Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental and epidemiological studies of risk factors for hepatocellular carcinoma (HCC): cirrhosis, male sex, oral contraceptives, alcohol, smoking, and aflatoxins, are evaluated, with meta-analysis for oral contraceptives, alcohol, and smoking. It is likely that an initiating event and one or more promoting events interact, probably with prolonged inflammation, necrosis and regeneration, to cause cancer in several types of cirrhosis. Over 90% of HCC patients have cirrhosis, usually from hepatitis B virus. The viral post-necrotic liver is often chronically dysplastic, but other types of cirrhosis are associated with HCC if they endure long enough. The proportion of men with HCC increases as hepatitis progressors to cirrhosis and then to HCC. Meta-analyses of 3 oral contraceptive studies resulted in a risk of 2.8 for 8 years of use, but 9.9 for 8 years. Population studies do not show any concentration of HCC in countries with high pill use, so the rarity of this cancer may have biased the results. Large epidemiologic studies are needed to refine risk estimates for oral contraceptives and HCC. Alcohol abuse of 80 g/day gives a risk of about 1.65 in pooled studies, compared to a risk of 1.1 for 80 g/day. Smoking gives a risk of 1.9, but there is no evidence for a secular trend by country in proportion to dose, as is evident for lung cancer. There is good experimental evidence that aflatoxin acts as an initiator for liver cancer, but there is not practical way to judge exposure for clinical studies.
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PMID:Hepatocellular carcinoma: risk factors other than HBV. 166 Mar 33

Hepatitis B virus (HBV) infection was evaluated in serum and liver specimens of eight Italian children with primary liver cancer. All children were negative for HBV markers in serum but four of them showed HBV-DNA sequences and/or HBs antigen expression in the liver. In one case, viral DNA was present in both neoplastic and non-neoplastic tissue, while in one case HBV-DNA was detectable only in nontumoral tissue and in one case only in the tumor area. In these cases, scattered HBsAg was expressed in the cytoplasm of cells in normal part of the liver and in another case neoplastic cells secreted HBsAg in culture. In two cases, the histologic diagnosis was HCC; one case had mixed HPB and one had macrotrabecular HPB. All children were more than 1 year of age. The remaining four children were histologically diagnosed as HPB and were less than 1 year of age. These findings suggest that HBV may be a cofactor for the development of liver cancer also in children of Western countries and that the risk of infection progressively increases with age.
Cancer Detect Prev 1991
PMID:Does hepatitis B virus play a role in primary liver cancer in children of Western countries? 166 Dec 2

From January 1976 to October 1989, 15 patients with hepatoblastoma who underwent surgery at the National Cancer Center Hospital were evaluated by clinico-radiological techniques. Eight patients were boys and seven were girls; their average age was 3 years and 5 months. Abdominal mass or distention was initially noted in 12 patients. Alpha-fetoprotein level was extremely high (average, 327 micrograms/ml) in all cases but one. Hepatitis B surface antigen was negative in all cases. Tumors occupied mainly the right lobe of the liver in 67% of patients, and the mean tumor diameter was 11.1 cm. Of 15 hepatoblastomas, 10 were grossly classified as massive type and five as multinodular. Histopathological diagnosis was well differentiated (fetal type) hepatoblastoma in 10 patients and poorly differentiated (embryonal type) hepatoblastoma in five. Fibrous capsule was also recognized in eight. The noncancerous liver was normal in all cases. Ultrasonography (US) (n = 7 patients) demonstrated an inhomogeneous internal echo with well demarcated margin in five cases and without such margin in two. Nonenhanced CT (n = 6) showed an isodense or low density mass in all cases. Drip infusion CT (n = 5) revealed isodensity in the early phase. Dynamic CT performed in one patient showed a well enhanced mass that appeared hypervascular on angiography. Preoperative chemotherapy and radiation therapy provoked histological changes such as necrosis, fibrosis and calcifications. These changes were reflected on CT images. Both US and CT demonstrated the characteristic internal structure and gross appearance of hepatoblastoma.
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PMID:[Hepatoblastoma: clinico-radiological study of fifteen cases]. 166 99

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.
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PMID:Viruses and cancer. Causal associations. 166 91

The development of hepatocellular carcinoma (HCC) presumably occurs in multiple steps and is influenced by numerous factors. Hepatitis B virus (HBV) is strongly associated with the development of HCC in people chronically infected with the virus, but the mechanism of viral involvement remains unclear. One possibility is that the gross chromosomal alterations frequently observed in HCC DNA at the site of HBV integration may alter the expression of important nearby cellular genes. We previously reported the cloning and characterization of a HBV insert from a Chinese HCC. The viral insert mapped to chromosome 17p11.2-12, and cellular sequences were duplicated at the site of viral integration. In the present study a DNA probe derived from cellular DNA sequences adjacent to the previously characterized HBV insert was used to analyze a set of 19 matched normal liver and HBV-positive hepatoma samples obtained from the same region of China, near Shanghai. Tumor-specific DNA changes were detected in two additional HCCs, suggesting that the small region of chromosome 17p defined by the flanking cell DNA probe is commonly altered in hepatomas. Restriction fragment length polymorphism studies demonstrated that the loss of one copy of portions of chromosome 17 occurred in 10 (53%) of the 19 patients. The loss of one allele of the p53 gene (located on chromosome 17p13) occurred in at least 6 (60%) of the 10 patients who were heterozygous at the p53 locus. As the p53 gene is known to possess tumor suppressor activity, the functional loss of this gene may be a significant step in the development of a subset of HCCs. High levels of allele loss also were detected for chromosomes 8q (4 of 9; 44%) and 16p (5 of 6; 83%) and may indicate the presence of additional cellular genes whose functional loss is important in the development of HCCs.
Cancer Res 1991 Jan 01
PMID:Hepatitis B virus integration event in human chromosome 17p near the p53 gene identifies the region of the chromosome commonly deleted in virus-positive hepatocellular carcinomas. 167 Sep 94

Accumulation of mutations in oncogenes and tumor suppressor genes transforms a normal cell to a malignant cell by allowing it to escape from normal control of growth. In order to learn (a) how many tumor suppressor genes are involved in the tumor progression of hepatocellular carcinoma, (b) whether there is any association among allelic losses of chromosomes, or (c) whether integration of hepatitis B virus into host DNA influences any particular chromosomal losses, we have examined loss of heterozygosity with 44 restriction fragment length polymorphism markers in 46 cases of hepatocellular carcinoma. The markers represented all chromosomal arms except 5p, 8p, 9p, 18p, and acrocentric chromosomes. Allelic losses in tumors indicated that five tumor suppressor genes, located on chromosomes 5q, 10q, 11p, 16q, and 17p, may be involved in this cancer. However, no significant associations were observed among the various allelic losses or between the integration of hepatitis B virus and chromosomal losses. Furthermore, a deletion map for chromosome 16q indicated the localization of a tumor suppressor gene between q22 and q24 and that for chromosome 17p suggested the existence of a second tumor suppressor gene in addition to the p53 gene.
Cancer Res 1991 Jan 01
PMID:Allelotype study of primary hepatocellular carcinoma. 167 Sep 95

Hepatocellular carcinoma (HCC) is a prevalent cancer in sub-Saharan Africa and eastern Asia. Hepatitis B virus and aflatoxins are risk factors for HCC, but the molecular mechanism of human hepatocellular carcinogenesis is largely unknown. Abnormalities in the structure and expression of the tumour-suppressor gene p53 are frequent in HCC cell lines, and allelic losses from chromosome 17p have been found in HCCs from China and Japan. Here we report on allelic deletions from chromosome 17p and mutations of the p53 gene found in 50% of primary HCCs from southern Africa. Four of five mutations detected were G----T substitutions, with clustering at codon 249. This mutation specificity could reflect exposure to a specific carcinogen, one candidate being aflatoxin B1 (ref. 7), a food contaminant in Africa, which is both a mutagen that induces G to T substitution and a liver-specific carcinogen.
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PMID:Selective G to T mutations of p53 gene in hepatocellular carcinoma from southern Africa. 201 Nov 86

Loss of tumor suppressor genes is involved in the mechanism of tumorigenesis of many solid tumors. We tested 9 hepatitis B virus (HBV)-positive and 10 HBV-negative hepatocellular carcinomas for loss of somatic heterozygosity using 14 polymorphic probes mapping to chromosomes 4, 11, 13, and 17. Losses were found on all chromosome arms tested. The highest frequency of loss was observed at the D13S1 locus (67%) at band 13q12. Losses were also observed at three other loci on 13q. Twenty-one % of informative cases showed loss on 17p using the probe pYNZ22 which maps near the p53 locus. Losses on 4q were infrequent with 17% found at one locus and no loss at two others. The retinoblastoma gene and the locus on 17p were only inactivated in our HBV-negative tumors, although the numbers were too small for statistical significance. For all loci tested, we found no significant differences in the frequency of losses with HBV status, ethnic background, cirrhosis, grade of tumor, or presence of hemochromatosis.
Cancer Res 1991 Aug 15
PMID:Loss of somatic heterozygosity in hepatocellular carcinoma. 167 14

One hundred thirty-five hepatocellular carcinomas were examined for the presence of antigenic tumor markers by the avidin-biotin-peroxidase complex method. Ninety-seven were from the US and 38 came from Argentina. The following markers were tested: alpha-fetoprotein (AFP), alpha-1-antitrypsin (AAT), hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), hepatitis D delta antigen (HD delta Ag), and Mallory's bodies (MB). In the US cases, AFP was present in 43%, AAT in 41%, HBsAg in 17%, and MB in 48%. Both HBcAg and HD delta Ag were absent. In the cases from Argentina, AFP was found in 26% and AAT in 18%. None of the other antigens were seen. Thirteen US tumors expressed three antigens and two four antigens simultaneously. This study reveals in humans a heterogenous expression of antigens by neoplastic hepatocytes with geographic differences, possibly due to multiple factors such as alcohol consumption or prevalence of hepatitis B infection.
Cancer 1990 Jan 01
PMID:Antigenic markers of hepatocellular carcinoma. 168

Hep G2, a human hepatocellular carcinoma, was grown s.c. in nude mice, as well as in tissue culture. This line retains the normal liver parenchymal cell capacity to synthesize human plasma proteins such as albumin, but there is no indication that it harbors the hepatitis B virus. We have detected the oncofetal antigens alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) in both Hep G2 xenografts and spent tissue culture media by Ouchterlony double diffusion assays, enzyme-linked immunosorbent assay, and immunohistology. By enzyme-linked immunosorbent assay, the AFP levels were 544.9 ng/ml in the cell culture and 1.6 microgram/g in saline extracts of the xenograft. The CEA levels were 35.2 ng/ml in the cell culture and 5.4 micrograms/g in the xenograft. The biodistribution of a radioiodinated anti-AFP murine monoclonal antibody and an anti-CEA monoclonal antibody were studied separately in nude mice bearing s.c. Hep G2 xenografts in comparison to an isotype-matched irrelevant IgG (Ag8). Anti-CEA antibody showed a preferential localization for Hep G2, but anti-AFP antibody did not. Immunohistochemical studies of the Hep G2 tumor, using biotinylated anti-AFP and anti-CEA, indicate both cytoplasmic and luminal staining of CEA and AFP in the tumor. These results suggest that Hep G2 may be a useful cell line for radioimmunodetection and radioimmunotherapy studies using anti-CEA and possibly anti-AFP monoclonal antibodies.
Cancer Res 1990 Feb 01
PMID:Carcinoembryonic antigen and alpha-fetoprotein expression and monoclonal antibody targeting in a human hepatoma/nude mouse model. 168 35


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