• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.8
• /
• pp.3651-3657
• /
• 2014

Hepatocellular carcinoma (HCC) has a relatively higher incidence in many countries of Asia. Globally, HCC has a high fatality rate and short survival. Epirubicin, a doxorubicin analogue, may be administered alone or in combination with other agents to treat primary liver cancer and metastatic diseases. However, the toxic effects of epirubicin to normal tissues and cells have been one of the major obstacles to successful cancer chemotherapy. Here, we investigated the effects of epirubicin in combination with kappa-selenocarrageenan on mice with H22 implanted tumors and HepG-2 cell proliferation, immune organ index, morphology, cell cycle and related protein expressions in vivo and in vitro with sequential drug exposure. The inhibitory rate of tumor growth in vivo was calculated. Drug sensitivity was measured by MTT assay, and the King's principle was used to evaluate the interaction of drug combination. Morphological changes were observed by fluorescent microscopy. Cell cycle changes were analyzed by flow cytometry. Expression of cyclin A, Cdc25A and Cdk2 were detected by Western blotting. In vivo results demonstrated that the inhibitory rate of EPI combined with KSC was higher than that of KSC or EPI alone, and the Q value indicated an additive effect. In addition, KSC could significantly raise the thymus and spleen indices of mice with H22 implanted tumors. In the drug sensitivity assay in vitro, exposure to KSC and EPI simultaneously was more effective than exposure sequentially in HepG-2 cells, while exposure to KSC prior to EPI was more effective than exposure to EPI prior to KSC. Q values showed an additive effect in the simultaneous group and antagonistic effects in the sequential groups. Morphological analysis showed similar results to the drug sensitivity assay. Cell cycle analysis revealed that exposure to KSC or EPI alone arrested the cells in S phase in HepG-2 cells, exposure to KSC and EPI simultaneously caused accumulation in the S phase, an effect caused by either KSC or EPI. Expression of cyclin A, Cdc25A and Cdk2 protein was down-regulated following exposure to KSC and EPI alone or in combination, exposure to KSC and EPI simultaneously resulting in the lowest values. Taken together, our findings suggest that KSC in combination with EPI might have potential as a new therapeutic regimen against HCC.

• Radiation Oncology Journal
• /
• v.11 no.2
• /
• pp.311-319
• /
• 1993

The retrospective analysis was performed on 37 patients with stage III non small cell lung cancer who received the radiotherapy from Feb. 1986 to Dec. 1990 at the Dept. of Radiation Oncology, National Medical Center. This analysis, with 29 patients $(78.4\%)$ having been followed from 10 to 60 months, was done to know the survival rate and significant prognostic factor. The actuarial 2,5-year survival rates were $20.6\%,6.9\%$ in our all patients and median survival time was 10 months. Of patients with KPS (Karnofsky prformance status) greater than $80\%,$ the 2, 5 year survival rate and median survival time were $29.2\%,9.7\%$ and 13 months, respectively. The 2-year survival rate and median survival time of patients with KPS less than $80\%\;were\;13.7\%$ and 7 months, respectively. The survival difference according to performance status was statisticaly significant $(29.2\%\;vs.\;13.7\%)(p<0.05).$ In stage IIIa, the 2,5-year survival rate and median survival rate and median survival time were $29.2\%,9.7\%$ and 12 months, respectively. The 2-year survival rate and metian survival time of stage IIIb were $8.6\%$ and 10 months, respectively. The survival difference between stage IIIa and IIIb did not show statistical significance (p>0.1). Of the prognostic factors, the difference of survival rate by initial performance status was statistically significant (p<0.05). But the difference of survival rates by pathologic cell type, stage, total radiation dose, radiotherapy response, and cmbination with chemotherapy were not statistically significant.