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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Formalin-fixed, paraffin-embedded specimens from 110 cases of primary hepatocellular carcinoma were stained for hepatitis B x antigen (HBxAg), hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg). Eighty-four % of these patients were HBxAg positive in their tumor cells. Among the 110 cases studied, 80 had adjacent nontumorous tissue in the same block, and 65 of these nontumorous liver tissues stained positive for HBxAg (81%). HBsAg was positive in 19% of cases within tumor tissue and 61% in surrounding nontumorous tissue. HBcAg was positive in 11% of cases within tumor tissue and 26% in surrounding nontumorous tissue. These findings show that HBxAg is a common marker in the liver of patients with hepatitis B virus (HBV)-associated primary hepatocellular carcinoma and that it is closely associated with tumor cells in these individuals. In addition, the finding of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues of many HBsAg carriers suggests that HBxAg could be expressed independent of HBV replication and implies that the synthesis of this antigen may be directed from integrated HBV DNA templates. The finding of HBxAg in the nucleus of hepatocytes from primary hepatocellular carcinoma patients with dysplasia, combined with the known trans-activating properties of HBxAg, implies that HBxAg plays one or more important roles in hepatocarcinogenesis. The finding of HBxAg in bile duct epithelium and cholangiocarcinoma tissues is compatible with the hypothesis that HBV may contribute to this other primary tumor type in the liver. Together, these results further implicate HBxAg in the pathogenesis of primary liver cancers.
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PMID:Hepatitis B x antigen in hepatitis B virus carrier patients with liver cancer. 165 8

Hepatocellular carcinoma (HCC) is the most frequent cancer of the liver and, worldwide, is the seventh most common tumor in males and the ninth in females; the annual incidence is estimated to be 1,000,000 cases newly diagnosed, with a male to female ratio of 4:1. The incidence of HCC is Italy is 6.9 cases for males and 2.7 for females as for the regions with intermediate risk for this tumor. During the last ten years many epidemiological studies, case-control and cohort, have associated HCC to hepatitis B virus (HBV) infection establishing that among HBsAg carriers the relative risk of HCC is between 10 and 20 to demonstrate the strength of the association. In addition to HBV infection, cirrhosis, aflatoxins, alcohol, tobacco smoking and oral contraceptives have been evaluated as risk factors for HCC. The importance of the contribution of these risk factors to the development of HCC and the perspectives for prevention in different geographical areas will be discussed.
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PMID:[Epidemiology of hepatocellular carcinoma]. 166 Mar 11

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.
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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

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

The hybridization test for duck hepatitis B virus DNA was performed in 34 ducks with hepatoma from Qidong, Jiangsu province. Among the 34 hepatoma ducks, 18 were positive for DHBV DNA in the serum and 27 were positive in the tumor and/or liver tissue. Tissue sections were stained with Victoria blue nuclear fast red for detecting DHBV surface antigen. Victoria blue positive cells were found in 11 tumors and 15 paratumorous regions of 23 ducks with hepatocellular carcinoma. Although paratumorous regions were positively stained in 3 of 8 ducks with cholangiocarcinoma, all were negative within their tumors. All paratumorous regions and 2 tumor regions of 3 ducks with hepatocellular-cholangiocarcinoma were positive for Victoria blue. The results suggest that duck hepatocellular carcinoma be closely related to DHBV infection.
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PMID:[Duck hepatitis B virus (DHBV) and viral DNA in duck hepatocellular carcinoma and liver tissue]. 166 70

Hepatocellular carcinoma mainly affects patients with cirrhosis or with various degrees of fibrosis. From 1979 to 1990, among 87 patients who underwent hepatic resection for non fibrolamellar hepatocellular carcinoma, 12 (14%) had a non fibrolamellar hepatocellular carcinoma developed in a normal liver. There were 8 men and 4 women, aged 29 to 74 years. In 7 patients (58%) hepatocellular carcinoma was associated with clinical manifestations. Serum hepatitis B surface antigen were absent in all patients. Serum alphafetoprotein level was less than 100 mg/ml in 10 (83%), size of the tumor was greater than or less than 5 cm in 10 (83%) and capsule was present in 10 (83%). Resections included removal of 2 segments or more in 11 (91%). One patient died postoperatively. Actuarial survival rate at 3 and 5 years were respectively 57% and 38%. Intra or extrahepatic recurrence was recognized in 8 (67%), 2 patients were alive respectively 28 and 16 months after treatment of their intrahepatic recurrence (resection in one and intra-arterial embolisation in one). In conclusion, our results suggest that aggressive surgical efforts are justified in non fibrolamellar hepatocellular carcinoma arising in normal liver.
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PMID:[Hepatocellular carcinoma in undamaged liver]. 166 90

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.
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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.
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PMID:Allelotype study of primary hepatocellular carcinoma. 167 Sep 95

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.
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PMID:Loss of somatic heterozygosity in hepatocellular carcinoma. 167 14


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