by a unique genetic aberration, the BCR-ABL1 fusion gene. CML is also the best example for molecular target therapy. The development of protein tyrosine kinase inhibitor, imatinib, has entirely changed the strategy of therapy for CML. Nonetheless, many fields of pathogenesis for CML have not been elucidated, such as the mechanisms of blastic crisis, the causes of genetic instability including the inactivation of tumor suppressor genes, and oncogenic signaling pathways downstreams of the BCR-ABL1 fusion gene product. Herein, we review current knowledge on the molecular pathogenesis of CML.
Sasaki
Ko
K
Department of Hematology, Dokkyo Medical University School of Medicine.
Mitani
Kinuko
K
D001549:Benzamides; D001752:Blast Crisis; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D020868:Gene Silencing; D018390:Gene Targeting; D016147:Genes, Tumor Suppressor; D006412:Hematopoietic Stem Cells / Q000473:pathology; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D014411:Neoplastic Stem Cells / Q000473:pathology; D010677:Philadelphia Chromosome; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology
D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl