American Society of Hematology

Figure 2.

$Figure 2. Kinetics of the BCR-ABL transcript and its clinical correlation in 29 patients with Ph+ ALL treated with imatinib interim therapy. (A) Plot showing quantitative MRD levels for 15 patients with hematologic CR after imatinib interim therapy. (B) Plot showing quantitative MRD levels for 7 patients with molecular CR after imatinib interim therapy. Their median BCR-ABL/ABL ratios decreased by 0.83 log after the first imatinib cycle and 0.34 log after the second imatinib cycle, respectively. (C) Plot showing quantitative MRD levels for 4 patients with a primary refractoriness to imatinib therapy. One patient (patient no. 10) died of septicemia before transplantation. (D) Plot showing quantitative MRD levels for 3 refractory patients after induction chemotherapy. These patients achieved CR with a decrease in MRD after imatinib therapy. Twenty-five patients underwent allogeneic SCT with a first CR (A + B + D), while the remaining 3 patients had resistant leukemia at the time of SCT (C). Of these, 7 patients (patient nos. 3, 6, 12, 16, 19, 24, 26) still had residual leukemia at 3 or 6 months after SCT. However, with the exception of 2 cases (patient nos. 16, 19), their BCR-ABL/ABL ratios rapidly decreased to an undetectable level after the development of acute (patient no. 24) or chronic (patient nos. 3, 6, 12, 26) GVHD induced by the rapid withdrawal of cyclosporine. Of 2 patients without GVHD, 1 (patient no. 16) showed an increase in MRD at 6 months (1.35 × 10-5 → 6.78 × 10-5) and subsequently died of overt hematologic relapse following a further increase in MRD (8.12 × 10-2) at 12 months after SCT. The overall treatment outcomes of the patients receiving imatinib interim therapy are listed in Table 4. Dx indicates diagnosis; p, post (ie, after); Ind, induction; C, consolidation; IM, imatinib; S, salvage chemotherapy; M, months; aGVHD, acute GVHD; cGVHD, chronic GVHD.$

Kinetics of the BCR-ABL transcript and its clinical correlation in 29 patients with Ph⁺ ALL treated with imatinib interim therapy. (A) Plot showing quantitative MRD levels for 15 patients with hematologic CR after imatinib interim therapy. (B) Plot showing quantitative MRD levels for 7 patients with molecular CR after imatinib interim therapy. Their median BCR-ABL/ABL ratios decreased by 0.83 log after the first imatinib cycle and 0.34 log after the second imatinib cycle, respectively. (C) Plot showing quantitative MRD levels for 4 patients with a primary refractoriness to imatinib therapy. One patient (patient no. 10) died of septicemia before transplantation. (D) Plot showing quantitative MRD levels for 3 refractory patients after induction chemotherapy. These patients achieved CR with a decrease in MRD after imatinib therapy. Twenty-five patients underwent allogeneic SCT with a first CR (A + B + D), while the remaining 3 patients had resistant leukemia at the time of SCT (C). Of these, 7 patients (patient nos. 3, 6, 12, 16, 19, 24, 26) still had residual leukemia at 3 or 6 months after SCT. However, with the exception of 2 cases (patient nos. 16, 19), their BCR-ABL/ABL ratios rapidly decreased to an undetectable level after the development of acute (patient no. 24) or chronic (patient nos. 3, 6, 12, 26) GVHD induced by the rapid withdrawal of cyclosporine. Of 2 patients without GVHD, 1 (patient no. 16) showed an increase in MRD at 6 months (1.35 × 10^-5 → 6.78 × 10^-5) and subsequently died of overt hematologic relapse following a further increase in MRD (8.12 × 10^-2) at 12 months after SCT. The overall treatment outcomes of the patients receiving imatinib interim therapy are listed in Table 4. Dx indicates diagnosis; p, post (ie, after); Ind, induction; C, consolidation; IM, imatinib; S, salvage chemotherapy; M, months; aGVHD, acute GVHD; cGVHD, chronic GVHD.

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