背景:磁性热疗(MHT)已成为放射肿瘤学领域中一种有前途的治疗方法,因为与常规热疗相比,它在控制温度和管理加热区域方面具有出色的精度。最近的研究提出了解决与MHT相关的临床安全问题的解决方案。这是由于使用高浓度的磁性纳米颗粒和引起高热效应所需的强磁场而产生的。尽管做出了这些努力,在量化治疗结果和开发MHT与放射治疗(RT)相结合的治疗计划系统方面仍然存在挑战.
目的:本研究旨在定量测量治疗效果,包括磁热-辐射联合治疗(MHRT)中的辐射剂量增强(RDE),采用等效辐射剂量(EQD)估算方法。
方法:要对MHRT进行EQD估算,我们比较了常规热疗-放疗联合治疗(HTRT)和MHRT在人前列腺癌细胞系中的治疗效果,PC3和LNCaP。我们采用克隆实验来验证RDE和MHT诱导的放射增敏作用。使用线性四元模型和Arrhenius模型分析了存活分数的数据,以通过最大似然估计来估计描述RDE和MHRT对两种细胞系的放射增敏作用的生物学参数。基于这些参数,提出了一种新的生存分数模型来估计MHRT的EQD。
结果:新设计的描述MHRT效应的模型,有效地捕获两种细胞系的热和辐射剂量的变化(R2>0.95),并通过残差正态检验证实了其适用性。该模型适当地描述了在仅RT条件下PC3细胞高达10Gy和LNCaP细胞高达8Gy的存活分数。此外,使用新定义的参数r,RDE效应在PC3细胞中为29%,在LNCaP细胞中为23%。当给予2Gy和MHT30分钟时,通过该模型计算的EQDMHRT对于PC3为9.47Gy,对于LNCaP为4.71Gy。与EQDHTRT相比,EQDMHRT显示PC3增加26%,LNCaP增加20%。
结论:提出的模型有效地描述了两种细胞系中MHRT诱导的存活分数的变化,并通过残差分析充分代表了实际数据值。新建议的RDE效应参数r显示了HTRT和MHRT之间定量比较的潜力,并优化MHRT对前列腺癌的治疗效果。
BACKGROUND: Magnetic hyperthermia (MHT) has emerged as a promising therapeutic approach in the field of radiation oncology due to its superior precision in controlling temperature and managing the heating area compared to conventional hyperthermia. Recent studies have proposed solutions to address clinical safety concerns associated with MHT, which arise from the use of highly concentrated magnetic nanoparticles and the strong magnetic field needed to induce hyperthermic effects. Despite these efforts, challenges remain in quantifying therapeutic outcomes and developing treatment plan systems for combining MHT with radiation therapy (RT).
OBJECTIVE: This study aims to quantitatively measure the therapeutic effect, including radiation dose enhancement (RDE) in the magnetic hyperthermia-radiation combined therapy (MHRT), using the equivalent radiation dose (EQD) estimation method.
METHODS: To conduct EQD estimation for MHRT, we compared the therapeutic effects between the conventional hyperthermia-radiation combined therapy (HTRT) and MHRT in human prostate cancer cell lines, PC3 and LNCaP. We adopted a clonogenic assay to validate RDE and the radiosensitizing effect induced by MHT. The data on survival fractions were analyzed using both the linear-quadradic model and Arrhenius model to estimate the biological parameters describing RDE and radiosensitizing effect of MHRT for both cell lines through maximum likelihood estimation. Based on these parameters, a new survival fraction model was suggested for EQD estimation of MHRT.
RESULTS: The newly designed model describing the MHRT effect, effectively captures the variations in thermal and radiation dose for both cell lines (R2 > 0.95), and its suitability was confirmed through the normality test of residuals. This model appropriately describes the survival fractions up to 10 Gy for PC3 cells and 8 Gy for LNCaP cells under RT-only conditions. Furthermore, using the newly defined parameter r, the RDE effect was calculated as 29% in PC3 cells and 23% in LNCaP cells. EQDMHRT calculated through this model was 9.47 Gy for PC3 and 4.71 Gy for LNCaP when given 2 Gy and MHT for 30 min. Compared to EQDHTRT, EQDMHRT showed a 26% increase for PC3 and a 20% increase for LNCaP.
CONCLUSIONS: The proposed model effectively describes the changes of the survival fraction induced by MHRT in both cell lines and adequately represents actual data values through residual analysis. Newly suggested parameter r for RDE effect shows potential for quantitative comparisons between HTRT and MHRT, and optimizing therapeutic outcomes in MHRT for prostate cancer.