Low temperature of radiofrequency ablation at the target sites can facilitate rapid progression of residual hepatic VX2 carcinoma.
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 degrees 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 degrees 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 degrees 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.
Ke
Shan
S
Department of Hepatobiliary Surgery, West Campus, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Ding
Xue-mei
XM
Kong
Jian
J
Gao
Jun
J
Wang
Shao-hong
SH
Cheng
Yan
Y
Sun
Wen-bing
WB
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000201:enzymology / Q000473:pathology / Q000601:surgery*; D017115:Catheter Ablation / Q000379:methods*; D049109:Cell Proliferation; D003080:Cold Temperature; D018450:Disease Progression; D017228:Hepatocyte Growth Factor / Q000378:metabolism; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000378:metabolism; D008113:Liver Neoplasms / Q000201:enzymology / Q000473:pathology / Q000601:surgery*; D008175:Lung Neoplasms / Q000556:secondary; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D018365:Neoplasm, Residual; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011817:Rabbits; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D015850:Interleukin-6; D018809:Proliferating Cell Nuclear Antigen; D042461:Vascular Endothelial Growth Factor A; D017228:Hepatocyte Growth Factor; D020780:Matrix Metalloproteinase 9