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)

Circulating immune complexes (CIC), complement and alpha-fetoprotein (AFP) were detected in 93 hepatitis B surface antigen (HBsAg)-positive patients with hepatocellular carcinoma (HCC), 16 patients with liver cirrhosis (LC) and 54 healthy controls. The CIC and complements were significantly higher in HCC patients than in LC patients. The complement and polyethylene glycol(PEG)-CIC in HCC patients with LC were higher than those in LC only (P less than 0.0001). The complement levels in LC patients were significantly lower than in controls. There was no difference in C3 and C4 between HCC patients and controls, while the C3 proactivator was higher in HCC patients (P less than 0.02). The C1q-CIC was higher in HCC and LC patients when compared to controls (P less than 0.0001). In patients with HCC, there was no difference in the CIC and complement levels between patients with cirrhosis and those without. There were inverse correlations between C1q-CIC and C3 (P less than 0.05), C1q-CIC and C4 (P less than 0.04). The mean level of 3% PEG-CIC and C1q-CIC increased significantly as AFP elevated, but decreased as AFP was higher than 1599 ng/ml (P less than 0.05). These results imply that CIC increase with tumor growth but further tumor burden may result in a fall in CIC, there was a shifting of CIC from complement-fixing to non-complement-fixing as AFP increased gradually.
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PMID:Relationship of serum alpha-fetoprotein to circulating immune complexes and complements in patients with hepatitis B surface antigen-positive hepatocellular carcinoma. 169 50

We have reviewed retrospectively the records of 157 patients, less than or equal to 30 years of age with nasopharyngeal carcinoma (NPC) from 218 such cases identified in the tumor registry files of three major teaching hospitals in Taipei, Taiwan. These cases were diagnosed between 1 January 1982 and 31 December 1985, with a minimum follow-up of 2 years. The average age was 25, with a male/female ratio of 1.67. The TNM (tumor size, nodes, metastases) classification of 127 patients showed T1, 22%; T2, 33.1%; T3, 23.6%; T4, 21.3%; N0, 26%; N1, 16.5%; N2, 27.6%; N3, 30%; and M1, 13.4%. Antibody titer to Epstein-Barr virus capsular antigen (EBVCA) were elevated in 45 of 48 patients tested. Of the 29 patients who had hepatitis B (HB) viral survey done 34.5% were positive for HB surface antigen (HBsAg). Of 13 patients with elevated EBVCA antibody who were also tested for HB, six were HBsAg carrier. Actuarial survival rates of 2 and 3 years are 70 and 62%, respectively, among the 90 patients who were followed regularly or to death. HBsAg carriers and patients with M1 disease had a shorter survival time. We concluded that patients less than 30 years of age seemed to have an increased incidence of NPC, compared to that in an earlier report. Our patients frequently presented with advanced stage and poor prognosis. The high rate of HB carrier raises the possibility that HBV may play a role in the carcinogenesis and tumor growth in some NPC patients. Future prospective studies are needed.
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PMID:Nasopharyngeal carcinoma in young patients. 184 56

To determine the clonal evolution of hepatocellular carcinoma, the integrated hepatitis B virus DNA patterns of the main tumor, satellites and/or metastatic lesions were analyzed by Southern-blot hybridization in 28 hepatocellular carcinomas, including three HBsAg-seronegative cases. Unicentric or multicentric hepatocellular carcinoma was confirmed by histopathological criteria in 89% of the cases. Among 17 unicentric hepatocellular carcinomas, minor changes of the integration pattern--including partial loss or addition of the integration sites or both--were detected in the metastatic lesions in 29% of the cases. Furthermore, none of five cases with free-form hepatitis B virus DNA in the primary tumor had detectable free hepatitis B virus DNA in the metastatic lesions. These results suggest that the alteration of integrated hepatitis B virus DNA pattern during the course of tumor growth and metastasis may occur more often than previously perceived and that the switch-off of virus replication may be related to tumor metastatic potential. In eight cases with unilateral, multicentric hepatocellular carcinoma, two clones were detected in six cases, three were seen in another and four were seen in one. One case of note was a 9-yr-old boy with two histological types and two different integration patterns, one associated with vascular invasion and lung metastasis. Three patients with bilateral hepatocellular carcinoma were confirmed to have bicentric or tricentric hepatocellular carcinoma rather than intrahepatic dissemination and had survival rates similar to those in unicentric hepatocellular carcinoma. Three invasive HBsAg-seronegative hepatocellular carcinomas were found to have hepatitis B virus DNA integration and were of unicentric origin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clonality and clonal evolution of hepatocellular carcinoma with multiple nodules. 185 94

The ribose moiety of 5-fluorouridine (FUR) was oxidized with periodate and the product was bound through a poly(L-lysine) bridge to monoclonal antibodies, denoted SF25MAb, reactive with a human colon carcinoma LS180. The antibody was linked via its polysaccharide (previously oxidized with periodate) to the poly(L-lysine)-drug conjugate. The linking of FUR-poly(L-lysine) to the antibody markedly increased the latter's binding to the tumor cells. A relatively lower increase was also observed with conjugates of nonrelated antibodies, such as anti-hepatitis B surface antigen and anti-epidermal growth factor receptor antibodies. The pharmacological activity of the specific conjugate FUR-poly(L-lysine) -SF25MAb was higher than that of the drug-substituted polymer alone. The poly(L-lysine) bridge caused toxic effects in vivo, even though substituted both by FUR and by antibody. Therefore, the additional unreacted lysyl residues were blocked by succinylation. Partial blocking of free amino groups on the conjugate rendered it nontoxic but decreased its cell-binding capacity, though to a level still higher than that of the original unmodified antibody. The pharmacological activity of the specific conjugate after blocking was also reduced and necessitated prolonged incubation periods or higher concentrations. Following periodate oxidation and reduction, FUR was as effective as the clinically preferred compound 5-fluoro-2'-deoxyuridine in vitro and in vivo, against the LS180 colon carcinoma. Experiments in nude mice, with LS180 tumor subcutaneous xenotransplants, showed that FUR-poly(L-lysine)-SF25MAb (blocked by succinylation) was not toxic and was effective in the retardation of tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A conjugate of 5-fluorouridine-poly(L-lysine) and an antibody reactive with human colon carcinoma. 209 21

To investigate the hepatitis B virus (HBV) DNA status in the liver when hepatocellular carcinoma (HCC) has developed, 35 paired nontumorous and tumorous liver tissues from 27 hepatitis B surface antigen (HBsAg)-seropositive and 8 HBsAg-negative patients with HCC were studied by Southern blot analysis. The hybridization patterns of HBV DNA were different in the nontumor and tumor parts in 26 (96.3%) of the 27 HBsAg-positive patients. In the nontumor parts, integration of HBV DNA into the host genome was significantly less when compared to the tumor parts (15/27 vs. 25/27, P less than 0.05), whereas free replicative viral forms were significantly more frequent (17/27 vs. 7/27). The integrated HBV DNA in the nontumor parts showed discrete band patterns in the majority of cases (13/15). Hepatitis B e antigen (HBeAg) was significantly associated with the expression of free replicative forms of HBV DNA in the tumor tissues. An integrated HBV DNA sequence was detected in the tumor part of one HBsAg-negative patient, but not in her nontumor counterpart. Our observation that discrete integrated HBV DNAs are present in the nontumor part, representing subclinical clonal expansion that precedes the development of HCC, suggests the risk of future new tumor growth from these cell clones.
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PMID:Status of hepatitis B virus DNA in hepatocellular carcinoma: a study based on paired tumor and nontumor liver tissues. 284 76

Primary liver cancer, particularly HCC, is increasing in certain countries, notably Japan. Although hepatitis B virus has been etiologically linked to hepatocarcinogenesis and integration of its DNA into hepatocyte chromosomal DNA has been emphasized, other etiologic factors seem to have an interplay with virus infection. Histopathology of HCC has geographic variations. An expanding encapsulated HCC is most common in Japan, whereas it is nearly nonexistent in the West; such regional differences can only be explained by differences in the major etiologic factors. Early detection of HCC is now possible with ultrasound examination combined with AFP measurement, and this strategy has been executed with success in the Far East where HCC is endemic among cirrhotics. The speed of tumor growth can be measured with accuracy by ultrasound examination. Preneoplastic or early lesions of HCC in a cirrhotic liver seem to be adenomatous hyperplastic nodules or foci, and the conventional histological criteria for malignant liver cells do not seem applicable to such lesions. Although advanced cirrhosis is a real deterrent for hepatic surgery, hepatic resection affords a better survival compared with any nonsurgical therapeutic modality. Transcatheter arterial embolization is one of the current preferences of the hepatologist for inoperable patients. Lastly, a new staging scheme has been proposed for the assessment of prognosis and for comparison of efficacy of various therapeutic modalities.
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PMID:Primary liver cancer. Quadrennial review lecture. 301 22

The clonality of tumor cells was studied in a patient with metastasizing hepatocellular carcinoma (HCC). Using hepatitis B virus (HBV) DNA as a genetic marker, the pattern of integration of viral DNA into the tumor cell genome was determined by Southern blot analyses of DNAs extracted from different HCC lesions in the liver and both lungs. All tumor tissues examined were found to have viral DNA integrated into the same site(s) of the cellular genome. This finding provides direct molecular evidence for a monoclonal origin and expansion of malignantly transformed hepatocytes during tumor growth and metastasis. This characteristic is similar to other human cancers associated with viral infections, such as adult T-cell leukemia, Burkitt's lymphoma, or cervical cancer, and is important for our understanding of viral oncogenesis in man.
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PMID:Hepatocellular carcinoma and hepatitis B virus infection: molecular evidence for monoclonal origin and expansion of malignantly transformed hepatocytes. 304 Jul 66

Anti-thymocyte serum (ATS) treated newborn rats were used to assess the tumorigenic potential of mammalian cell and mammalian cell culture derived substances. Injection of as much as 100 micrograms of Chinese hamster ovary (CHO) DNA, an amount in excess of 10(8) fold more than might be present in one dose of a typical final product derived from mammalian cell cultures, failed to initiate a tumor in immunosuppressed animals. In addition, injection of 10 micrograms of activated oncogene cloned from a human bladder carcinoma was also insufficient to initiate a tumor in immunosuppressed animals. Injection of some but not all CHO cell lines did result in tumor growth which upon isoenzyme analysis was verified to be of hamster origin. Of importance was the finding that recombinant tissue plasminogen activator (rt-PA) and hepatitis B surface antigen (HBsAg) vaccine failed to induce tumors in either normal or immunosuppressed rats. The results suggest that the presence of minute quantities of CHO derived nucleic acid fragments in these final products have no discernable tumorigenic potential.
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PMID:Safety issues related to the use of recombinant DNA-derived cell culture products. I. Cellular components. 358 42

A human primary liver cancer cell line which retains the property of synthesizing hepatitis B surface antigen has been successfully transplanted into nude (athymic) mice. The morphology of the heterotransplanted tumor is similar to that of a well-differentiated human primary liver cell cancer. It produces hepatitis B surface antigen, but there is no evidence of hepatitis B virion production: Hepatitis B core antigen is not detected in the PLC tissue, and serum is negative for hepatitis B e antigen. The nude mouse exhibits a resistance to the transplantation of the human primary liver cancer cells which can be modified by sublethal total body irradiation, suggesting involvement of an immunologic rejection mechanism. The heterotransplanted primary liver cell cancer also produces alpha-fetoprotein, as did the original tumor in vivo, although this marker was not detected during in vitro cell culture. The serum level of alpha-fetoprotein rises exponentially, enabling quantitative evaluation of tumor growth. The human primary liver cell cancer in nude mice provides an in vivo model for determination of tumor response to chemotherapeutic agents.
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PMID:Hepatitis B surface antigen and alpha-fetoprotein secreting human primary liver cell cancer in athymic mice. 615 47

The histologic pattern of tumor growth at tumor-nontumor boundaries was studied in 60 livers bearing hepatocellular carcinoma. Three growth patterns, arbitrarily described as "sinusoidal," "replacing," and "encapsulated," were distinguished. Cancer cells growing in the sinusoids between liver cell cords (sinusoidal pattern) were anaplastic; those growing in an expansile fashion and acquiring a fibrous capsule (encapsulated pattern) were most differentiated; and those growing into the cord of liver cells and replacing them (replacing pattern) were differentiated to an intermediate degree. There was certain relation between the histologic growth patterns and gross morphologic features of the tumors. Test results for 20 of the 60 cases were positive for serum hepatitis B surface antigen (HBsAg), and the livers also contained orcein-positive cells. Orcein-positive cells were frequently seen at the border between tumor and parenchyma. Cells containing HBsAg as an orcein-positive inclusion were present in cancer tissue in three cases. When serial sections were made from such areas and stained alternately with hematoxylin and eosin and orcein, it was found that these cells were hepatocytes blended with cancer cells. This phenomenon was related to the growth pattern of tumor cells. Orcein-positive cells were never found in metastatic lesions.
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PMID:Histologic growth pattern of hepatocellular carcinoma: relationship to orcein (hepatitis B surface antigen)-positive cells in cancer tissue. 617 25


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