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

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

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

This is a study of aetiological associations in patients with primary hepatocellular carcinoma (PHC). Thirty new patients with PHC were seen in a five-year period. The most common aetiological association was alcoholic cirrhosis. This was implicated in the development of PHC in 13 patients. However, since the introduction of radioimmunoassay for hepatitis B surface antigen (HBsAg) there have been six patients with HBsAg-associated PHC. Thus, for the first time, an association of hepatitis B virus with PHC is described in this country.
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PMID:Primary hepatocellular carcinoma in Australia: Aetiological considerations. 22 95

Although hepatocellular carcinoma is probably caused by one or more environmental carcinogens, a genetically determined susceptibility to the development of the tumor has not been excluded. In looking for such a predisposition, we have compared the histocompatibility antigens (HLA) of 102 southern African blacks with histologically proved HCC with those of 208 healthy blacks. The standard two-stage lymphocyte microcytotoxicity method was used to test for 40 antigens: 17 in the A locus, 20 in the B locus, and 3 in the C locus. None of the HLA antigens had a frequency that was significantly different in the patients and the controls. A close association undoubtedly exists between chronic hepatitis B virus infection and hepatocellular carcinoma. If this virus is proved to be oncogenic with respect to hepatocellular carcinoma, a genetic predisposition to the hepatitis B virus carrier state may have an indirect bearing on the etiology of the tumor. Sera from the hepatocellular carcinoma patients were therefore tested for hepatitis B virus markers (HBV surface antigen and antibody against HBV core antigen), and these were related to the patients' histocompatibility antigens. None of the HLA antigen frequencies was significantly different in the surface antigen-positive and the surface antigen-negative patients. As 88% of the patients were anticore positive, no meaningful correlation could be carried out with this marker. Analysis of histocompatibility antigens thus failed to show evidence of a genetic predisposition either to hepatocellular carcinoma or to chronic hepatitis B surface antigenemia in patients with this tumor.
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PMID:Histocompatibility antigens in patients with hepatocellular carcinoma and their relationship to chronic hepatitis B virus infection in these patients. 22 45

Family member of 13 patients with hepatitis B surface antigen (HBsAg) positive primary hepatocellular carcinoma (PHC) were tested for the presence of hepatitis B virus-associated antigens and antibodies. Of the 122 members examined, circulating HGsAg was detected in 47 (39%), antibody to HBsAg (anti-HBs) was found in 37 (30%), and antibody to hepatitis B core antigen (anti-HBc) alone was present in 13 (11%). The relatives with the highest frequency of HBsAg positivity were the offspring of the propositus, followed by the nieces and nephews and the grandchildren. Anti-HBs and anti-HBc were detected most often in the spouses and non-blood relatives. Evidence for past and present hepatitis B virus (HBV) infection was more frequently found in the Asian family members when compared to the non-Asians. The e antigen (HBeAg) was present in 38% of the HBsAg positive individuals, including four with PHC; antibody to HBcAg (anti-HBe) was rarely detected. These results indicate that clustering of HBV infection was commonly present in family members of patients with PHC. The HBsAg positive individuals may be major contributors to the endemic pool of the virus, and may themselves be potential cases of chronic active type B hepatitis, cirrhosis, and PHC.
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PMID:Evidence for clustering of hepatitis B virus infection in families of patients with primary hepatocellular carcinoma. 22 43

Serologic tests for evidence of hepatitis B virus (HBV) infection were performed on family members of Asian and non-Asian patients with either hepatitis B surface antigen (HBsAg)-positive hepatocellular carcinoma or chronic HBV infection. Asian family members had a significant increase of HBsAg (34% higher) and of antibody to HBsAg or of antibody to hepatitis B core antigen (50% higher) when they were compared with non-Asian family members. In the Asian group, viral markers were detected more frequently in blood relatives than in nonblood relatives of the index cases. Within this group, birthplace did not influence the frequency of antigenemia, since HBsAg was positive in 55 (44%) of 125 Asians born in Asia and in 36 (38%) of the 94 Asians who were born in the United States. Also, HBsAg positivity frequently was seen in offspring from HBsAg-positive carrier mothers as well as from HBsAg-positive carrier fathers whose spouses were either HBsAg-negative or who had antibody. The e antigen was found more often in individuals 30 years of age or younger than in older individuals. This study indicates that intrafamilial spread of HBsAg in Asian families plays an important role in the perpetuation of HBV infection and in the eventual development of chronic liver disease in this ethnic group.
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PMID:A comparative study of hepatitis B viral markers in the family members of Asian and non-Asian patients with hepatitis B surface antigen-positive hepatocellular carcinoma and with chronic hepatitis B infection. 22 73

A sensitive method for the detection of hepatitis B surface antigen (HBsAg) is described whereby the separation of specific antibody by affinity chromatography is incorporated into one of the assay reagents. HBsAg, which may be obtained from tissue culture fluids of a human hepatoma cell line, is first reacted with polystyrene beads. Unoccupied spaces on the plastic are next covered with a non-specific protein (e.g. albumin). The plastic is then reacted with either whole antiserum or an IgG fraction of anti-HBs. Care must be taken to cover all of the reacting sites of the first layer of HBsAg with sufficient anti-HBs. This results in a reagent of detecting antigen. No affinity purified antibody was necessary because the reagent, at this stage, contains only specific antibody on the surface. Antigen reacting with this reagent can be detected by the addition of radioactively labeled IgG fraction of anti-HBs, which will complete the 'sandwich'. This assay has been evaluated and found to be as sensitive as those commerically available.
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PMID:'Aspira': a new sensitive assay for the detection of hepatitis B surface antigen. 23 Feb 61

Most series in Africa show a high percentage of hepatitis B surface antigen in hepatocellular carcinoma. Two groups of cases were investigated in this study. The one was derived from the autopsy material at Baragwanath hospital from subjects who had lived in Soweto, a large Black urban town. The second group consisted of male Black mineworkers generally originating from rural areas. A combination of the aldehydefuchsin stain and immunoperoxidase technique was used. The two groups showed totally different results. The Baragwanath series consisted of 24 hepatocellular carcinomas of which only 4 (17%) were HBsAg positive. Of the 24 cases, 14 had cirrhosis of which 9 were macronodular and 5 micronodular. Ten of these cases showed heavy iron overload. The series of male Black mineworkers comprised 22 cases of which 16 (72%) were HBsAg positive. Twelve of the 22 cases showed a macronodular cirrhosis and there were no micronodular cirrhoses. Only one case showed severe iron overload. These findings delineate two different populations of hepatocellular carcinoma in Southern Africa.
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PMID:Hepatitis B surface antigen and hepatocellular carcinoma in Southern Africa. 23 51

A significant aspect of primary hepatic carcinoma in man is the high positive correlation of hepatocellular carcinoma with infection with hepatitis B virus (HBV)1. Analysis of the relationship between HBV infection and oncogenesis is difficult because natural infection with HBV is limited to man and experimental infection has been achieved only in chimpanzees and gibbons. Furthermore, because HBV has not been successfully propagated in cell culture, basic study of virus-cell interaction of the aetiological agent of one of the most widespread infections of man has been impossible. Recently, however, a cell line (PLC/PRF/5) derived from a human hepatoma biopsy was described which produces the HRV surface antigen (HBsAg) and so provides a tool for the experimental investigation of HBV in viro. We now report the derivation and characterisation of two additional cell lines primary liver carcinomas. In contrast to the PLC/PRF/5 cell line, these cell lines retain the capacity to synthesise many human plasma proteins, including both albumin and alpha-fetoprotein (AFP). One of these lines also produces BHsAg. We also present evidence that HBsAg synthesis and secretion in this cell line are correlated with the growth state of the culture. This finding is in contrast to the continuous HBsAg production found in the PLC/PRF/5 cell line.
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PMID:Controlled synthesis of HBsAg in a differentiated human liver carcinoma-derived cell line. 23 37


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