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

Chronic hepatitis B virus infection is often associated with major structural rearrangements of both the integrated viral DNA and the associated cellular sequences. We present here the structure of a single-copy hepatitis B virus insert cloned from human hepatocellular carcinoma DNA recently reported to encode a novel transcriptional trans-activator function. The hepatitis B virus portion of the clone consists of two colinear fragments covering the X gene with its promoter and enhancer (nucleotides 717 to 1796) and a 3' truncated pre-S/S gene (nucleotides 2703 to 423). The lack of the entire pre-C/C gene caused a fusion of the 3' end of the X gene with sequences upstream from the pre-S gene. The structure of the integrated viral DNA fragments suggests insertion of hepatitis B virus replication intermediates into cellular DNA and subsequent recombination between these primary integrations to generate the final structure of the clone. The 5' and 3' cellular flanking sequences mapped to the centromeric alpha-satellite DNA of chromosome 17 and to the short arm of chromosome 7 (p14-pter), respectively, indicating that chromosomal translocation was associated with the hepatitis B virus DNA integration. Because this is the fourth case reported in which hepatitis B virus-associated rearrangements have affected chromosome 17, it is conceivable that a loss of important cellular genes (such as the p53 antioncogene on chromosome 17) may be a crucial step in hepatitis B virus-related hepatocarcinogenesis.
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PMID:A chromosome 17:7 translocation is associated with a hepatitis B virus DNA integration in human hepatocellular carcinoma DNA. 131 86

The role of contraceptive steroids in the etiology or pathogenesis of hepatocellular carcinoma in urban South African black women was investigated in a hospital-based case and control study. Participating were 46 women, 19 to 54 yr old, with carcinoma, and 92 matched controls. South African blacks have a high incidence of hepatocellular carcinoma, and urban black women have used contraceptive steroids fairly widely for a number of years. Use of contraceptive steroids for longer than 6 mo (mean duration 46.7 mo) was not found to pose a risk for development of hepatocellular carcinoma in this population--relative risk 0.8 (95% confidence interval [C.I.] 0.4 to 1.7). This was also true of use for longer than 8 yr--relative risk 0.6 (95% C.I. 0.2 to 2.5), and if a combination of an estrogen and a progestogen or a progestogen alone was used (relative risk 1.7 [95% C.I. 0.7 to 4.2] and 0.4 [95% C.I. 0.1 to 1.2], respectively). Chronic hepatitis B virus infection was confirmed to have an etiological association with hepatocellular carcinoma, but there was no evidence that contraceptive steroids acted as a co-carcinogen with the virus or, conversely, that they played a causal role in patients negative for hepatitis B surface antigenemia. We cannot, however, exclude the possibility that contraceptive steroids may play a causal role in hepatocellular carcinoma in black women who have never been infected with the hepatitis B virus. Nor was there evidence that contraceptive steroids acted in concert with either cigarette smoking or chronic alcohol abuse in hepatocarcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contraceptive steroids as a risk factor for hepatocellular carcinoma: a case/control study in South African black women. 215 69

Case-control studies were initiated to investigate possible risk factors (life style, etc.) for hepatocellular carcinoma (HCC) and liver cirrhosis (LC). One hundred and fifty-four patients with HCC and 97 patients with LC who had no evidence of HCC were compared with frequency-matched 298 control subjects. Chronic hepatitis B virus infection and histories of blood transfusion and familial liver diseases were highly and significantly associated with both HCC and LC. Heavy drinkers in their younger years showed about 2 to 3 times risk increase for HCC or LC as compared with non-drinkers. Smoking was suspected as a risk factor, but a dose-response relationship was not clear, and further investigations are needed. To study the factors in the development of HCC from LC, 120 HCC patients with LC were compared with LC patients. No significant factors were observed. Ex-drinkers among LC patients experienced a slightly decreased risk for HCC in contrast to some belief that ex-drinkers with LC have higher risk for HCC.
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PMID:[Case-control studies of hepatocellular carcinoma and liver cirrhosis in relation to life style and other risk factors]. 215 92

Chronic hepatitis B virus (HBV) infection is etiologically related to human hepatocellular carcinoma (HCC). Most HCCs contain integrated HBV DNA in the liver cellular DNA, suggesting that the integration may be involved in carcinogenesis. From a comparison of a single HBV integration site present in a hepatoma with the corresponding unoccupied site in the non-tumourous tissue of the same liver, we have shown that HBV DNA inserted in a putative cellular exon with striking similarity to the DNA-binding domain of the thyroid/steroid hormone receptors. The corresponding cDNA has been isolated (hap gene) and shown to encode the retinoic acid receptor. In the original patient, integration took place so that the first codons of the viral surface protein gene became fused in frame with most of the hap gene. Because retinoic acid is known to regulate the transcription of target genes crucial for cellular growth and differentiation, it is most probable that consequent to the HBV insertion, hap, usually transcribed at a very low level in normal hepatocytes, became inappropriately expressed as an altered chimaeric retinoic acid receptor, thus contributing to the cell transformation. These results strongly support the possibility that HBV may play a direct role in liver carcinogenesis by insertional mutagenesis.
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PMID:Hepatitis B virus as an insertional mutagene in a human hepatocellular carcinoma. 217 Aug 9

Chronic hepatitis B infection is an important cause of cirrhosis and subsequent hepatocellular carcinoma in South Africa. The disease can now be prevented by vaccination, but second-generation genetically engineered vaccines still necessitate planned allotment. We have tested 29,312 black southern African mineworkers for hepatitis B surface antigen (HBsAg) to indirectly ascertain the relative prevalence of hepatitis B infection in diverse linguistic and ethnic groups. The overall prevalence of HBsAg in this cohort of predominantly rural men was 9.9%, but the prevalence in men from different regions varied from 5.5% to 14%. The relative prevalence in 200 magisterial districts was ranked; these percentage prevalences ranged from 0% to 17%. A significantly lower mean prevalence was detected in Southern Sotho subjects than in those from coastal districts (Nguni). Based on these data, we believe that there are perhaps 2 million hepatitis B carriers in South Africa. The collected data in this report could provide a basis for a broad-based vaccine campaign whereby hepatitis B vaccine could be targeted to high-priority districts initially. This strategy could rapidly reduce the critical mass of carriers, and hasten control of the disease.
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PMID:Differences in the regional prevalence of chronic hepatitis B in southern Africa--implications for vaccination. 252 93

Chronic hepatitis B virus infection is far less common in urban born than in rural born southern African blacks, who also have a high incidence of hepatocellular carcinoma. A case-control study was carried out to determine the relative frequency of hepatocellular carcinoma and its relation to hepatitis B virus infection in urban born blacks. Three hundred and ninety two black patients with hepatocellular carcinoma and matched controls seen at two city hospitals were classified by questioning as urban born or rural born. The ratio of rural born to urban born blacks among the controls was 1.1:1.0 (207/185), whereas in the patients with cancer the ratio was 4.8:1.0 (324/68) (p less than 0.0001). Analysis of the prevalence of hepatitis B markers in 62 urban born and matched rural born blacks with hepatocellular carcinoma showed no differences in the frequency of current or past hepatitis B virus infection. It is concluded that urban born blacks are less likely than rural born blacks to develop hepatocellular carcinoma, but when they do the tumour is equally likely to be related to infection with hepatitis B virus. The findings lend further support to an important role for chronic hepatitis B virus infection in the aetiology of hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma in urban born blacks: frequency and relation to hepatitis B virus infection. 302 71

Primary Hepatocellular Carcinoma (HCC) is the most common form of liver cancer and is now one of the leading causes of cancer in the world. Chronic Hepatitis B carriage is now recognised to contribute to at least 80% of the liver cancers seen today. Hepatic toxins (such as Aflatoxin) are responsible for a smaller proportion of HCC and may have an additional synergistic effect in Aflatoxin-endemic areas where HCC occurs early. Prevention and control programmes require control of Aflatoxins and hepatic carcinogen contamination of human food material (from direct or indirect sources), and the control and prevention of Hepatitis B transmission to prevent the carrier state. Opportunities to treat the chronic carrier state may be possible in the future, since there have been considerable advances in genetic engineering and molecular biology in the last few years.
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PMID:Prevention of primary liver cancer. 609 75

100 consecutive British chronic carriers of hepatitis B surface antigen seen in a London teaching hospital are described. 77 were male homosexuals and only 19 had either symptoms or signs of chronic liver disease. 27 had normal liver function tests and 69 of the remaining patients had minimal changes, chronic persistent hepatitis, chronic active hepatitis, cirrhosis, or hepatocellular carcinoma diagnosed on liver biopsy. The 4 remaining patients did not have a biopsy but did have abnormal liver function tests. Chronic hepatitis B virus infection was an important cause of these conditions. Most patients showed no clinical, biochemical, or histological change during a mean follow-up period of 44 months, and only 9.7% spontaneously seroconverted from hepatitis B antigen positivity to become anti-hepatitis B e antibody carriers. Although the prognosis is good in the medium term, 7 patients died from hepatocellular carcinoma.
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PMID:Natural history of liver disease in chronic hepatitis B surface antigen carriers. Survey of 100 patients from Great Britain. 611 90

We prospectively analysed the liver histology and clinical data of 45 patients with a clinical diagnosis of chronic hepatitis. There was more chronic active hepatitis than chronic persistent hepatitis. In both, there were more men than women except in the subgroup of lupoid hepatitis, where all were women. As a group, chronic persistent hepatitis patients tended to have less severe abnormalities in biochemical liver function tests. Chronic hepatitis B infection accounted for 38% (17/45) of all patients. Of these, 53% (9/17) were Maori or Polynesian, although they only account for approximately 1/5 of the European population in Auckland. This correlated with the known high hepatitis B surface antigen carrier frequency in the Maori and Polynesian and the high incidence of primary hepatocellular carcinoma in this ethnic group. The present study also showed there are relatively few chronic active hepatitis patients, those with immunological abnormalities (lupoid hepatitis, 5/45), who are likely to respond to steroid treatment.
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PMID:A clinical-pathological study on chronic hepatitis in Auckland. 659 Oct 11

146 patients (62 female, 84 male) with chronic hepatitis B and 80 patients (34 female, 46 male) with chronic hepatitis C were regularly examined in 1 to 2 year intervals with an average follow-up period of 12 years (mean). Each time patients were evaluated by physical examination, routine laboratory data, immunological and serological testing, ultrasonography, and laparoscopy and/or percutaneous liver biopsy. No patient of the study underwent immunosuppressive or antiviral treatment at any time.-The average time data in years are given as the median value (mean). Chronic hepatitis B: Histologic diagnoses and their long-term prognosis: Chronic persistent hepatitis (CPH) on first biopsy: 10% of cases complete recovery after 15 years, 70% progression to chronic active hepatitis (CAH) after 5 years; CAH: 30% advanced remission/complete recovery 8 years after the first diagnosis of CAH, 40% progression to liver cirrhosis after 5 years; liver cirrhosis: 50% advanced remission/recovery 4 years after the first diagnosis of cirrhosis, 5% developed a hepatocellular carcinoma (HCC) 11 years after the first diagnosis of cirrhosis. Natural history: In the 11 years following initial diagnosis of HBV-infection spontaneous recovery was observed in 49% of cases. In 3% of the patients the disease eventually caused death (1 x hemorrhage of oesophageal varices, 3x HCC after 14 to 20 years). Chronic hepatitis C: All patients were anti-HCV- and HCV-RNA-positive.-There was no spontaneous elimination of virus in any patient (maximal follow-up 27 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term prognosis of chronic B and C viral hepatitis]. 750 Aug 7


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