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RT-PCR.10 Before the advent of imatinib for the treatment of CML, the only therapeutic modality capable of inducing a complete molecular remission was allogeneic HSCT. In fact, molecular relapse or failure to induce molecular remission after HSCT predicts hema-tologic relapse and is an indication for salvage therapy including donor lymphocyte infusions.11 Thus, a complete molecular remission is tantamount to cure after HSCT and is the ultimate goal of non-HSCT therapies if they aspire to cure CML.

Imatinib can induce molecular remission, though not as uniformly or as quickly as with an allogeneic HSCT. At a dose of 400 mg daily in untreated patients with chronic-phase CML, imatinib induces a complete molecular remission in fewer than 5% of patients.12 Although higher doses of imatinib may induce a higher rate of complete molecular remission, most patients in CCR still have detectable bcr/abl transcripts.13 For these patients in CCR who still have detectable bcr/abl transcripts, a reduction in the number of these transcripts may be just as important as complete molecular remission.

A note of caution must be inserted when considering the definition of a complete molecular response as determined by RT-PCR analysis. RT-PCR techniques may fail to detect extremely low levels of bcr/abl, and lab-to-lab differences in methodology preclude the practical comparison of results generated between laboratories. To account for variations in methodology and RT-PCR sensitivity, optimal post-therapy moni toring of disease is better accomplished using quantitative rather than qualitative RT-PCR assays. The log reduction in bcr/abl transcripts compared to a baseline level obtained at the time CCR was achieved has been introduced as a method to standardize the reporting of molecular responses after treatment for CML.12 In general, a 3-log reduction in the number of detectable bcr/abl transcripts constitutes a major molecular remission.

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