Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum erythropoietin (Epo) levels are depressed in anemic AIDS patients relative to controls. The basis for abnormal regulation of Epo has not been defined. The hepatoma cell line Hep3B produces Epo in response to hypoxia and serves as a model for the study of Epo regulation. Hep3B cells are infectible with human immunodeficiency virus-1 (HIV-1) and were used as a model for evaluating potential direct effects of HIV on Epo expression. HIV-1 infected or transfected Hep3B cells produced Epo at significantly lower levels than uninfected Hep3B cells under low O2 conditions or following exposure to cobalt chloride. Epo production induced by hypoxia of HIV-1 infected Hep3B cells was depressed compared with non-HIV containing Hep3B cells when normalized for cell number, total cellular protein or albumin, but not depressed when normalized for alpha-fetoprotein production. The cellular levels of Epo mRNA were not diminished in the HIV-1+ Hep3B cells, indicating a probable posttranscriptional effect of HIV-1 on Epo production. Cellular protein production or secretion rates as measured by precipitable 3H-leucine were not affected by the presence of HIV-1. HIV-1 appeared to depress the production of Epo and some, but not all, other cellular proteins. These results suggest that impaired production of Epo may be a direct effect of HIV-1 infection possibly contributing to anemia in AIDS.
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PMID:HIV-1 suppresses erythropoietin production in vitro. 839 Mar 70

Translational incorporation of the unusual amino acid selenocysteine in eukaryotes requires a coding region UGA codon (which otherwise serves as a termination signal), a selenocysteine insertion sequence (SECIS) in the 3'-untranslated region of the mRNA, and selenocysteyl-tRNA. The mechanisms involved in SECIS recognition by the eukaryotic translational machinery remain unknown. We report the detection of RNA-binding proteins that specifically recognize the SECIS from human cellular glutathione peroxidase (GPX1) transcripts. RNA gel shift assays showed three retarded bands after incubation with COS-1 whole cell lysate or S-100 cytosol fraction or with extracts from hepatoma cell lines HepG2 and Hep3B. The specificity of the binding was demonstrated by competition by cold unlabeled SECIS RNA and by lack of competition by other RNA species with similar stem-loop secondary structures, such as the human immunodeficiency virus (HIV) transactivation-response region of HIV mRNA element, and mutated SECIS constructs. UV cross-linking and SDS-polyacrylamide gel electrophoresis revealed at least two proteins, with estimated molecular masses of 55,000 and 65,000 Da, that bind to the SECIS. Examination of a series of insertion and deletion SECIS mutants indicated recognition of the SECIS primarily through the basal stem region, although the upper stem, loop, and two of three short conserved sequences also appear to contribute to the affinity of the binding.
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PMID:RNA-binding proteins that specifically recognize the selenocysteine insertion sequence of human cellular glutathione peroxidase mRNA. 853 Apr 73

The genomic region encoding the hepatitis C virus (HCV) core protein was cloned into a mammalian expression vector to study its role on the transcriptional regulation of cellular proto-oncogene and viral promoters. Using a transient transfection assay in human hepatocellular carcinoma (HepG2) cells, we demonstrate that the HCV core protein activates the human c-myc, Rous sarcoma virus long terminal repeat (LTR), and simian virus 40 (SV40) early promoters; and suppresses the c-fos promoter and human immunodeficiency virus type 1 (HIV-1) LTR activity. The transcriptional regulation of cellular proto-oncogenes by the HCV core protein suggests possible involvement of the core protein in the deregulation of normal hepatocyte growth and hepatocarcinogenesis.
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PMID:Transcriptional regulation of cellular and viral promoters by the hepatitis C virus core protein. 853 58

A case/control study was conducted in Bujumbura, Burundi, from 1991 to 1992 to assess the relationship between chronic liver disease and hepatitis C virus (HCV). Patients presenting chronic liver disease (n = 80) were selected based on clinical, laboratory, ultrasonographic, and/or endoscopic findings. Patients with AIDS or hepatocellular carcinoma were excluded. Controls (n = 159) matched with regard to age and sex were recruited from outpatients who had blood tests at a liver disease clinic. Patients and controls were tested for anti-HCV antibodies by ELISA and LIA. Screening for hepatitis B virus (HBs antigen, anti-HBs and anti-HBc antibodies) and human immunodeficiency virus (HIV) was achieved by ELISA with confirmation of HIV infection by LIA. The incidence of anti-HCV antibodies was significantly higher in patients (55.0%) than controls (33.3%) (p < 0.001). The incidence of HBs antigens was significantly higher in patients (28.8%) than controls (7.5%) (p < 0.0001). The incidence of anti-HIV antibodies was not significantly different in the two groups. Multifactorial analysis indicated that anti-HCV antibodies and HBs antigens were risk factors for chronic liver disease, but did not detected a significant interaction between these two risk factors. Prevention of hepatitis C and B would reduce the incidence of chronic liver disease but cost currently limits widespread use of this approach.
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PMID:[Relationship between chronic liver diseases and hepatitis C in Burundi adults]. 855 18

Substantial evidence indicates that several common viruses are clearly or probable causal factors in the etiology of specific malignancies. These viruses either normally establish latency or can become persistent infections. Oncogenesis is probably linked to an enhanced level of viral activation in the infected host, reflecting heavy viral dose or compromised immune control. The major virus-malignancy systems include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatocellular carcinoma; human lymphotropic virus-type 1 (HTLV-1) and adult T-cell leukemia/lymphoma (ATL); Epstein-Barr virus (EBV) and endemic Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's disease; and human papilloma virus (HPV) and cervical cancer. Of these, a vaccine is available only for HBV. These malignancies tend to occur in early to mid-life and account for a substantial amount of morbidity and person-years lost. They are also likely to occur as "opportunistic malignancies" among individuals infected with human immunodeficiency virus type-1, particularly among those who experience prolonged survival.
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PMID:Overview: viral agents and cancer. 874 95

Small cell undifferentiated carcinoma (oat cell carcinoma) is a malignant epithelial neoplasm with neuroendocrine features. It can appear as a primary tumor in many organs besides the lung, including the colon. We report a case of primary small cell undifferentiated carcinoma of the left colon with omental metastases in a 23-year-old man with a history of X-linked hyper-IgM syndrome. The patient had a simultaneous primary hepatocellular carcinoma. A literature review of this rare colonic malignancy is presented together with a discussion of the possible relationship of this tumor with hepatic malignancy and immunodeficiency.
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PMID:Small cell undifferentiated carcinoma of the colon associated with hepatocellular carcinoma in an immunodeficient patient. 881

The molecular mechanisms involved in the regulation of human immunodeficiency virus type 1 (HIV-1) replication may differ in various cell types and with various exogenous stimuli. TAR/Tat interactions play important roles in HIV-1-long terminal repeat (LTR)-directed transcription, and have become specific targets in molecular therapies for blocking HIV-1 replication. As we previously reported, astrocytic glial cells, which can support HIV-1 replication in cell culture and may be infected in vivo, provide an intracellular milieu in which TAR mutant HIV-1 viruses may replicate. In further studies of this molecular model, several divergent human cell types were analyzed for both TAR- and Tat-independent HIV-1 replication. Human hepatoma cell lines, which can be productively infected by HIV-1 after the hepatoma cells are transduced with the human CD4 receptor gene, were found to support high levels of HIV-1 replication. In these studies, utilizing a transient transfection system with wild-type and various TAR, Tat, or combined TAR/Tat mutant HIV-1 proviral constructs, we demonstrate TAR-independent replication in unstimulated human hepatoma cells. Remarkably, in human hepatoma cells, HIV-1 replication is not only independent of TAR but also can be independent of Tat expression. It is further demonstrated, using electrophoretic mobility shift assays (EMSAs) and an in situ UV cross-linking system, that human hepatoma cells contain novel endogenous cellular proteins that bind to the proviral HIV-1 5' LTR in the downstream region, between nucleotides +38 to +125 on proviral DNA. This alternative regulatory pathway of TAR- and Tat-independent viral production may provide a new system to dissect further the interactions of Tat/TAR and determine the role of the TAR element, in its DNA form, in HIV-1 replication.
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PMID:TAR- and Tat-independent replication of human immunodeficiency virus type 1 in human hepatoma cells. 884 14

The natural history of hepatitis C is complex and still poorly known. Hepatitis C virus (HCV) replication can be detected very soon after exposure and, at least in the transfusional setting, it persists indefinitely in up to 90% of the cases. While liver damage during the acute phase of hepatitis is almost invariably mild (fulminant cases are exceptions), chronic sequelae of HCV infection may be severe in the long run. Chronic hepatitis C, in fact, is a long-lasting indolent process which leads to cirrhosis in approximately 20% of all infected patients. Hepatocellular carcinoma is a well-recognized complication of old infections, as are a number of extrahepatic manifestations, including type II cryoglobulinaemia. The determinants of the severity of the liver disease are still unclear. However, the risk of cirrhosis seems to be greater for patients with old infections, those infected with the genotype 1b and those with associated conditions. The latter are a heterogeneous and increasing group of 'problem' patients, including patients who are co-infected with the human immunodeficiency virus (HIV1), or who are being treated with cytotoxic or immunomodulating drugs. Data suggest that the natural history of hepatitis C is altered in patients with associated conditions, and this might have an impact on strategies of patient management and treatment.
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PMID:The natural history of hepatitis C. 886 34

Persistent human immunodeficiency virus (HIV) infection induces an immuno-suppressive state and therefore malignant tumors are a very common complication. Hepatocellular carcinoma is very rare, however, because it is associated with chronic liver disease by the persistent infection of hepatitis B or C virus (HBV or HCV). We reported a case of HCC with HIV infection who had no evidence of HBV or HCV infection, and that had a rapid growth and active pulmonary metastases. Pathological findings of the resected liver showed moderately differentiated HCC and no chronic liver disease. Despite efforts to find potential HBV integration in tumor and non-tumor tissue, none was observed. To our knowledge, this is the first report of HCC in HIV-infected patient with no evidence of hepatitis virus infection.
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PMID:A case of hepatocellular carcinoma in HIV-infected patient. 888 41

We investigated the presence of hepatitis C virus (HCV) infection in 58 patients with humoral immunodeficiencies. Forty-three of these patients had common variable immunodeficiency (CVI), 2 had sporadic hyperimmunoglobulin M (HIM) syndrome, 2 had immunoglobulin G subclass deficiency, 4 had ataxia-telangiectasia (AT), and 7 had X-linked agammaglobulinemia (XLA). Patients with late-onset hypogammaglobulinemia (those with CVI, HIM, or immunoglobulin G subclass deficiency) had a 38.2% prevalence of HCV infection. In patients with XLA or AT, HCV infection was not detectable. Most of the HCV-infected patients had persistent viremia, with histologic findings of chronic hepatitis. Although patients positive for HCV ribonucleic acid (RNA) had received several lots of immunoglobulin, we were unable to detect any correlation between the time that alanine aminotransferase levels increased and the time that intravenous immunoglobulin therapy was given, except in one patient with CVI. Moreover, we found no differences in the number of blood transfusions, surgical procedures, or administrations of intravenous or intramuscular immunoglobulin between HCV RNA-positive and HCV RNA-negative groups. We concluded that: (1) the incidence of HCV infection in patients with hypogammaglobulinemia is much higher than that reported in the Italian general population; (2) although patients with hypogammaglobulinemia have persistent viremia, they do not show an aggressive course of HCV disease, nor does hepatocarcinoma develop; and (3) intravenous immunoglobulins are only one of several possible causes of HCV transmission in patients with humoral immunodeficiencies.
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PMID:Hepatitis C virus infection in Italian patients with hypogammaglobulinemia. 893 Apr 47


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