ABSTRACT
PURPOSE: To explore the effect of combined antiviral therapy in patients with hepatitis B-related hepatocellular carcinoma. METHODS: 82 patients with hepatitis B-related primary liver cancer were selected and divided into two groups. Among them, the control group was treated with routine liver protection, the observation group was treated with antiviral therapy and nucleoside analogues (including lamivudine, entecavir and tibivudine). RESULTS: The alanine transferase (ALT) of the observation group (54.79±13.23) U/L was significantly lower than that in the control group (150.27±18.75) U/L (p<0.05). The unpredictable rate of HBV DNA in the observation group was 48.1% in the 12th month, which was obviously improved compared with the conventional therapy, p<0.05. Among the 18 patients (43.9%) in the observation group, 7 patients with positive HBeAg turned negative and 3 were converted to HBeAb, among which, the HBeAg negative conversion rate was 38.9% and the HBeAg conversion rate was 16.7%. Child-Pugh score of patients with hepatitis B-related primary liver cancer increased with the extension of treatment. In the observation group for 6 and 12 months, Child-Pugh score was significantly lower than that in the control group, p<0.05. The survival rate was 97.6% and 92.7% at the 6th month, 85.4% and 78.0% at the 12th month, 78.0% and 56.1% at the 18th month, the difference was statistically significant (p<0.05). CONCLUSION: Combined antiviral therapy on the basis of conventional treatment can significantly improve the liver function, reduce the viral load and prolong the survival time of patients with hepatitis B-related hepatocellular carcinoma associated.
Subject(s)
Antiviral Agents/therapeutic use , Carcinoma, Hepatocellular/drug therapy , Carcinoma, Hepatocellular/virology , Hepatitis B, Chronic/complications , Hepatitis B, Chronic/drug therapy , Liver Neoplasms/drug therapy , Liver Neoplasms/virology , Female , Humans , Male , Middle Aged , Treatment OutcomeABSTRACT
BACKGROUND: The incidence of gallbladder carcinoma (GBM) in China has increased in recent years. Here, the functional mechanism of lncRNA TTN-AS1 in GBC was preliminary elucidated. METHODS: The expression levels of lncRNA TTN-AS1, miR-107, and HMGA1 in tissues and cell lines were assessed by RT-qPCR. Cell proliferation was measured by MTT assays. Cell invasion and migration abilities were evaluated by Transwell assays. The relationship between miR-107 and lncRNA TTN-AS1 or HMGA1 was confirmed by luciferase reporter assay. RESULTS: Upregulation of lncRNA TTN-AS1 and downregulation of miR-107 were detected in GBC. Furthermore, the expressions between TTN-AS1 and miR-107 were mutually inhibited in GBC. Functionally, lncRNA TTN-AS1 promoted cell viability and motility in GBC by sponging miR-107. In addition, miR-107 directly targets HMGA1. And HMGA1 can be positively regulated by lncRNA TTN-AS1 in GBC. Furthermore, HMGA1 promoted GBC progression by interacting with lncRNA TTN-AS1/miR-107 axis. CONCLUSION: LncRNA TTN-AS1 acted as a tumor promoter in GBC by sponging miR-107 and upregulating HMGA1.
