American Society of Hematology

Figure 1.

$Figure 1. Sequential assessment of the BCR-ABL kinetics. The 118 bone marrow samples from 14 Ph+ ALL patients treated with a first-line interim therapy of imatinib prior to allogeneic SCT were assessed by RQ-PCR. (A) Plot shows quantitative BCR-ABL values for 12 responders. After the first imatinib cycle, 11 patients remained in sustained CHR with a decrease in their BCR-ABL/ABL ratios (0.89 logs), and one patient (no. 12) who was refractory achieved a CHR. Of these, 10 patients received the second imatinib cycle following consolidation and showed a sustained CHR, including 2 molecular CRs, with a further decrease in the BCR-ABL/ABL ratios (0.19 logs). All patients underwent SCT in a favorable status, and of these, 11 are alive in a leukemia-free status 9 to 28+ months after SCT. An interesting phenomenon involving a decreased BCR-ABL/ABL ratio to a PCR-negative status after the development of GVHD induced by rapid cyclosporine withdrawal was observed in patient nos. 3, 6, and 12. (B) Plot shows quantitative BCR-ABL values for 2 nonresponders. One patient (no. 10) showing a CHR after chemotherapy developed an overt hematologic relapse with an increase in the BCR-ABL/ABL ratio after each imatinib cycle and died of sepsis prior to SCT. The other patient (no. 14) showed no response to the first imatinib cycle and proceeded directly to SCT. The patient died of refractory grade IV acute GVHD. The patients' characteristics and treatment outcomes are listed in Table 1. Dx indicates diagnosis; p, post; Ind, induction; C, consolidation; IM, imatinib; S, salvage chemotherapy; M, months; and UD, undetectable.$

Sequential assessment of the BCR-ABL kinetics. The 118 bone marrow samples from 14 Ph⁺ ALL patients treated with a first-line interim therapy of imatinib prior to allogeneic SCT were assessed by RQ-PCR. (A) Plot shows quantitative BCR-ABL values for 12 responders. After the first imatinib cycle, 11 patients remained in sustained CHR with a decrease in their BCR-ABL/ABL ratios (0.89 logs), and one patient (no. 12) who was refractory achieved a CHR. Of these, 10 patients received the second imatinib cycle following consolidation and showed a sustained CHR, including 2 molecular CRs, with a further decrease in the BCR-ABL/ABL ratios (0.19 logs). All patients underwent SCT in a favorable status, and of these, 11 are alive in a leukemia-free status 9 to 28+ months after SCT. An interesting phenomenon involving a decreased BCR-ABL/ABL ratio to a PCR-negative status after the development of GVHD induced by rapid cyclosporine withdrawal was observed in patient nos. 3, 6, and 12. (B) Plot shows quantitative BCR-ABL values for 2 nonresponders. One patient (no. 10) showing a CHR after chemotherapy developed an overt hematologic relapse with an increase in the BCR-ABL/ABL ratio after each imatinib cycle and died of sepsis prior to SCT. The other patient (no. 14) showed no response to the first imatinib cycle and proceeded directly to SCT. The patient died of refractory grade IV acute GVHD. The patients' characteristics and treatment outcomes are listed in Table 1. Dx indicates diagnosis; p, post; Ind, induction; C, consolidation; IM, imatinib; S, salvage chemotherapy; M, months; and UD, undetectable.

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