Author:
Ke Shan,Ding Xue-mei,Kong Jian,Gao Jun,Wang Shao-hong,Cheng Yan,Sun Wen-bing
Abstract
Abstract
Background
Rapid progression of residual tumor after radiofrequency ablation (RFA) of hepatocellular carcinoma has been observed increasingly. However, its underlying mechanisms remain to be clarified. The present study was designed to determine whether low temperature of RFA at the target sites facilitates rapid progression of residual hepatic VX2 carcinoma and to clarify the possible underlying mechanisms.
Methods
The residual VX2 hepatoma model in rabbits was established by using RFA at 55, 70 and 85°C. Rabbits that were implanted with VX2 hepatoma but did not receive RFA acted as a control group. The relationship between rapid progression of residual hepatic VX2 carcinoma and low temperature of RFA at the target sites was carefully evaluated. A number of potential contributing molecular factors, such as proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 9 (MMP-9), vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF) and Interleukin-6 (IL-6) were measured.
Results
The focal tumor volume and lung metastases of RFA-treated rabbits increased significantly compared with the control group (P < 0.05), and the greatest changes were seen in the 55°C group (P < 0.05). Expression of PCNA, MMP-9, VEGF, HGF and IL-6 in tumor tissues increased significantly in the RFA-treated groups compared with the control group, and of the increases were greatest in the 55°C group (P < 0.05). These results were consistent with gross pathological observation. Tumor re-inoculation experiments confirmed that low temperature of RFA at the target sites facilitated rapid progression of residual hepatic VX2 carcinoma.
Conclusions
Insufficient RFA that is caused by low temperature at the target sites could be an important cause of rapid progression of residual hepatic VX2 carcinoma. Residual hepatic VX2 carcinoma could facilitate its rapid progression through inducing overexpression of several molecular factors, such as PCNA, MMP-9, VEGF, HGF and IL-6.
Publisher
Springer Science and Business Media LLC
Subject
General Biochemistry, Genetics and Molecular Biology,General Medicine
Reference41 articles.
1. Shariff MI, Cox IJ, Gomaa AI, Khan SA, Gedroyc W, Taylor-Robinson SD: Hepatocellular carcinoma: current trends in worldwide epidemiology, risk factors, diagnosis and therapeutics. Expert Rev Gastroenterol Hepatol. 2009, 3 (4): 353-367. 10.1586/egh.09.35.
2. Sun WB: How is radiofrequency ablation going in treating hepatocellular carcinoma in China?. Austral-Asian Journal of Cancer. 2008, 7 (4): 221-224.
3. Lau WY, Lai EC: The current role of radiofrequency ablation in the management of hepatocellular carcinoma: a systematic review. Ann Surg. 2009, 249 (1): 20-25. 10.1097/SLA.0b013e31818eec29.
4. Rhim H, Kim YS, Choi D, Lim HK, Park K: Percutaneous radiofrequency ablation of hepatocellular carcinoma: analysis of 80 patients treated with two consecutive sessions. Eur Radiol. 2008, 18 (7): 1442-1448. 10.1007/s00330-008-0902-4.
5. Thanos L, Mylona S, Galani P, Pomoni M, Pomoni A, Koskinas I: Overcoming the heat-sink phenomenon: successful radiofrequency thermal ablation of liver tumors in contact with blood vessels. Diagn Interv Radiol. 2008, 14 (1): 51-56.