Although the mechanisms of CML transformation remain poorly understood, recent therapeutic advances moderately have improved the prognosis of patients in AP and BP. Treatment with IFN-αbased regimens are minimally effective for patients in AP and ineffective for those in BP. Imatinib mesylate has a significant but generally transient response rate in patients in AP and BP. Hope for progress in this area lies mainly in the development of novel targeted therapies. The more promising agents that are being investigated include decitabine, HHT, troxacitabine, clofarabine, farnesyl transferase inhibitors, histone deacetylase inhibitors, and the VEGF and mTOR inhibitors. Many of these approaches may be synergistic with imatinib or the more powerful abl or Src inhibitors that are in development.
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