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David Galton and the evolution of somatic cell populations

proved recently to be correct. CML today is generally regarded as starting with the acquisition of a BCR-ABL1 fusion gene in a pluripotential haemopoietic stem cell, though the notion that this could be a secondary event gains some support from the 1982 work of Fialkow, from the observation that some patients with two existing cytogenetic lesions in leukemia cells lose only the Ph chromosome when treated with imatinib [7] and from the recent demonstration that the JAK2 V617F mutation is probably secondary in polycythaemia vera. Imatinib is impressively effective in controlling disease in 490% of patients with newly diagnosed chronic phase CML and seems to be associated with very substantial prolongation of survival, despite persistence in most cases of residual BCR-ABL1 transcripts at low level [8]. One possible explanation is that though leukemia stem cells are not eradicated by imatinib, the drug greatly reduces or indeed eliminates a more mature progenitor which would otherwise be the starting point for leukaemic transformation [9,10]. Various unresolved issues remain. For example, for how long should imatinib treatment be continued in the responding patient? Does the survival of small numbers of leukemia stem cells really matter? What are the mechanisms underlying primary and secondary resistance to imatinib, which may be different? How should resistant patients be treated? Perhaps most important, does the remarkable success of imatinib in treating CML offer important lessons for the investigation and management of other haematological malignancies, or will the imatinib story turn out to be unique? Some of the answers should emerge in the not too distant future.