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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera of patients with chronic hepatitis and chronic haemodialysed uraemia were tested for both Hepatitis B virus and Hepatitis Delta virus markers from 1985. Hepatitis Delta virus seroconversion was found in 10 of 88 haemodialysed patients and anti-Delta-IgG sero-positivity in 11 of 108 chronic hepatitis patients. The clinical course of Delta superinfections in haemodialysed patients was as follows: 3 infections were symptomless, 7 patients had acute hepatitis, two of the latter group died because of fulminant hepatitis. Of the 11 HBsAg and anti-Delta-IgG positive chronic hepatitis patients 3 had primary hepatocellular cancer.
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PMID:[Delta virus infection in hemodialyzed kidney patients and patients with chronic liver diseases]. 132 98

A Nigerian series of 890 patients with primary liver cell carcinoma, seen during the recent three years, has been examined with a view to establishing the natural history of the tumour in untreated cases. There were 60 males and the mean age of all the patients was 50 years. Hepatitis B surface antigen was positive in 70 pc of tested patients and there were higher pathologic levels of aflatoxins in these patients when compared to normal controls. Liver cirrhosis was associated with 81 pc of patients. Alcohol and smoking were unlikely to be aetiologically important in these patients. The macroscopic type of tumour was mainly diffusely nodular and the commonest microscopic pattern was the characteristic trabecular pattern. Metastases were present in 52 pc of the patients and were mainly to the lungs. Due to late presentation and underlying cirrhosis, most patients were critically ill with high incidence of ascites, jaundice and hepatic precoma. The mean survival time of all patients was six months after onset of the initial symptoms to death and only three weeks after admission to death. The major causes of death were advanced cancer in 78 pc, hepatic failure in 48 pc and rupture of tumour, 39 pc. These observations clearly show that the prognosis of liver cancer is dismal in this environment, as elsewhere. Medical education on earlier presentation in hospital and early operative removal of the tumour should be emphasised. It is suggested that an attempt through immunisation should be employed to reduce the incidence of liver cancer in the population.
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PMID:The natural history of primary liver cell carcinoma: a study of 89 untreated adult Nigerians. 132 87

Hepatitis B virus (HBV) and certain human papillomaviruses (HPV) have been suspected of playing a role in human malignancy. The long latency period (decades) and the fact that only a small proportion of infected individuals subsequently have cancer suggests that these viruses probably contribute in an indirect manner to the development of cancer. Analysis of viral gene function at the molecular level supports this conclusion. More studies are needed to understand the subtle interactions between host cell and viral functions and the genetic and environmental factors that may contribute to malignancy.
Cancer 1992 Sep 15
PMID:Viral role in cervical and liver cancer. 132 82

A personal view is presented reflecting some developments in human tumor virology during the past three decades. Since the discovery of the Epstein-Barr virus in 1964 members of additional viral groups have been linked to human tumors, e.g. hepatitis B virus, HTLV-1, and a number of different papillomavirus types. It became evident that the virus infection per se is not sufficient and that additional events modifying the host cell genome contribute to the development of virus-linked human cancers. At present approximately 15% of the worldwide cancer incidence can be linked to viral infections. The author describes his personal entry into the field and the research in his laboratory on human tumor viruses.
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PMID:Viruses in human tumors--personal reflections. 132 72

To elucidate the role of p53 mutation in hepatocarcinogenesis in Taiwan, a hepatitis B viral infection hyperendemic area, exons 5 to 8 of the p53 gene in the tumor tissue of 61 hepatocellular carcinomas were amplified and sequenced. A total of 20 cases (32.8%) were found to have mutations; 36.6% (15 of 41) for the hepatitis B surface antigen positive group and 25.0% (5 of 20) for the hepatitis B surface antigen negative group. The corresponding normal liver showed no mutation. The mutation is widely distributed throughout exons 5 to 8. Only 4 cases (6.6%), all positive for hepatitis B surface antigen, had a specific hot spot mutation at codon 249 with G to T transversion. Our results show that scattered point mutations in p53 are not uncommon in hepatocellular carcinoma samples from Taiwan and may be important in the development of this cancer. However, the aflatoxin related specific mutation seems much less related to the genesis of hepatocellular carcinoma in Taiwan.
Cancer Res 1992 Nov 01
PMID:Mutation of p53 gene in hepatocellular carcinoma in Taiwan. 132 23

Mutant p53 has been found in a wide variety of human malignancies including carcinomas of the lung, breast and colon. Because of the controversial mutational rate of the p53 gene in hepatocellular carcinoma, a large series of liver tumors from white patients with different risk factors was examined immunohistochemically for expression of the p53 mutant to assess its prevalence and the relationships between p53 overexpression and clinicopathological data. Nine of 58 specimens were found to have detectable evidence of p53 gene mutation by virtue of the immunohistochemical detection of mutant p53 protein. The p53 mutation was more frequent in patients with serological hepatitis B and C markers than in patients without these markers (p = 0.046). The prevalence of p53-positive tumors was also significantly higher in the group of tumors with invaded portal branches than in the group without (p = 0.02). Our results showed that p53-positive hepatocellular carcinoma is a rare finding in patients exposed to a low dietary aflatoxin intake and that p53 mutation seems to occur at a late stage of the tumoral process and could contribute to an aggressive tumoral phenotype.
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PMID:Overexpression of p53: a rare event in a large series of white patients with hepatocellular carcinoma. 133 Aug 67

The present paper reviews several studies performed between 1977 and 1986 in Singapore on the 10-year survival outcome of treatment for stage I and II hepatocellular carcinoma (HCC). Of 801 HCC patients evaluated, only 2 survivors (0.3%) remained in complete remission for 13 and 14 years, respectively. One had received four weekly cycles of prednisolone, Adriamycin, vincristine and 5-fluorouracil for an inoperable HCC with a 10-cm diameter, and the other had received localised synchronised hepatic irradiation and Adriamycin. As follow-up, the use of localised hepatic irradiation consisting of 131I-labeled (30 mCi) iodised oil in lipiodol infused via the hepatic artery appeared to benefit patients with small residual tumours but did not affect larger tumours measuring 2 cm in diameter. Prophylactic, intermittent long-term administration of lymphoblastoid interferon-alpha (Wellferon) was carried out in pre-cancerous, high-risk hepatitis B surface antigen (HBsAg)-positive patients with cirrhosis, in immediate male relatives of liver cancer patients, and in persons who had undergone hepatic resection. In the untreated group, 10/162 (6%) cirrhotics, 3/18 (17%) male family members, and 6/10 (60%) post-resection cases developed single or multiple HCCs within 1 year of screening done at 3-month intervals on the basis of alpha-fetoprotein (AFP) levels and real-time hepatic ultrasonography. In contrast, none of the Wellferon-treated group consisting of 518 cirrhotic patients, 82 male relatives of HCC patients and 20 post-resection cases developed HCC. Two HBsAg-positive individuals who had not been treated with interferon (IFN) developed hepatic nodules which that showed dysplasia, AFP elevation and chromosomal changes. These studies demonstrate the poor results of late diagnosis and show that early intervention and prophylaxis with Wellferon can reduce the incidence of HCC in high-risk persons. In addition, transhepatic chemoembolisation and liver resection are suitable methods for treating small HCCs (single or multiple) that are detected by screening. However, some of these early-detected HCCs remain highly malignant. Prophylactic treatment of pre-cancerous conditions appears to be a better option as a long-term programme for HCC.
Cancer Chemother Pharmacol 1992
PMID:Long-term survival following treatment of hepatocellular carcinoma in Singapore: evaluation of Wellferon in the prophylaxis of high-risk pre-cancerous conditions. 133

The incidence of hepatocellular carcinoma (HCC) in Japan has increased over the past two decades. Of the 379 patients with HCC treated at Shinshu University Hospital over the past 20 years, 112 underwent treatment between 1971 and 1980 and 267 were treated between 1981 and 1990. The prevalence of hepatitis B virus-associated HCC and hepatitis C virus-associated HCC was 54% and 34%, respectively, during the first decade and 31% and 60%, respectively, during the second decade. Major factors contributing to the increased incidence of HCC include an increase in the incidence of type C chronic hepatitis and an increase in the incidence of cirrhosis of the liver, which in turn are the result of blood transfusions received about 30 years ago. Donated blood testing positive for hepatitis C virus antibody is currently rejected from the blood supply. However, the occurrence of post-transfusion hepatitis with the potential to develop into HCC has not been entirely eliminated. In addition, there is an as yet unelucidated route of horizontal transmission of hepatitis C virus.
Cancer Chemother Pharmacol 1992
PMID:Clinical aspects and epidemiology of hepatitis B and C viruses in hepatocellular carcinoma in Japan. 133 1

Potential risk factors for the development of hepatocellular carcinoma were analysed in 40 Caucasian patients with this malignancy. A higher proportion (14 of 40; 35%) had evidence of hepatitis C virus (HCV) infection than had evidence of either hepatitis B virus (HBV) carriage (17.5%) or alcohol abuse (30%). In all 14 patients whose sera were reactive by HCV ELISA (Ortho second generation test), the presence of antibodies to HCV were confirmed by recombinant immunoblot assay (Ortho RIBA-2). Furthermore, two independent laboratories detected HCV-RNA in 10 of the 14 (71%) anti-HCV positive sera. Two additional sera were shown to contain HCV-RNA when reanalysed by a modified PCR using oligonucleotide primers designed to amplify a shorter fragment of the 5' noncoding region of the genome. Seven of the anti-HCV positive patients also had evidence of prior HBV infection and 2 admitted to alcohol abuse. HCV infection was the only identifiable risk factor in 6 patients. These data confirm the association between HCV infection and hepatocellular carcinoma and suggest that persistent viral replication accompanies tumour development in the majority of patients whose serum contains anti-HCV.
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PMID:Detection of hepatitis C viraemia in Caucasian patients with hepatocellular carcinoma. 133 30

Hepatitis B virus is a major etiologic agent in the development of human hepatocellular carcinoma, but the precise role of the virus in the tumorigenic process is still unclear. Recent studies of naturally occurring animal models, such as woodchucks and squirrels infected with hepatitis B-like viruses (hepadnaviruses) have revealed different oncogenic strategies and outlined the predominant role of myc genes in rodent hepatomas. Higher oncogenicity of woodchuck hepatitis virus has been correlated with a direct contribution of the virus as an insertional mutagen of myc genes: c-myc, N-myc and predominantly the woodchuck N-myc retroposon. In contrast, rare viral integration events but frequent amplifications of c-myc characterize ground squirrel hepatitis virus-induced tumors, indicating that hepadnaviruses may contribute in malignant transformation through different, direct or indirect ways.
Semin Cancer Biol 1992 Oct
PMID:Mammalian hepatitis B viruses and primary liver cancer. 133 94


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