Figure 2.
Figure 2. Serial measurement of BCR-ABL transcript levels in patients with a rise in BCR-ABL of more than 2-fold. Patient A (A) commenced imatinib in late chronic phase (≥ 12 months since diagnosis). The T315I mutation was detected prior to a steady rise in BCR-ABL, which highlights that mutation analysis is warranted when the rise in multiple samples exceeds 2-fold from the nadir level. Escalated doses of imatinib were ineffective, and the patient proceeded to an autologous transplantation. Patient B (B) was 1 of only 3 patients whereby the mutation was detected after the rise in BCR-ABL. The patient proceeded to an autologous transplantation after progression to accelerated phase (AP). In both patients A and B, the mutations remained detectable at the last measurement before transplantation. In patient C (C) a steady rise in the BCR-ABL level preceded a return to myeloid blast crisis (MBC); however, no mutations were detected. Patient D (D) commenced imatinib in early chronic phase (< 12 months since diagnosis), and the Y253H mutation was first detected at 6 months of imatinib. A rise in the BCR-ABL level on consecutive occasions followed; however, the patient maintained a CCR from 3 to 12 months.

Serial measurement of BCR-ABL transcript levels in patients with a rise in BCR-ABL of more than 2-fold. Patient A (A) commenced imatinib in late chronic phase (≥ 12 months since diagnosis). The T315I mutation was detected prior to a steady rise in BCR-ABL, which highlights that mutation analysis is warranted when the rise in multiple samples exceeds 2-fold from the nadir level. Escalated doses of imatinib were ineffective, and the patient proceeded to an autologous transplantation. Patient B (B) was 1 of only 3 patients whereby the mutation was detected after the rise in BCR-ABL. The patient proceeded to an autologous transplantation after progression to accelerated phase (AP). In both patients A and B, the mutations remained detectable at the last measurement before transplantation. In patient C (C) a steady rise in the BCR-ABL level preceded a return to myeloid blast crisis (MBC); however, no mutations were detected. Patient D (D) commenced imatinib in early chronic phase (< 12 months since diagnosis), and the Y253H mutation was first detected at 6 months of imatinib. A rise in the BCR-ABL level on consecutive occasions followed; however, the patient maintained a CCR from 3 to 12 months.

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