By Pasler F.A., Hassell T.
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278,279 Clonal cytogenetic evolution occurs in 60–80% of patients. 280 The specific role of chromosomal abnormalities in CML disease progression is not clear. 281 Similarly, an association between p53 mutations and the appearance of an isochromosome 17 was hypothesized, owing to the loss of the corresponding 17p coding for p53. 283 The underlying mutator phenotype of CML cells is probably the result of diverse mechanisms that cooperate to destabilize the genome of the leukemia cells. Evidently, the high cell turnover itself combined with the antiapoptotic activity of BCR-ABL must increase the mutation risk per unit of time.
297 Despite the durability of most imatinib responses in patients treated in early chronic phase, persistence of residual disease is the rule,298 suggesting that current therapy may be unable to efficiently target leukemic stem cells. If we define cure as the eradication of all leukemia cells then few patients may be curable with imatinib therapy. 261,299 Most importantly, defining whether persistence is a BCR-ABL-dependent or -independent phenomenon will be necessary to guide CYTOGENETICS AND MOLECULAR BIOLOGY the development of rational therapeutic approaches.
7. Bartram CR, de Klein A, Hagemeijer A et al. Translocation of c-abl oncogene correlates with the presence of a Philadelphia chromosome in chronic myelocytic leukaemia. Nature 1983; 306: 277–80. 8. Groffen J, Stephenson JR, Heisterkamp N et al. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell 1984; 36: 93–9. 33 9. Abelson HT, Rabstein LS. Lymphosarcoma: virus induced thymic-independent disease in mice. Cancer Res 1970; 30: 2213–22. 10. Scher CD, Siegler R.