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

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

Familial non-Hodgkin lymphoma (NHL) cases were classified according to the histologic criteria (modified) of Rappaport, to determine the extent of morphologic similarities of the tumors. In four families affected members had different tumor histologies that may be observed in an individual patient as the lymphoma progresses. In two families, the affected relatives had tumors of seemingly discordant histology. These tumors may nonetheless be etiologically related as indicated by the pattern of laboratory abnormalities, especially immunologic, in affected as well as unaffected members. The 20 cases had a reversal of the sex ratio (M/F) usually seen in NHL: 0.5 instead of 1.3. Other tumors observed in these families included primary hepatocellular carcinoma, pulmonary adenocarcinoma, Hodgkin disease, and acute lymphocytic leukemia - all of which have been associated with inborn or acquired immunodeficiency states.
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PMID:Familial non-Hodgkin lymphoma: histologic diversity and relation to other cancers. 27 64

To determine the interrelationship between hepatitis B viral markers (HBV), the human Immunodeficiency virus (HIV), and hepatocellular carcinoma (HCC) in HCC patients, a total of 282 subjects were included in the study. Out of 282 subjects, 182 were HCC patients as determined by raised alpha-feto-protein (AFP) of greater than 1,000 ng/ml. The other 100 control patients presented with other conditions and had detectable AFP of less than 1,000 ng/ml in their sera. On presentation, 10 ml of venous blood was drawn from each enrolled subject and taken to the laboratory. HBV markers were detected using commercial reagents; HIV antibodies were detected by the commercial ELISA tests and were confirmed by Western blot. AFP was detected using an RIA technique. Of 282 examined subjects 182 (64.5%) had detectable AFP of greater than 1,000 ng/ml. 113 (40.1%) and 103 (36.5%) had HBsAg and Anti-HBc respectively. However, HBeAg was found in 21 of 113 (18.6%) of the HBsAg positive only. Anti-HIV antibodies were present in 15 (5.3%) of the 282 tested individuals. Only 1 (1.0%) of the control group had detectable anti-HIV antibodies in the serum. Eleven percent and 4.0% of the same control group had HBsAg and anti-HBc in their sera respectively. The study shows a significant correlation between HCC and HBV-markers (P less than 0.0001). Similarly, a significant correlation between anti-HIV antibodies and HBV-markers, (P less than 0.0001) was found.
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PMID:The interrelationship between HBV-markers and HIV antibodies in patients with hepatocellular carcinoma. 127 8

The prevalence of antibodies to hepatitis C virus (anti-HCV) was investigated among different populations in Taiwan, where anti-HCV was detected in 0.8% (24/2,994) of adult volunteer blood donors, 0.1% (1/1,305) of youngsters and children, 12.5% (8/64) of adult volunteer blood donors with elevated alanine aminotransferase (ALT), 36.5% (23/63) of hemodialysis patients, 4.1% (13/318) of male homosexuals, 25.4% (16/63) of cases positive for antibodies to human immunodeficiency virus (anti-HIV), 82.2% (578/703) of intravenous drug users (IVDUs), and 10.3% (23/223) of female prostitutes (FPs). Among patients with chronic liver diseases including chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC), the overall prevalence rate for anti-HCV was 34.1% (42/123), and a higher prevalence was noted in hepatitis B surface antigen (HBsAg)-negative cases than in HBsAg-positive cases. The prevalence of anti-HCV in volunteer blood donors and high prevalence found in IVDUs, hemodialysis patients, anti-HIV positive cases, and FPs are consistent with those results from other countries. These findings suggest that hepatitis C virus (HCV) infection is transmitted by both blood-borne and sexual contact routes. Among flavivirus infections, anti-HCV was detected in 0.3% (1/289) and 1.3% (4/310) of Japanese encephalitis and dengue fever patients, respectively. In conclusion, in Taiwan, an area with high endemicity of hepatitis B virus (HBV) infection, the epidemiological status of HCV infection is similar to that observed in other countries, and no serum cross-reactivity was noticed between HCV and flavivirus infections.
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PMID:Prevalence of antibodies to hepatitis C virus (anti-HCV) in different populations in Taiwan. 165 45

Patients with the acquired immunodeficiency syndrome are at risk to develop a variety of different cancers. Based on epidemiological data, Kaposi's sarcoma and non-Hodgkin's lymphoma have been clearly associated with infection by the human immunodeficiency virus (HIV). Additional cancers such as basal cell and squamous cell carcinomas, melanoma, and hepatocellular carcinoma have also been reported to be associated with a diagnosis of acquired immunodeficiency syndrome. A direct causal role of HIV has yet to be established for any of these cancers. We now report that transgenic mice carrying the HIV tat gene develop a high incidence of hepatocellular carcinoma after a long latency and that these changes in the liver are likely to be initiated by extrahepatic growth signals from the tat expressing cells in these mice. We predict that as acquired immunodeficiency syndrome patients begin to respond to therapy and show prolonged survival, such "secondary" malignancies induced by HIV will become increasingly prevalent.
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PMID:Liver cancer in transgenic mice carrying the human immunodeficiency virus tat gene. 174 42

In populations with non-HIV immunodeficiency, non-Hodgkin lymphoma and soft tissue sarcoma, especially Kaposi's sarcoma, are the most prominent tumours, but Hodgkin's disease, gastric carcinoma, squamous cell skin cancer, malignant melanoma, hepatoma, myeloid leukaemia and/or colorectal carcinoma have been linked in various studies. Population based cancer registries and cohort studies of HIV infected persons have generally failed to detect HIV related increases in total cancer incidence or in specific tumours other than non-Hodgkin lymphoma and Kaposi's sarcoma; however, associations with anal carcinoma, hepatoma and Hodgkin's disease have been suggested by some studies. Although not indicating increased risk, HIV induced immunosuppression has been linked to an acceleration of cervical and anal neoplasia and to increased aggressiveness of Hodgkin's disease with a relative excess of the mixed cellularity type. Advances in treatment for HIV infection will delay progression to AIDS and may allow an altered natural history to emerge, including the occurrence of excesses of additional cancer types.
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PMID:HIV infection and cancers other than non-Hodgkin lymphoma and Kaposi's sarcoma. 182 20

The nucleotide sequences of cDNAs (275 base-pairs) in the non-structural protein 5 regions of Japanese isolates of hepatitis C virus (HCV-J) from the plasma of 11 patients with non-A, non-B hepatitis and the livers of five patients with hepatocellular carcinoma were analyzed. Approximately 14 to 17% of nucleotide sequences of the HCV-Js examined differed from that of the original isolate in the United States (HCV-US). Furthermore, 2.5 to 11% sequence diversity was found among the HCV-Js. The nucleotide sequences of the HCV-Js showed characteristic common differences from that of HCV-US, although they also showed some random substitutions. Plural HCV-J genomes were found in two of the cDNAs derived from liver specimens, and a deletion of 102 nucleotides was found in the cDNA derived from one plasma specimen. These results suggest that HCV-J is a strain different from the HCV-US and that mutation of the viral genome occurs at as high a frequency as in that of the human immunodeficiency virus.
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PMID:Sequence diversity of hepatitis C viral genomes. 196 17

For developing countries, the cost-benefit of vaccination to control the hepatitis B virus (HBV) infection is great since the acute infection is generally subclinical and the benefit is the prevention of small numbers of cases of cirrhosis and hepatocellular carcinoma. Since the pattern of HBV infection in Africa is such that compared with southeast Asia, the infection occurs later in childhood and spread is horizontal rather than vertical. Investigation of method of spread of HBV may result in a means of control other than by vaccination. In the interim, due to the overlap in means by which HBV and human immunodeficiency virus (HIV) are spread, it could be worthwhile to take advantage of existing AIDS prevention programs to educate people about how to avoid both HBV and HIV infections.
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PMID:How AIDS forces reappraisal of hepatitis B virus control in sub-Saharan Africa. 167 Aug 83

Five hepatoma cell lines, including CZHC/8571, PLC/PRF/5, Hep3B, HepG2, and HUH7, were inoculated with three diverse isolates of human immunodeficiency virus type 1 (HIV-1). Productive infection was noted in all hepatoma cell lines, and expression of viral p24 antigen lasted for over 3 months, but its level decreased in proportion to the number of viable cells. HIV-1 antigens were also found in the cells by immunohistochemical staining and radioimmunoprecipitation assay, as were viral RNA by in situ hybridization and HIV-1-like particles by electron microscopy. Virus yield assays were also positive on supernatant fluids collected from hepatoma cultures inoculated with HIV-1. Despite their susceptibility to infection, all five hepatoma cell lines were negative for CD4 by immunofluorescence and for CD4 mRNA by slot-blot hybridization. In addition, HIV-1 infection of hepatoma cell lines was not blocked by anti-CD4 monoclonal antibody or soluble CD4. Together, these findings clearly demonstrate that all five hepatoma cell lines were susceptible to productive infection by HIV-1 in vitro via a CD4-independent mechanism.
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PMID:CD4-independent, productive human immunodeficiency virus type 1 infection of hepatoma cell lines in vitro. 215 30

Because of the various neoplastic manifestations of human immunodeficiency virus (HIV) and the variable period between HIV infection and the development of tumors related to acquired immunodeficiency syndrome (AIDS), it is possible that certain behaviors, toxins, genes, or infectious agents--particularly viruses--may act as cofactors in the pathogenesis of AIDS-related neoplasms. Most epidemiologic and laboratory investigations of possible cofactors have been directed toward Kaposi's sarcoma (KS), by far the most common AIDS-related tumor and one closely associated with male homosexual lifestyle in the U.S. Nonetheless, epidemiologic investigations of putative associations have not demonstrated any clear association between KS and particular viruses. Furthermore, laboratory investigations, both serologic and molecular/genetic, have failed to definitively implicate as cofactors for KS these viruses: cytomegalovirus, Epstein-Barr virus (EBV), herpes simplex viruses, pathogenic human papillomaviruses, or human herpes virus type 6. Investigations of a suggested association between EBV and AIDS-associated non-Hodgkin's (B cell) lymphomas (NHLs) have also been inconclusive. However, HIV may act as a cofactor in accelerating the development of hepatitis B-associated hepatocellular carcinoma. In summary, viral or other cofactors have not been definitely identified as cofactors in AIDS-related tumors.
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PMID:Possible cofactors for the development of AIDS-related neoplasms. 216 69


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