Investigation of various growth mechanisms of solid tumour growth within the linear-quadratic model for radiotherapy
Investigation of various growth mechanisms of solid tumour growth within the linear-quadratic model for radiotherapy
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DOI：
10.1088/0031-9155/52/4/012
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发表时间：
2007-02-21
影响因子：
3.5
通讯作者：
O'Rourke, S. F. C.
中科院分区：
文献类型：
--
作者：
McAneney, H.;O'Rourke, S. F. C.
放射治疗的标准线性-二次生存模型被用来研究不同的放射治疗计划方案，以研究不同的治疗方案之间不同的肿瘤再生长动力学对这些方案的影响。肿瘤细胞再繁殖的定律包括Logistic模型和Gompertz模型，这扩展了Wheldon等人的工作(1977 b.J.Radiol。50 681)，涉及处理之间的指数再增长的情况。这里我们还考虑了受限指数模型。Panetta和Adam(1995 Math.电脑。在化疗计划的情况下，建模22 67)。所研究的治疗方案包括每日治疗的标准分割、工作日治疗、加速分割、优化的均匀分割以及剂量和α/ss比的变化，其中α和ss是相关肿瘤组织的放射生物学参数。这些治疗策略的参数摘自关于晚期头颈癌、前列腺癌以及放射敏感性参数的文献。标准化的治疗方案也被考虑。基于当前分析的计算表明，即使将增长规律按比例模拟初始增长，从而使增长机制具有可比性，但存活率出现了数量级的变化。计算表明，Logistic模型和指数模型在消除肿瘤方面产生了类似的结果。通过比较，Gompertz模型的计算表明，这一定律描述的肿瘤导致的肿瘤根除预后比指数或Logistic模型要差得多。目前的研究还表明，肿瘤生长速度越快，细胞株的修复能力越高，生存分数的结果变化就越大。治疗上的差距，无论是计划内的还是计划外的，也加剧了考虑到替代生长动态的存活率的差异。
The standard linear-quadratic survival model for radiotherapy is used to investigate different schedules of radiation treatment planning to study how these may be affected by different tumour repopulation kinetics between treatments. The laws for tumour cell repopulation include the logistic and Gompertz models and this extends the work of Wheldon et al (1977 Br. J. Radiol. 50 681), which was concerned with the case of exponential re-growth between treatments. Here we also consider the restricted exponential model. This has been successfully used by Panetta and Adam (1995 Math. Comput. Modelling 22 67) in the case of chemotherapy treatment planning. Treatment schedules investigated include standard fractionation of daily treatments, weekday treatments, accelerated fractionation, optimized uniform schedules and variation of the dosage and alpha/ss ratio, where alpha and ss are radiobiological parameters for the tumour tissue concerned. Parameters for these treatment strategies are extracted from the literature on advanced head and neck cancer, prostate cancer, as well as radiosensitive parameters. Standardized treatment protocols are also considered. Calculations based on the present analysis indicate that even with growth laws scaled to mimic initial growth, such that growth mechanisms are comparable, variation in survival fraction to orders of magnitude emerged. Calculations show that the logistic and exponential models yield similar results in tumour eradication. By comparison the Gompertz model calculations indicate that tumours described by this law result in a significantly poorer prognosis for tumour eradication than either the exponential or logistic models. The present study also shows that the faster the tumour growth rate and the higher the repair capacity of the cell line, the greater the variation in outcome of the survival fraction. Gaps in treatment, planned or unplanned, also accentuate the differences of the survival fraction given alternative growth dynamics.