Cell biology of CML--a model linking the chronic and terminal phases.
A model for the pathogenesis of chronic myeloid leukaemia (CML) is proposed. It relies on a comparison between normal steady-state and regenerating haemopoiesis and suggests that chronic phase CML stem cells have a finite capacity for self-renewal. According to the model, metamorphosis of the disease occurs once the potential for chronic phase cell production has been exhausted. The model considers also the generation of leukocytosis in the chronic phase and the origin of the terminal phase. Comparison with normal regenerating haemopoiesis allows discrimination between features of CML that are fundamentally abnormal and those which are normally associated with regeneration.
Gordon
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Leukaemia Research Fund Centre, Institute of Cancer Research, London.
D000818:Animals; D001752:Blast Crisis / Q000097:blood / Q000235:genetics / Q000473:pathology*; D001853:Bone Marrow / Q000503:physiopathology; D002454:Cell Differentiation; D002455:Cell Division; D002999:Clone Cells / Q000473:pathology; D015973:Gene Expression Regulation, Leukemic; D006410:Hematopoiesis; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000097:blood / Q000235:genetics / Q000473:pathology*; D015466:Leukemia, Myeloid, Chronic-Phase / Q000097:blood / Q000235:genetics / Q000473:pathology*; D007964:Leukocytosis / Q000209:etiology; D051379:Mice; D008954:Models, Biological; D014411:Neoplastic Stem Cells / Q000473:pathology*