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 etiologic relationship of parasitic liver disease to primary liver cancer has long been debated. For this reason, a review of 4611 necropsies was carried out to determine the frequency with which hepatocellular carcinoma occurred in association with schistosomiasis. Of 227 cases of hepatocellular carcinoma, 24 (10.6%) were associated with schistosomiasis japonica. This was significantly higher than the incidence of this carcinoma without schistosomiasis (2.78%). The majority of the 24 cases exhibited the features of a mixed macronodular and micronodular cirrhosis (Gall's posthepatitic cirrhosis); this was super-imposed upon and caused a masking of schistosomiasis fibrosis. By radioimmunoassay hepatitis B antigen was positive in 27% of these cases. A review of the literature indicated that chronic schistosomiasis, on its own, is unlikely to be the cause of primary liver cell carcinoma. Histologic features resembling post-hepatitic cirrhosis combined with a high frequency of hepatitis B antigen suggest that viral hepatitis rather than S. japonicum is the more likely etiologic factor involved, or has a synergistic effect on carcinogenesis.
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PMID:Primary liver cancer coincident with Schistosomiasis japonica. A study of 24 necropsies. 16 89

The high frequency of hepatitis B antigen (HBsAg) in hepatocellular carcinoma (HCC) patients has led to the hypothesis that immunoresponsiveness to hepatitis B virus (HBV) may be deficient in some patients, and that the immune response deficiency may have a genetic basis. Radioelectrocomplexing (REC), a radioimmunoassay in gel based on the principle of counterimmunoelectrophoresis (CIE), has been used to identify four HBV immune status subgroups: 1) HBsAg +ve/HBsAb +ve; 2) HBsAg +ve/HBsAb -ve; 3) HBsAb -ve/HBsAb +ve; 4) HBsAg -ve/HBsAb -ve/HBsAb -ve. These subgroups comprise 2, 6, 70, and 22 percent, respectively, among blood donors, and 32, 19, 23, and 26 percent, respectively, among HCC patients. Although the HBV exposure rates in the two groups were similar, the immune complexemic rates and HBs antigenemic rates were significantly higher in HBB patients than in the blood donors. It is proposed that the failure of termination of HBV infection revealed by these high rates reflects an immunodeficiency state characterized by an inability to produce high-avidity HBsAb. The immunodeficiency might have a primary genetic basis, or it might be secondary to the immunodepressive effects of concurrent viral or parasitic infections.
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PMID:Immunodeficiency to hepatitis B virus infection and genetic susceptibility to development of hepatocellular carcinoma. 17 28

During a 23 year period at Memorial Hospital, the diagnosis of liver cell carcinoma was made in 42 patients who were 11 to 40 years old. Ninety per cent were Caucasian, mostly born in the United states. No occupational hazard was detected. Serum hepatitis antigen was demonstrated in only one patient. Alpha fetoprotein was found in the serum of 55 per cent of nine patients tested. Eight-three per cent were Rh positive, 43 per cent were ABO groups, A or O, respectively. Twenty-three per cent of 13 patients with sufficient material for study had an associated cirrhosis. Of these, active hepatitis with cirrhosis was present in one patient; postnecrotic cirrhosis was present in another. Approximately 7 per cent had a history of previous liver disease. One patient had infectious mononucleosis, and nearly 13 per cent gave a family history of cancer. Weight loss or pain in the right upper abdominal quadrant was present in 65 per cent, and hepatomegaly was found in 88 per cent. Only one patient presented with hemoperitoneum simulating an acute condition within abdomen. The liver profile examinations characteristically revealed an elevation in serum alkaline phosphatase, 5 nucleotidase, and Bromsulphalein retention with normal bilirubin level. The most common finding, upon roentgenographic examination, was an elevated right hemidiaphragm. Selective celiac and superior mesenteric angiography and 99mTc sulfur colloid liver scans were both done in 13 patients. There was a 75 per cent accuracy rate in localization of the tumor. At laparotomy, the tumor was found to be confined to one lobe in seven patients and involved both lobes in ten. Twenty-seven patients were thought to have multicentric tumors and 15 unicentric lesions. Only ten were found to be candidates for hepatic lobectomy. Five and ten years survival rates were 20 per cent; the operative mortality rate was 40 per cent. Twenty per cent died within a year, ten per cent, one patient, is alive with disease at 28 months and another is free of disease at 31-months. Paraneoplastic syndromes were erythrocytosis in two patients, terminal stage of hypoglycemia in one patient, and hypocholesterolemia with associated excess beta globulin in one patient.
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PMID:Liver cell carcinoma during the prime of life. 17 34

In Asia, Africa, and other tropical areas, primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the postnecrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 patients with PHC had hepatitis B surface antigen (HBsAg) (controls, 8 of 98) and 56 of 63 (controls, 26 of 100) had antibody against hepatitis B core antigen (anti-HBc). In earlier studies, we demonstrated a maternal effect of HBsAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBsAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; P = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBsAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the west African hepatoma patients showed that there is a very high frequency of HBsAg in mothers (71.6%), while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. Several years ago, we described a vaccine which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis, and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:The relation of infection with the hepatitis B agent to primary hepatic carcinoma. 17 34

The clinical course and pathological patterns of a group of 13 patients with both primary liver cell carcinoma and Hepatitis B surface antigen (HBsAg) are described and contrasted with those of 43 patients with primary liver cell carcinoma but without HBsAg. HBsAg-positive carcinoma patients demonstrated a higher incidence of splenomegaly, transudative ascites, and the presence of alpha-fetoprotein, although none of these reached statistical significance. Serum bilirubin was significantly higher in patients with HBsAg. HBsAg-positive carcinoma patients most frequently originated from countries where the presence of HBsAg is high in the general population. Survival time from the diagnosis of primary liver cell carcinoma was shorter in patients with HBsAg.
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PMID:Primary liver cell carcinoma in the presence or absence of hepatitis B antigen. 18 15

The human hepatoma cell line, PLC/PRF/5, was shown to produce hepatitis B surface antigen (HBsAg). Immunologically reactive material was present in the supernatant tissue culture medium in significant amounts, and was associated with spherical particles approximately 20 nm in diameter. The rate of antigen production by the cells was estimated at 500 ng/day/10(6) cells by reference to a purified HBsAg standard. All immunological activity was neutralized by specific antibody and the subtype was ad. The studies reported here broaden the scope of investigations on both the in vitro production of HBsAg and the association between this antigen and primary liver cancer.
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PMID:Hepatitis B surface antigen produced by a human hepatoma cell line. 18 8

The core and coat of hepatitis B virus were found by electron microscopy in parenchymal cells of a liver biopsy from a 61 year old man with chronic active hepatitis and cirrhosis of the liver. Laparoscopy, 35 days after liver biopsy, and autopsy 42 days later confirmed the cirrhosis and showed in addition a well differentiated hepatoma. The possibility of a viral aetiology for the cirrhosis and primary carcinoma of the liver is considered.
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PMID:Hepatitis B virus, cirrhosis and primary carcinoma of the liver. An electron microscopic study. 18 67

Specimens of liver tissue obtained by biopsy from five patients and at necropsy from seven patients with postnecrotic liver cirrhosis and hepatocellular carcinoma were examined for the presence of hepatitis B surface antigen (HBs Ag) and hepatitis B core antigen (HBc Ag) by direct immunofluorescence. In all cases, samples of serum were tested for HBs Ag and antibody to HBs Ag (anti-HBs) by immunoelectroosmophoresis and for antibody to HBc Ag (anti-HBc) by indirect immunofluorescence. Of these 12 representative cases of the main histological types of hepatocellular carcinoma, six were found to be seropositive for anti-HBc, and three of them were negative for HBs Ag. HBs Ag was detected in the cytoplasm of hepatocytes in the cirrhotic nodules in one seronegative patient and in three of the seropositive cases. In the latter cases, HBs Ag was identified in the cytoplasm of cells in well-differentiated hepatocellular carcinoma. HBc Ag was not found in any of the specimens examined.
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PMID:Cellular localization of hepatitis B virus antigens in patients with hepatocellular carcinoma coexisting with liver cirrhosis. 19 Mar 31

In Asia, Africa and other tropical areas primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the post-necrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 PHC patients had hepatitis B surface antigen (HBSAg) (controls: 8 of 98) and 56 of 63 (controls: 26 of 100) had antibody against hepatitis B core antigen (anti-HBC). In earlier studies we demonstrated a maternal effect of HBSAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBSAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; p = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBSAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the African hepatoma patients showed that there is a very high frequency of HBSAg in mothers (71.6%) while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. We described a vaccine several years ago which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:[The relation of infection with the hepatitis B-agent to primary hepatic carcinoma (author's transl)]. 19 Apr 99

The antibody to hepatitis B core antigen (anti-HBc) is belived to be a marker for natural infection with hepatitis B virus (HBV). In order to study the etiological role of HBV in relation to primary hepatocellular carcinoma (PHC), the anti-HBc in sera of 31 PHC patients was surveyed by the immune adherence hemagglutination method which was about 10 times more sensitive than the complement fixation method. Twenty two out of 31 PHC cases were positive for anti-HBc (71.0%). The is a higher rate of incidence than that of HBs-Ag (51.6%). However, high anti-HBc titer above 2(10) which might reflect current infection with HBV was observed in 15 of these 22 cases. The remaining 7 cases had a titer lower than 2(8); 5 of these patients had neither HBs-Ag nor anti-HBs in their sera. As control, 37 anti-HBs positive blood donors with no definite liver disease were surveyed for anti-HBc titer. Thirty-four of them were positive, but in the majority of cases, the serum titer was less than 2(9), which might only reflect previous infection with HBV. These findings indicate that not only the prevalence of anti-HBc, but also the determination of its real titer is quite important for studying the relationship of HBV to PHC.
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PMID:Anti-HBc titer in relation to the etiological role of hepatitis B virus in primary hepatocellular carcinoma. 19 28


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