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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of the serological markers of Hepatitis B virus (HBV) including e antigen (HBe Ag) and antibody against HBe Ag (anti-HBe) was performed in Senegalese patients suffering from cirrhosis and primary hepatocellular carcinoma, and in a control group (blood donors). It was not possible to diagnose additional HBV infections in primary hepatocellular carcinoma patients using HBe Ag or anti-HBe Ab alone as serological markers. The lower prevalence of HBe Ag among primary hepatocellular carcinoma patients as compared with cirrhotic patients suggests that active replication of HBV becomes increasingly defective during the course of the malignant process.
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PMID:Incidence and significance of hepatitis B e antigen and antibody in postnecrotic cirrhosis and primary hepatocellular carcinoma. 21 Nov 44

Tumour, cirrhotic, and metastatic tissues from four patients with primary hepatocellular carcinoma have been investigated for the presence of hepatitis B viral DNA by nucleic acid hybridization. Tumours from two of three patients with a current HBV infection contained 1--2 genomes per cell of unintegrated viral DNA, while tumours from the third HBs antigen-positive patient contained less than one genome equivalent per ten cells. A tumour from one patient with anti-HBs contained no detectable HBV DNA. A variety of models involving HBV as an etiologic agent may be advanced to explain the statistical correlation of HBV infection with primary hepatocellular carcinoma (PHC). The data presented here argue against the model that HBV DNA integrated into every cell is required to maintain the oncogenic transformation of hepatocytes, but they do not rule out other models.
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PMID:Hepatitis B virus DNA in primary hepatocellular carcinoma tissue. 21 25

Particles with properties similar to those associated with human hepatitis B were found in serum from woodchucks with chronic hepatitis and hepatocellular carcinoma. It is suggested that woodchuck hepatitis virus is a second member of a novel class of viruses represented by the human hepatitis B virus.
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PMID:A virus similar to human hepatitis B virus associated with hepatitis and hepatoma in woodchucks. 21 58

Numerous cases of chronic hepatitis have been shown to be closely associated with persistent infection with hepatitis B virus (HBV). A group of 100 patients suffering from chronic active hepatitis (CAH) was investigated for HBV serologic markers. Of these, 35 patients were HbsAg-positive; in 26 HBsAg-negative subjects, anti-HBc were detected using counterimmune electrophoresis and complement-fixation tests. These data suggest that chronic liver disease in patients who were only anti-HBc-positive might be related to persistent infection with hepatitis B virus. Epidemiological clinical and histopathological data were different when we compared CAH patients who were HBsAg-negative, but anti-HBc-positive, with HBsAg-positive CAH patients. A sequence is proposed leading from HBsAg-positive to HBsAg-negative CAH, cirrhosis, and hepatoma in temperate areas, according to a model similar to the one described in intertropical Africa.
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PMID:HBsAg-negative chronic active hepatitis related to hepatitis B virus. 21 84

Three hundred and eighty-five patients mostly with chronic liver diseases and 729 apparently healthy adults were studied for hepatitis B surface antigen (HBsAg) with reversed passive hemagglutination and antibody (anti-HBs) with passive hemagglutination. In healthy adults around 15% was HBsAg positive and in 45% was anti-HBs positive, estimating hepatitis B virus (HBV) infection in nearly two thirds of the population. The infection already occurred before adulthood. The prevalences of HBsAg were invariably over 80% in chronic hepatitis, cirrhosis and hepatocellular carcinoma (hepatoma) indicating an intimate relationship to HBV. On the contrary, the positive rates of anti-HBs in these diseases were far lower than those in healthy people and patients with other diseases, this is similar to the situation in chronic HBsAg carriers. The prevalence of HBsAg in hepatoma patients was unusually high, being 82.7% in contrast to 11.9% in patients with other malignancies. Not only hepatoma patients with cirrhosis but also those without cirrhosis were found to have high prevalence of HBsAg. The fact indicates an even more intimate relationship between hepatoma and HBV.
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PMID:Hepatitis B virus infection and chronic liver disease in Taiwan. 21 87

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

Risk factors can be used to formulate hypotheses on the aetiology and pathogenesis of site specific cancers. Persistent infection with hepatitis B virus (HBV), chronic liver disease, and maleness are associated with a greatly increased risk of developing primary hepatocellular carcinoma (PHC). A model for the pathogenesis of this tumour is proposed that does not involve integration of the HBV genome into the tumour cell. If chronic infection with HBV is necessary for the development of chronic liver disease and PHC, prevention of PHC could be accomplished by prevention of infection with HBV. A vaccine against HBV could be accomplished by prevention of infection with HBV. A vaccine against HBV has been developed; if it is effective, we can predict that its use in endemic areas will be accompanied by an eventual fall in the incidence of PHC.
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PMID:Hepatocellular carcinoma (an approach to the study of risk factors in human cancer). 21 70

Liver tissues of 180 autopsy cases of cirrhosis and hepatoma and 285 consecutive autopsy cases of other diseases were studied for liver cell dysplasia correlated with hepatitis B surface and core antigens (HBsAg and HBcAg) in liver cells and sera, and antibody to HBsAg (anti-HBs) in sera. Liver cell dysplasia was characteristic in cirrhotic livers, particularly with hepatoma. No significant difference was found in age and sex between cirrhotic cases with and without dysplasia. Rate of positive HBsAg in liver cells and sera was significantly high in cirrhotic cases with dysplasia with or without hepatoma. Massive pattern distribution of orcein-positive liver cells was statistically significant in cirrhotic livers with or without hepatoma, but morphological characteristics of orcein-positive liver cells could not be correlated in significance with dysplasia and hepatoma. HBcAg showed neither correlation with liver cell dysplasia nor hepatoma. It appears to correlate with active cirrhosis, marked liver cell degeneration and necrosis, and membranous diffuse type HBsAg in liver cells.
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PMID:Liver cell dysplasia and hepatitis B surface and core antigens in cirrhosis and hepatocellular carcinoma of autopsy cases. 21 29

Hepatitis B surface antigen (HBsAg) was identified with aldehyde fuchsin and immunoperoxidase stain and by immunofluorescence in malignant hepatocytes with a ground-glass appearance in only one needle biopsy specimen of a series of biopsies from 130 consecutive cases of hepatocellular carcinoma. The patient was 14 years old. HBsAg was identified by aldehyde fuchsin stain in nonmalignant hepatocytes of 48 (58%) of 83 biopsy specimens that contained nonmalignant liver tissue. The antigen was demonstrable in significantly greater proportions of cases in younger age groups. A similar but not identical age relationship has been found for hepatitis B antigenemia in Hong Kong. It appears that the ability to produce HBsAg declines with age. The usual absence of demonstrable HBsAg in cells of hepatocellular carcinoma may be due to a failure of this characteristic to survive into the malignant cell line, and so does not invalidate the possibility that the hepatitis B virus (HBV) plays a direct role in the pathogenesis of hepatocellular carcinoma. In exceptional circumstances, as when hepatocellular carcinoma appears at an unusually early age, this marker is identifiable in cells of the tumor.
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PMID:Cytoplasmic hepatitis B surface antigen and the ground-glass appearance in hepatocellular carcinoma. 21 45

Sera of 173 patients with various forms of liver disease along with serum precipitates produced by polyethylene glycol were screened for the presence of a microsomal antigen referred to as ubiquitous tissue antigen (UTA) and its antibody by double diffusion precipitation in agarose gel. UTA was detected in 7 or 26 patients with chronic active hepatitis, 1 of 5 with alcoholic hepatitis, 2 of 14 with alcoholic cirrhosis and 18 of 98 with hepatoma. Antibodies to UTA were found only in 2 patients with chronic active hepatitis, 1 with alcoholic cirrhosis and 1 with hepatoma. No UTA or its antibody were noted in sera of 5 patients with alcoholic fatty liver, 10 patients with hepatitis B, and 15 asymptomatic carriers of HBsAg. Positivity for the UTA or its antibody was restricted to severe, chronic cases irrespective of diagnosis, indicating that persistent tissue destruction might be necessary for antigen release or antibody formation.
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PMID:Detection of a microsomal antigen and its antibody in human liver diseases. 22 26


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