Chen Li, Liu Zhi-Xing, Bi Qiu-Chen, Zhao Jun, Liang Qing-Rong, Tang Qun
Department of Ultrasonic Radiology, The First Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China.
Institute for Advanced Study, Nanchang University, Nanchang, People's Republic of China.
J Hepatocell Carcinoma. 2021 Apr 20;8:263-270. doi: 10.2147/JHC.S301083. eCollection 2021.
It is difficult to achieve whole tumor ablation using percutaneous ethanol ablation therapy (PEAT) due to the limited diffusion of ethanol.
To determine whether chemotherapy can be an adjuvant therapy to benefit PEAT, we investigated ultrasound-guided percutaneous ethanol-paclitaxel combined therapy (PEPCT) of VX2 carcinoma, a rabbit liver cancer model.
A six-arm study was designed to quantify the correlation between paclitaxel (PTX) dose and tumor necrosis or cell proliferation, including sham group (2 mL saline, n=6), incremented dose of PTX (0, 12.5, 25, 37.5 mg) in 2.0 mL ethanol (n=6) and a conventional PEAT group (n=6) as comparison. The test was followed by contrast-enhanced ultrasonic (CEUS) before 7-day sacrifice, tumor harvest, and sectioning. Tumor necrosis ratio was radiologically and histologically quantified; modified proliferation index (-PI) was proposed to quantify the PTX's pharmacological effects. A linear regression model was set to correlate the PTX dose with tumor necrosis ratio or cell proliferation index. The difference of radiological, histological necrosis ratio (HNR) and modified PI in six groups was analyzed via Kruskal-Wallis -test, Welch analysis of variance and one-way ANOVA.
Incremental increases of PTX (0, 12.5, 25, 37.5 mg) correlated with greater fraction of tumor necrosis (R = 0.946, P<0.001 for radiological necrosis ratio [RNR], R = 0.843, P<0.001 forHNR), indicating that one week after procedure PTX's anti-proliferation and ethanol's dehydration co-induced severe tumor necrosis. Correlation analysis further testified a significant association between PTX dose and -PI (R = 0.860, P<0.001).
These results suggest a clear role for PTX-induced cytotoxicity and support the use of chemotherapeutic drugs in ablation therapy.
由于乙醇扩散有限，经皮乙醇消融治疗（PEAT）难以实现对整个肿瘤的消融。
为了确定化疗是否可作为辅助治疗以增强PEAT的疗效，我们研究了超声引导下经皮乙醇 - 紫杉醇联合治疗（PEPCT）兔VX2肝癌模型的效果。
设计了一项六组研究，以量化紫杉醇（PTX）剂量与肿瘤坏死或细胞增殖之间的相关性，包括假手术组（2 mL生理盐水，n = 6）、在2.0 mL乙醇中递增剂量的PTX（0、12.5、25、37.5 mg，n = 6）以及作为对照的传统PEAT组（n = 6）。在处死前7天、切除肿瘤并切片之前进行对比增强超声（CEUS）检查。对肿瘤坏死率进行影像学和组织学定量分析；提出改良增殖指数（-PI）以量化PTX的药理作用。建立线性回归模型以关联PTX剂量与肿瘤坏死率或细胞增殖指数。通过Kruskal-Wallis检验、Welch方差分析和单因素方差分析对六组的影像学、组织学坏死率（HNR）和改良PI的差异进行分析。
PTX剂量递增（0、12.5、25、37.5 mg）与更大比例的肿瘤坏死相关（放射学坏死率[RNR]：R = 0.946，P < 0.001；HNR：R = 0.843，P < 0.001），表明术后一周PTX的抗增殖作用和乙醇的脱水作用共同导致严重的肿瘤坏死。相关性分析进一步证实PTX剂量与 -PI之间存在显著关联（R = 0.860，P < 0.001）。
这些结果表明PTX诱导的细胞毒性具有明确作用，并支持在消融治疗中使用化疗药物。
