Department of Haematology, SA Pathology Centre for Cancer Biology, University of Adelaide, Adelaide, Australia.
Leukemia. 2011 Feb;25(2):193-200. doi: 10.1038/leu.2010.197. Epub 2010 Sep 16.
Previous experience in the treatment of chronic myeloid leukaemia (CML) has shown that the achievement of clinical, morphological and cytogenetic remission does not indicate eradication of the disease. A complete molecular response (CMR; no detectable BCR-ABL mRNA) represents a deeper level of response, but even CMR is not a guarantee of elimination of the leukaemia, because the significance of CMR is determined by the detection limit of the assay that is used. Two studies of imatinib cessation in CMR are underway, cumulatively involving over 100 patients. The current estimated rate of stable CMR after stopping imatinib is approximately 40%, but the duration of follow-up is relatively short. The factors that determine relapse risk are yet to be identified. The intrinsic capacity of any residual leukaemia [corrected] cells to proliferate following the withdrawal of treatment may be important, but there may also be a role for immunological suppression of the leukaemia [corrected] clone. No currently available test can formally prove that the leukaemic clone is eradicated. Here we discuss the sensitive measurement of minimal residual disease, and speculate on the biology of BCR-ABL-positive cells that may persist after effective therapy of CML.
先前在慢性髓性白血病（CML）治疗方面的经验表明，实现临床、形态学和细胞遗传学缓解并不能表明疾病的根除。完全分子缓解（CMR；无法检测到 BCR-ABL mRNA）代表了更深层次的反应，但即使是 CMR 也不能保证白血病的消除，因为 CMR 的意义取决于所使用的检测方法的检测极限。有两项关于 CMR 中停用伊马替尼的研究正在进行中，总共涉及 100 多名患者。目前停止伊马替尼后稳定 CMR 的估计率约为 40%，但随访时间相对较短。决定复发风险的因素尚待确定。任何残留白血病[已更正]细胞在治疗停止后增殖的内在能力可能很重要，但白血病[已更正]克隆的免疫抑制也可能发挥作用。目前没有可用的测试可以正式证明白血病克隆已被根除。在这里，我们讨论了微小残留疾病的敏感测量，并推测了在 CML 有效治疗后可能持续存在的 BCR-ABL 阳性细胞的生物学。
