Radiofrequency ablation (RFA) is a new, minimally invasive treatment for hepatocellular carcinoma (HCC). However, there is little available information regarding local recurrence after a single ...session of RFA with a single electron insertion.
From February 1999 to September 2001, we treated 104 HCC tumors with an expandable needle with four hooks. Ninety-nine of the 104 tumors were successfully treated by single-session RFA with a single electrode insertion. We investigated the relationships between pretreatment factors (tumor size, tumor staining, tumor capsule, and tumor location) and local recurrence in these 99 tumors.
The mean size of the 99 tumors was 21.5 mm in diameter (range, 10 to 33 mm). The overall local recurrence rates were 9.7%, 15.4%, and 20.4%, at 1, 2, and 3 years, respectively. For small tumors (smaller than 25 mm), the local recurrence rates at 1, 2, and 3 years were 4.0%, 8.0%, and 14.6%, respectively. The local recurrence rates were 21.1% and 32.3% at 1 and 2 years, respectively, for large tumors (25 mm or larger), and at 3 years the rate was over 50% for tumors located close to the liver surface. Tumor size and tumor location relative to the liver surface were significantly associated with a higher local recurrence rate. However, other variables tested showed no significant relationship to the local recurrence rate.
This study demonstrated that both tumor size and location relative to the liver surface influence the local efficacy of single-session RFA with a single electrode insertion.Radiofrequency ablation (RFA) is a new, minimally invasive treatment for hepatocellular carcinoma (HCC). However, there is little available information regarding local recurrence after a single session of RFA with a single electrode insertion.
Background/Aims: Hepatocellular carcinoma (HCC) is closely associated with chronic liver diseases, particularly cirrhosis. However, the genes involved in hepatocarcinogenesis in the context of ...developing cirrhosis remain unknown. This study aims to identify genes associated with early cirrhosis-associated hepatocarcinogenesis.
Methods: We examined genes differentially expressed between the livers of normal rats and rats fed a choline-deficient,
l-amino acid-defined (CDAA) diet using suppression subtractive hybridization. We examined both the expression in the liver and HCC tissues of osteoactivin (OA), isolated in this screen, and its effect on invasiveness and metastasis.
Results: OA mRNA was strongly expressed in the livers of rats fed the CDAA diet for 1–3 months. Moderate expression was sustained for 18 months. OA overexpression increased the invasiveness and metastasis of rat hepatoma cells in vitro and in vivo. In humans, OA expression was not detectable in normal liver tissues. While OA transcripts were detectable in cirrhotic nontumorous liver tissues surrounding HCCs, the majority of HCC tissue samples exhibited higher levels of OA expression than the surrounding normal tissue.
Conclusions: These results indicate that OA is a novel factor involved in the progression of HCC via stimulation of tumor invasiveness and metastatic potential.
In a rat model of hepatocarcinogenesis induced by a choline-deficient,
l-amino acid-defined (CDAA) diet, hepatocellular carcinoma (HCC) occurs in conjunction with fatty liver, hepatocyte injury and ...regeneration, fibrosis and cirrhosis. This is similar to human HCC development with cirrhosis. The aim of this study is to clarify sequential changes in the expression of growth and growth inhibitory factors, and hepatocyte proliferation and apoptosis during development of preneoplastic nodules in rats fed a CDAA diet. The expression of hepatocyte growth factor was stimulated at about the same time as CDAA diet-induced liver injury within 1 week. Hepatocyte growth factor reached a maximum level of expression from 4 to 8 weeks. Transforming growth factor (TGF)-α expression increased from 4 to 40 weeks. Although TGF-β, a growth inhibitory factor for hepatocytes, was also expressed with a peak from 4 to 8 weeks followed by a gradual decrease until 48 weeks, expression of cyclin D1 and hepatocyte proliferation continued to be stimulated throughout the experimental period. Additionally, the number of apoptotic hepatocytes was markedly reduced after peaking at 8 weeks. These results suggest that some hepatocytes in the livers of rats fed a CDAA diet may escape from TGF-β-induced growth inhibition and apoptosis, leading to development of preneoplastic nodules.
We previously reported that the retroviral vector expressing the herpes simplex virus-thymidine kinase gene under the control of 0.3-kb human alpha-fetoprotein (AFP) gene promoter (AF0.3) provided ...the cytotoxicity to ganciclovir (GCV) in high-AFP-producing human hepatoma cells but not in low-AFP-producing cells. Therefore, specific enhancement of AFP promoter activity is likely to be required to induce enough cytotoxicity in low-AFP-producing hepatoma cells. In this study, we constructed a hybrid promoter, HREAF, in which a 0.4-kb fragment of human vascular endothelial growth factor 5'-flanking sequences containing hypoxia-responsive element (HRE) was fused to AF0.3 promoter. By means of the reporter gene transfection assay, hypoxia-inducible transcriptions that were mediated by HREAF promoter were detected in low- and non-AFP-producing human hepatoma cells, but not in nonhepatoma cells. When the herpes simplex virus-thymidine kinase gene controlled by HREAF promoter was transduced into hepatoma and nonhepatoma cells by a retroviral vector, the exposure to 1% O2 induced GCV cytotoxicity specifically in the hepatoma cells. Moreover, in nude mice bearing solid tumor xenografts, only the tumors consisting of the virus-infected hepatoma cells gradually disappeared by GCV administration. These results indicate that the hypoxia-inducible enhancer of the human vascular endothelial growth factor gene, which is directly linked to human AFP promoter, involves selective and enhanced tumoricidal activity in gene therapy for hepatocellular carcinoma.
A previously well 18-year-old female was referred to our hospital because of abnormalities of blood biochemistry and slight jaundice. Because serum aspartate aminotransferase (AST) and alanine ...aminotransferase (ALT) levels were elevated more than 6000 IU/L, the patient was suspected to have acute viral hepatitis. The platelet count on admission was 9.7×10
4/μl, which was decreased from the initial value of 21×10
4/μl for 3 days. The coagulation tests revealed marked elevation of
d-dimmer, fibrinogen degradation products and thrombin–antithrombin III complex suggesting increase in fibrinolysis. Serum levels of high density lipoprotein cholesterol and ferritin were markedly decreased and increased, respectively. The bone marrow smears revealed proliferation of mature histiocytes ingesting platelets and erythrocytes, these pathological findings were consistent with those of hemophagocytic syndrome (HPS). In addition, anti-hepatitis A IgM antibody in the serum and hepatitis A virus (HAV) RNA in the stool were positive. Therefore, the patient was diagnosed as having acute hepatitis A with probable HPS. Since a fulminant clinical course was suspected, glucocorticoid pulse therapy was started immediately 7 days after onset and a favorable clinical outcome resulted.
We report a case of hepatocellular carcinoma (HCC) associated with autoimmune hepatitis in an 80-year-old female. The patient exhibited the presence of a liver injury 10 years previously. However, ...because the etiology was not identified, she did not receive specific treatment such as glucocorticoid therapy. She was admitted to our hospital because of the presence of a mass lesion in the S
8 region of the liver detected by ultrasonography. Serum alanine and aspartate aminotransferase levels were elevated and the serum
γ-globulin level was increased to more than 2.5 g/dl. Serum autoantibodies such as antinuclear antibody and anti-DNA antibody were positive. Hepatitis virus markers and their genes for hepatitis B virus (HBV) and hepatitis C virus (HCV) were negative in the serum. The biopsied specimen from the non-tumorous lesion showed a marked infiltration of chronic inflammatory cells, particularly plasma cells, and the tumorous lesion was well to moderately differentiated HCC. HBV DNA and HCV RNA were not detected in the tissue specimen from the non-tumorous lesion.
