Objective: To study the importance of percutaneous radiofrequency ablation (PRFA) guided by ultrasound for inoperable recurrent hepatocellular carcinoma.Methods: Forty-seven patients with inoperable recurrent hepatoce...Objective: To study the importance of percutaneous radiofrequency ablation (PRFA) guided by ultrasound for inoperable recurrent hepatocellular carcinoma.Methods: Forty-seven patients with inoperable recurrent hepatocellular carcinoma underwent percutaneous radiofrequency ablation (PRFA) under ultrasond between October 1999 and July 2001. Twenty-four patients had single recurrent tumor and 23 patients had multiple lesions. Twelve patients had single lesion with less than 3.5 cm in diameter. All patients were followed up to examine the value of AFP, MRI or CT after PRFA. Kaplan-Meier estimation was used to analyze the survival rate.Results: The 1-, 2- and 3-year survival rate in single lesion group was 65.2%, 37.5% and 37.5% respectively. The survival rate of 1 and 2 years was 41.7% and 19.5% in the multiple lesions group. The 1-, 2-and 3-year survival rate in single lesion groups with less than 3.5 cm in diameter was 83.3%, 51.4% and 51.4% respectively.Conclusion: PRFA is one of the important comprehensive methods for recurrent hepatocellular carcinoma. According to the size, number and recurrent time, PRFA can be performed separately or combined with transcatheter arterial chemoembolization for inoperable recurrent hepatocellular carcinoma. This method can control the recurrence and increase the survival rate effectively. Key words recurrence - hepatocellular cacinoma - radiofrequency ablation展开更多
Objective To evaluate the role of nuclear factor-kappa B (NF-κB) and inhibitory κB alpha (IκBα) in hepatocellular cacinoma (HCC) SMMC7721 cells, the consequence of NF-κB inhibition in SMMC7721 cells transfected...Objective To evaluate the role of nuclear factor-kappa B (NF-κB) and inhibitory κB alpha (IκBα) in hepatocellular cacinoma (HCC) SMMC7721 cells, the consequence of NF-κB inhibition in SMMC7721 cells transfected with mutated IκBα (mIκBα) plasmid and the effect of stable inhibition of NF-κB activity in combination with Doxorubicin.Methods Western blot was used to determine the expression of NF-κB and IκBα in SMMC7721 cells and normal liver cells. Nuclear protein was used to evaluate the binding of the 32P-labeled tandem κB sequence using electrophoretic mobility shift assay and the expression of NF-κB using Western blot between SMMC7721 cells transfected with mIκBα plasmid (SMMC7721-MT) and control cells. Furthermore, cell viability was plotted between SMMC7721-MT and control cells. The binding of κB sequence and cell viability between SMMC7721-MT and control cells at different concentrations of Doxorubicin were also investigated.Results Western blot analysis for nuclear extract showed more P50 (NF-κB1) and P65 (RelA) expression in SMMC7721 cells compared with normal liver cells. The expression of cytosolic IκBα protein in SMMC7721 cells was less than that in normal cells. SMMC7721-MT cells inhibited NF-κB nuclear translocation at 0, 24, 48 and 96 hours. Furthermore, NF-κB cannot be detected in the nuclear protein of SMMC7721-MT cells by Western blot. By calculating cell viability, the proliferation of SMMC7721-MT cells was shown to be suppressed more significantly than that of control cells. NF-κB in untransfected cells was activated by Doxorubicin in a dose-dependent manner, but that in SMMC7721-MT cells was not induced at low concentrations of Doxorubicin. Compared with untransfected cells, the viability of SMMC7721-MT cells was significantly suppressed at the same concentration of Doxorubicin (P<0.01).Conclusions The present study demonstrates that upregulation of NF-κB and downregulation of inhibitory kappa B (IκBα) in SMMC7721 cells are related with the growth of hepatocellular cacinoma cells. Stable expression of mIκBα in SMMC7721-MT cells can inhibit NF-κB nuclear translocation and suppress cell growth. Furthermore, stable inhibition of NF-κB activity in combination with Doxorubicin can significantly inhibit cell proliferation in SMMC7721-MT cells. Thus, modulation of NF-κB may represent an improvement in the efficacy of HCC therapies and be worthy of further research and investigation.展开更多
文摘Objective: To study the importance of percutaneous radiofrequency ablation (PRFA) guided by ultrasound for inoperable recurrent hepatocellular carcinoma.Methods: Forty-seven patients with inoperable recurrent hepatocellular carcinoma underwent percutaneous radiofrequency ablation (PRFA) under ultrasond between October 1999 and July 2001. Twenty-four patients had single recurrent tumor and 23 patients had multiple lesions. Twelve patients had single lesion with less than 3.5 cm in diameter. All patients were followed up to examine the value of AFP, MRI or CT after PRFA. Kaplan-Meier estimation was used to analyze the survival rate.Results: The 1-, 2- and 3-year survival rate in single lesion group was 65.2%, 37.5% and 37.5% respectively. The survival rate of 1 and 2 years was 41.7% and 19.5% in the multiple lesions group. The 1-, 2-and 3-year survival rate in single lesion groups with less than 3.5 cm in diameter was 83.3%, 51.4% and 51.4% respectively.Conclusion: PRFA is one of the important comprehensive methods for recurrent hepatocellular carcinoma. According to the size, number and recurrent time, PRFA can be performed separately or combined with transcatheter arterial chemoembolization for inoperable recurrent hepatocellular carcinoma. This method can control the recurrence and increase the survival rate effectively. Key words recurrence - hepatocellular cacinoma - radiofrequency ablation
文摘Objective To evaluate the role of nuclear factor-kappa B (NF-κB) and inhibitory κB alpha (IκBα) in hepatocellular cacinoma (HCC) SMMC7721 cells, the consequence of NF-κB inhibition in SMMC7721 cells transfected with mutated IκBα (mIκBα) plasmid and the effect of stable inhibition of NF-κB activity in combination with Doxorubicin.Methods Western blot was used to determine the expression of NF-κB and IκBα in SMMC7721 cells and normal liver cells. Nuclear protein was used to evaluate the binding of the 32P-labeled tandem κB sequence using electrophoretic mobility shift assay and the expression of NF-κB using Western blot between SMMC7721 cells transfected with mIκBα plasmid (SMMC7721-MT) and control cells. Furthermore, cell viability was plotted between SMMC7721-MT and control cells. The binding of κB sequence and cell viability between SMMC7721-MT and control cells at different concentrations of Doxorubicin were also investigated.Results Western blot analysis for nuclear extract showed more P50 (NF-κB1) and P65 (RelA) expression in SMMC7721 cells compared with normal liver cells. The expression of cytosolic IκBα protein in SMMC7721 cells was less than that in normal cells. SMMC7721-MT cells inhibited NF-κB nuclear translocation at 0, 24, 48 and 96 hours. Furthermore, NF-κB cannot be detected in the nuclear protein of SMMC7721-MT cells by Western blot. By calculating cell viability, the proliferation of SMMC7721-MT cells was shown to be suppressed more significantly than that of control cells. NF-κB in untransfected cells was activated by Doxorubicin in a dose-dependent manner, but that in SMMC7721-MT cells was not induced at low concentrations of Doxorubicin. Compared with untransfected cells, the viability of SMMC7721-MT cells was significantly suppressed at the same concentration of Doxorubicin (P<0.01).Conclusions The present study demonstrates that upregulation of NF-κB and downregulation of inhibitory kappa B (IκBα) in SMMC7721 cells are related with the growth of hepatocellular cacinoma cells. Stable expression of mIκBα in SMMC7721-MT cells can inhibit NF-κB nuclear translocation and suppress cell growth. Furthermore, stable inhibition of NF-κB activity in combination with Doxorubicin can significantly inhibit cell proliferation in SMMC7721-MT cells. Thus, modulation of NF-κB may represent an improvement in the efficacy of HCC therapies and be worthy of further research and investigation.
