Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to investigate the relation between the recurrence of hepatocellular carcinoma (HCC) and the histologic status of underlying chronic liver disease from a viewpoint of multicentric hepatocarcinogenesis. Sixty-eight patients who underwent curative resection of HCC and have been followed for more than 2 years are reported. Based on the microscopic findings of the noncancerous part of the liver, the patients were divided into normal liver (N,n = 2), chronic persistent hepatitis (CPH,n = 6), chronic aggressive hepatitis (CAH,n = 31), and liver cirrhosis (LC,n = 29) according to a classification by the European Association for the Study of the Liver. Background data for the groups showed no significant differences. Recurrence was observed in none of the patients in the N and CPH groups, 26 (83.9%) of the patients in the CAH group, and 12 (41.4%) of the patients in the LC group. The cumulative disease-free survival rate of the CAH group was significantly lower than that of the CPH group (p < 0.05) and LC group (p < 0.01). This study revealed that the histologic status of the underlying chronic liver disease influenced the recurrence rate in patients with HCC. CAH was considered to be a risk factor for recurrence after resection of HCC.
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PMID:Influence of associated viral hepatitis status on recurrence of hepatocellular carcinoma after hepatectomy. 879 68

HCV is ubiquitous. In 50% of all cases it causes chronic hepatitis that often evolves into liver cirrhosis and hepatocellular carcinoma. Recently HCV has been classified in 5 genotypes by Okamoto. The purpose of this study is to evaluate the prevalence of 5 genotypes in Campania, a region of southern Italy, where the prevalence of anti-HCV antibodies ranges from 0.87 to 4%, and to evaluate the correlation between the HCV genotypes and the severity of histological damage. One-hundred- and-thirty-five anti-HCV positive patients were enrolled and tested by PCR to identify HCV-RNA. One-hundred-and-twenty-four patients resulted HCV-RNA positive. Genotyping was performed as described by Okamoto et al. with minor modifications of the specific primer to type III proposed by Silini et al. Eight patients were negative for all genotypes. Eight patients were positive for type I(1a), 61 for type II(1b), 39 for type III(2a), 11 for type IV(2b) and 1 for type V(3a). In 4 cases two different genotypes were present in the same sample [II(1b)-IV(2b), III(2a)-II(1b) twice, III (2a)-IV(2b)]. Histological evaluation of liver damage showed: CPH (22 cases), minimal CAH (56), severe CAH (31) and liver cirrhosis (15). There was no statistically significant correlation between the 5 genotypes and the severity of histological damage. Data on the prevalence of genotype II (1b) in Italy are similar to those reported for other European countries. The prevalence of genotypes in southern Italy is similar to that reported in the population of northern Italy.
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PMID:Prevalence of hepatitis C virus genotypes in southern Italy. 906 79

Soluble HLA-class I and CD8 molecules were determined by sandwich ELISA in patients with viral-induced hepatic disorders. As a whole, the patients with hepatic disorders (acute hepatitis: AH; chronic hepatitis: CH; liver cirrhosis: LC; hepatocellular carcinoma: HCC) showed higher sHLA-class I and sCD8 levels than normal controls (P < 0.001). AH patients had the highest sHLA-class I levels (mean, 3513 +/- 2112 ng/ml), followed by CH (2896 +/- 1290 ng/ml), LC (2293 +/- 1266 ng/ml), and HCC (2221 +/- 1212 ng/ml) sCD8 levels wer highest in AH, followed by HCC, LC, and CH, in that order. Among histologically defined C virus-positive patients, sHLA-I levels were higher in those with chronic active hepatitis (CAH) 2A (3802 +/- 1124 ng/ml) than in those with chronic persistent hepatitis (CPH; 2200 +/- 711 ng/ml; P < 0.01), the levels then decreased as the disease progressed (CAH2B, 3564 +/- 1783 ng/ml, LC, 2376 +/- 1265 ng/ml). In contrast, sCD8 values showed little difference among the disorders. sHLA-class I levels showed a positive correlation with sCD8 values both in whole patients and in patients with AH (P < 0.01), but no correlation was shown, in any patients, with biochemical parameters such as GPT and GOT. These findings, taken together, suggest that hepatic destruction is not the only cause of sHLA-class I production, but that sHLA-class I levels, together with sCD8 levels, may reflect immunological activity in hepatic disorders.
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PMID:Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders. 921 47


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