Background. The aims of this study were to define the clinical characteristics of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in young adult patients without cirrhosis and to evaluate the efficacy o...Background. The aims of this study were to define the clinical characteristics of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in young adult patients without cirrhosis and to evaluate the efficacy of interferon (IFN) therapy on HCC recurrence. Methods. Of 187 patients with HBV-related HCC treated at our hospital, 4 had no liver cirrhosis and were less than 30 years of age (10, 22, 23, and 26 years). Results. At the time of diagnosis of HCC, all cases had antibody to hepatitis Be antigen (anti-HBe) and histological staging of nontumorous liver was F0 or F1, i.e., low-grade hepatitis. The mothers of all 4 young adult patients with HCC had HBV-related liver disease. Three cases developed recurrence of HCC. In these patients, long-term intermittent IFN therapy after reresection of HCC resulted in long-term survival without recurrence for more than 3 years of follow-up. Conclusions. (1) Young adult patients with HCC are positive for anti-HBe, lack cirrhosis,and the route of infection seems to be mother-to-infant transmission.Transplacental transmission of HBV and HBV DNA integration into the cellular genomic DNA during fetal life is a possible explanation of HBV-related hepatocarcinogenesis in young adults; and (2) long-term IFN therapy seems to be useful for prevention of tumor recurrence after radical operation for HBV-related HCC.展开更多
Background. Silencing of the suppressor of cytokine signaling(SOCS-1) by aberrant methylation at the CpG island in the coding region gene has been reported in hepatocellular carcinoma(HCC). However, principally, it is...Background. Silencing of the suppressor of cytokine signaling(SOCS-1) by aberrant methylation at the CpG island in the coding region gene has been reported in hepatocellular carcinoma(HCC). However, principally, it is methylation in the 5-noncoding region but not that in the coding region which determines the regulation of gene expression. Methods. Methylation-specific PCR was performed for the analysis of methylation status both in the 5-noncoding region and the CpG island of SOCS-1 from 22 HCC tissue samples with adjacent non-HCC tissue samples and from two cell lines. Results. Using primers in the CpG island, 9 of 22 HCC samples exhibited aberrant methylation of SOCS-1, while only 1 of 22 adjacent non-HCC samples did so.The unmethylation pattern was detected in 1 of 22 HCC and in 5 of 22 non-HCC samples. Thus, aberrant methylation of SOCS-1 was significantly associated with HCC (P = 0.0076 by Fisher s exact test). Using primers in the 5-noncoding region,aberrant methylation was observed in 12 of 22 HCC and in 2 non-HCC samples. The unmethylated pattern was observed in 5 of 22 HCC and in 10 of 22 non-HCC samples (P = 0.0042). There was no significant correlation between the methylation status of SOCS-1 and clinicopathological findings, such as the presence or absence of cirrhosis or the histological grade of HCC. Conclusions. Aberrant methylation of the SOCS-1 had a significant correlation with HCC. The rate of aberrant methylation was similar in the 5-noncoding region and in the CpG island. Aberrant methylation of SOCS-1 may be associated with hepatocarcinogenesis, although further studies are necessary.展开更多
Background. The gap junction (GJ) plays important roles in the maintenance of tissue homeostasis, the control of cell growth and differentiation, and the prevention of experimental hepatocarcinogenesis. In this study,...Background. The gap junction (GJ) plays important roles in the maintenance of tissue homeostasis, the control of cell growth and differentiation, and the prevention of experimental hepatocarcinogenesis. In this study, we examined the relationship between the expression of the GJ protein connexin (Cx) 32 in 24 human hepatocellular carcinomas (HCCs) and 29 non carcinomatous liver specimens (NCLs) of 31 patients. Methods. An immunohistochemical study of Cx32 was done in 24 HCCs and 29 NCLs from 31 patients who had undergone hepatic resection. Results. The Cx32 expression decreased gradually as the disease progressed to cirrhosis and HCC. In all Cx32 positive HCCs, the expression was mostly recognized in cytoplasm, not only on the cell membrane. This internalization of Cx32 was also recognized in liver specimens showing hepatitis and cirrhosis, although it was less frequent than in the HCCs. Conclusions. These findings suggest the possibility that changes in both the amount and the distribution of Cx32 may be implicated in human hepatocarcinogenesis.展开更多
文摘Background. The aims of this study were to define the clinical characteristics of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in young adult patients without cirrhosis and to evaluate the efficacy of interferon (IFN) therapy on HCC recurrence. Methods. Of 187 patients with HBV-related HCC treated at our hospital, 4 had no liver cirrhosis and were less than 30 years of age (10, 22, 23, and 26 years). Results. At the time of diagnosis of HCC, all cases had antibody to hepatitis Be antigen (anti-HBe) and histological staging of nontumorous liver was F0 or F1, i.e., low-grade hepatitis. The mothers of all 4 young adult patients with HCC had HBV-related liver disease. Three cases developed recurrence of HCC. In these patients, long-term intermittent IFN therapy after reresection of HCC resulted in long-term survival without recurrence for more than 3 years of follow-up. Conclusions. (1) Young adult patients with HCC are positive for anti-HBe, lack cirrhosis,and the route of infection seems to be mother-to-infant transmission.Transplacental transmission of HBV and HBV DNA integration into the cellular genomic DNA during fetal life is a possible explanation of HBV-related hepatocarcinogenesis in young adults; and (2) long-term IFN therapy seems to be useful for prevention of tumor recurrence after radical operation for HBV-related HCC.
文摘Background. Silencing of the suppressor of cytokine signaling(SOCS-1) by aberrant methylation at the CpG island in the coding region gene has been reported in hepatocellular carcinoma(HCC). However, principally, it is methylation in the 5-noncoding region but not that in the coding region which determines the regulation of gene expression. Methods. Methylation-specific PCR was performed for the analysis of methylation status both in the 5-noncoding region and the CpG island of SOCS-1 from 22 HCC tissue samples with adjacent non-HCC tissue samples and from two cell lines. Results. Using primers in the CpG island, 9 of 22 HCC samples exhibited aberrant methylation of SOCS-1, while only 1 of 22 adjacent non-HCC samples did so.The unmethylation pattern was detected in 1 of 22 HCC and in 5 of 22 non-HCC samples. Thus, aberrant methylation of SOCS-1 was significantly associated with HCC (P = 0.0076 by Fisher s exact test). Using primers in the 5-noncoding region,aberrant methylation was observed in 12 of 22 HCC and in 2 non-HCC samples. The unmethylated pattern was observed in 5 of 22 HCC and in 10 of 22 non-HCC samples (P = 0.0042). There was no significant correlation between the methylation status of SOCS-1 and clinicopathological findings, such as the presence or absence of cirrhosis or the histological grade of HCC. Conclusions. Aberrant methylation of the SOCS-1 had a significant correlation with HCC. The rate of aberrant methylation was similar in the 5-noncoding region and in the CpG island. Aberrant methylation of SOCS-1 may be associated with hepatocarcinogenesis, although further studies are necessary.
文摘Background. The gap junction (GJ) plays important roles in the maintenance of tissue homeostasis, the control of cell growth and differentiation, and the prevention of experimental hepatocarcinogenesis. In this study, we examined the relationship between the expression of the GJ protein connexin (Cx) 32 in 24 human hepatocellular carcinomas (HCCs) and 29 non carcinomatous liver specimens (NCLs) of 31 patients. Methods. An immunohistochemical study of Cx32 was done in 24 HCCs and 29 NCLs from 31 patients who had undergone hepatic resection. Results. The Cx32 expression decreased gradually as the disease progressed to cirrhosis and HCC. In all Cx32 positive HCCs, the expression was mostly recognized in cytoplasm, not only on the cell membrane. This internalization of Cx32 was also recognized in liver specimens showing hepatitis and cirrhosis, although it was less frequent than in the HCCs. Conclusions. These findings suggest the possibility that changes in both the amount and the distribution of Cx32 may be implicated in human hepatocarcinogenesis.
