Department of Ecology and Evolutionary Biology, University of California-Irvine, Irvine, CA 92607, USA.
Proc Biol Sci. 2010 Jun 22;277(1689):1875-80. doi: 10.1098/rspb.2009.2179. Epub 2010 Feb 10.
Previous studies have shown that during imatinib therapy, the decline of chronic myeloid leukaemia BCR-ABL transcript numbers involves a fast phase followed by a slow phase in averaged datasets. Drug resistance leads to regrowth. In this paper, variation of treatment responses between patients is examined. A significant positive correlation is found between slopes of the fast and the slow phase of decline. A significant negative correlation is found between slopes of the slow phase of decline and the regrowth phase. No correlation is found between slopes of the fast phase of decline and the regrowth phase. A mathematical model that is successfully fitted to diverse clinical profiles explains these correlations by invoking the immune response as a key determinant of tumour decline during treatment. Boosting immunity during drug therapy could enhance the response to treatment in patients.
先前的研究表明，在伊马替尼治疗期间，慢性髓性白血病 BCR-ABL 转录本数量的下降涉及到一个快速相和一个缓慢相，这在平均数据集上表现明显。耐药性导致肿瘤再生。本文考察了不同患者之间的治疗反应变化。快速下降相和缓慢下降相之间的斜率呈显著正相关。缓慢下降相斜率和再生相斜率之间呈显著负相关。快速下降相斜率和再生相斜率之间没有相关性。一个成功拟合不同临床特征的数学模型，通过将免疫反应作为治疗过程中肿瘤消退的关键决定因素，解释了这些相关性。在药物治疗期间增强免疫力可以增强患者对治疗的反应。
