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

The paper present a brief review of progress in cancer immunology in the past 50 years and its use in the immunodiagnosis, immunoprevention, and immunotherapy of cancer. Tumor markers have been a basis of the serological diagnosis of some tumors and the immunophenotyping of leukemia. Hepatitis B virus vaccination should reduce the incidence of hepatic cell carcinoma. Investigations have provided impetus to the design of molecular genetic anticancer vaccines which are being tested in the clinical setting.
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PMID:[Immunology of cancer]. 1037 79

This study was carried out at Nil Ratan Sarkar Medical College, Calcutta from December 1993-95 among 450 patients with hepatic and nonhepatic disorders and 100 normal individuals. The study was conducted to examine the association between serum Hepatitis B surface antigen (HBsAg) and Delta virus (HDV) antigen, and different clinical disorders. Serum was tested for bilirubin and serum glutamic pyruvic transaminase (SGPT) and detection of HBsAg and HDV antigen. Results showed that the presence of HBsAg was found highest in cirrhosis of liver (42.3%), followed by leukemia (32.1%), hepatitis (29.1%), and jaundice (26%). About 65% of HBsAg positive jaundiced patients had a serum bilirubin level of more than 2mg/dl, with a mean SGPT level of 488iu/l. Only two cases were positive for HDV antigen among 60 HBsAg positive jaundice patients, indicating a lower prevalence rate of infection. It also showed that the mean SGPT level was directly proportional to the serum bilirubin level. Age distribution varied from 19.5% to 23.6% among extreme ages, and only 24.8% among the sexually active group.
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PMID:Hepatitis D infectivity profile among hepatitis B infected hospitalised patients in Calcutta. 1038 22

Chemotherapy, which has greatly improved the prognosis of children with malignant diseases, is potentially hepatotoxic. Furthermore, there is a risk for viral hepatitis acquired by blood products. In this study we looked for hepatotoxicity and for chronic viral hepatitis during and after chemotherapy in 50 unselected children with malignant diseases. 29 children had been treated for leukemia or lymphoma, 19 for solid tumors, 2 for histiocytosis. All patients had been treated before 1991 and had received blood products not screened for hepatitis C-antibodies. In 18 girls and 32 boys aged 12.3 years (range 6.7-24.5 years) hepatitis B- and hepatitis C-serology and liver function tests were measured during a routine check-up 3.6 years (range 0.5-11.8 years) after the last chemotherapy. Liver function tests during chemotherapy were reviewed retrospectively. During chemotherapy 86% of children showed increased ALT and AST levels, 10% had levels above 500 U/l. At follow up 16 children (32%) had pathological liver function tests, especially slightly increased AST and ALT, 13 of these 16 patients had chronic hepatitis C. In contrast only 2 of 34 patients with normal liver function tests had a viral hepatitis (p = 0.001). Patients with elevation of AST and ALT above 100 U/l during chemotherapy had significantly more often a viral hepatitis than those with normal or slightly elevated aminotransferases. Our study shows that hepatocellular damage is a frequent complication following chemotherapy. However this progresses to chronic liver disease very rarely unless the patient acquired a viral hepatitis. The prevalence of chronic hepatitis C was very high in our patients. As screening of blood products for hepatitis C-antibodies is routinely performed since 1991 this problem is likely to have decreased.
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PMID:[Chronic liver disease after treatment of malignancies in children]. 1040 9

The RNA and DNA tumor viruses have made fundamental contributions to two major areas of cancer research. Viruses were vital, first, to the discovery and analysis of cellular growth control pathways and the synthesis of current concepts of cancer biology and, second, to the recognition of the etiology of some human cancers. Transforming retroviruses carry oncogenes derived from cellular genes that are involved in mitogenic signalling and growth control. DNA tumor viruses encode oncogenes of viral origin that are essential for viral replication and cell transformation; viral oncoproteins complex with cellular proteins to stimulate cell cycle progression and led to the discovery of tumor suppressors. Viral systems support the concept that cancer development occurs by the accumulation of multiple cooperating events. Viruses are now accepted as bona fide etiologic factors of human cancer; these include hepatitis B virus, Epstein-Barr virus, human papillomaviruses, human T-cell leukemia virus type I and hepatitis C virus, plus several candidate human cancer viruses. It is estimated that 15% of all human tumors worldwide are caused by viruses. The infectious nature of viruses distinguishes them from all other cancer-causing factors; tumor viruses establish long-term persistent infections in humans, with cancer an accidental side effect of viral replication strategies. Viruses are usually not complete carcinogens, and the known human cancer viruses display different roles in transformation. Many years may pass between initial infection and tumor appearance and most infected individuals do not develop cancer, although immunocompromised individuals are at elevated risk of viral-associated cancers. Variable factors that influence viral carcinogenesis are reviewed, including possible synergy between viruses and environmental cofactors. The difficulties in establishing an etiologic role for a virus in human cancer are discussed, as well as the different approaches that proved viral links to cancer. Future directions for tumor virus studies are considered.
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PMID:Viral carcinogenesis: revelation of molecular mechanisms and etiology of human disease. 1068 61

The latest experimental data on the role of viruses in the origin of human tumors are discussed. This group of viruses consists of T-cell leukemia virus type 1 (HTLV 1), herpes viruses (HHV 8 and Epstein-Barr virus), hepatitis B virus, and human papilloma viruses. The most typical feature of this group of viruses is a very long latent period from the initial infection to the development of the disease that varies between 10 and 40 years. The mechanism of malignant cell conversion is specific for each viral type but is mainly associated with a disruption of functions of cellular genes participating in the control of cell division and proliferation. It can be a direct inactivation of tumor suppressor genes by their interaction with viral gene products (papilloma viruses), or a trans-activation of cellular genes modulating cell proliferation by viral gene products (hepatitis B virus and HTLV 1). Viruses play an initiative role and additional genetic changes in the genome of infected cells are necessary for complete expression of the oncogenic potential of the viral genes. Only these cells will give rise to a monoclonal cell population with uncontrolled proliferation. New approaches for the creation of vaccines against cancers associated with hepatitis B virus and papilloma viruses (hepatocellular carcinomas and cervical tumors, respectively) are in progress. These vaccines have been found to be effective in prevention of the disease in the experimental models and are now beginning to be used for human vaccination.
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PMID:Virus-associated human tumors: cervical carcinomas and papilloma viruses. 1070 42

Cancer prevention has been the stated goal of molecular cancer epidemiology for the past 17 years. In this review, progress toward that goal is evaluated by using as examples well-studied environmental exposures-i.e., tobacco smoke, polycyclic aromatic hydrocarbons, aflatoxin B(1), benzene, and hepatitis B virus-and their roles in lung, breast, and liver cancers and leukemia. The contributions of molecular epidemiology discussed here include providing evidence that environmental agents pose carcinogenic risks, helping establish the causal roles of environmental factors in cancer, identifying environment-susceptibility interactions and populations at greatest risk, and developing new intervention strategies. Molecular epidemiologic and other data indicate that assessment of carcinogenic risks should address both the range of risk across the population and the risk to subgroups who may be at high risk because of genetic or acquired susceptibilities, including young children. However, for the most part, research results have not yet been effectively translated into risk assessments and preventive health policies. An infrastructure linking scientists, policy makers, and other constituencies is needed to facilitate this process. To extend our knowledge, the second generation of molecular epidemiologic research should include large-scale, collaborative studies incorporating validated biomarkers and automated technologies. An incentive to make the necessary investment is the recognition that prevention of only 20% of cancer in the United States would result in 200000 fewer new cases diagnosed each year and an annual savings of $21.4 billion in direct costs alone.
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PMID:Molecular epidemiology: on the path to prevention? 1077 77

Bone marrow histology after bone marrow transplantation has rarely been studied. Here, we reviewed the pre- and post-transplant bone marrow biopsies (BMB) of 40 acute myelogenous leukemia (AML) patients autografted in our center, 28 with normal and 12 with delayed peripheral recovery. The two groups were comparable in terms of previous therapy, disease phase and the number of infused cells, and received the same conditioning regimen. In the former group, reduced bone marrow cellularity and mild reticulin abnormalities were usual histological findings; in the latter, five patients had the same pattern, but the other seven had an almost undetectable hematopoietic parenchyma and severe reticulin derangement. One of these seven patients died of reactivated hepatitis B virus infection; the others eventually achieved peripheral recovery, with none of them experiencing a relapse. Autografted AML patients are excellent subjects for histological investigations. They account for the majority of delayed engraftments, the contribution of extramedullary components to the timing of engraftment is minimal, and leukemia relapse cannot be ruled out. These results suggest that BMB is a useful investigation in the work-up of late engraftment. A high degree of reticulin derangement with an almost undetectable hematopoietic parenchyma appear to be the morphological hallmarks of late engraftment.
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PMID:Histological alterations in bone marrow in patients with late engraftment after autologous bone marrow transplantation. 1080 4

The blood borne viruses must be separated into major and minor agents. Major viruses transmissible by blood transfusion are human immunodeficiency virus (HIV) and hepatitis B and C viruses (respectively HBV, HCV). The prevalence of virological markers in French blood donors has been continuously decreasing since the implementation of serological screening methods as soon as they were available. In 1998, the prevalences (per 10,000 donations) were 0.17 for antibody to HIV, 0.08 for antibody to human T-cell leukemia virus (HTLV), 2.23 for hepatitis B surface antigen (HBs Ag) and 2.52 for antibody to HCV. The values are, of course, higher in new donors when compared to regular donors: approximately five-fold for HIV, 50-fold for HCV and 300-fold for HBs Ag. The remaining major questions concern the residual risk due to infectious donations which could escape the preventive measures. It seems evident that the major risk is imputable mainly to donations collected during the window period. During the 1996-1998 period, the residual risk for HIV was 1 out of 1,350,000 donations, 0 for HTLV, 1 out of 375,000 for HCV, and 1 out of 220,000 for HBV. A few cases of "immunosilent" patients have been reported. They remain exceptional. The first data collected after the implementation of nucleic acid technology (NAT) confirm the very low residual risk. The recent introduction of leukodepletion probably brought an important contribution to diminishing the risk of transmission of leucotropic viruses such as cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesviruses-6, -7 and -8, and HTLV. If the purification process of plasma-derived medicinal products including inactivation procedures makes it possible to be confident with the elimination of infectivity due to enveloped viruses, the detection of nucleic acid sequences derived from naked viruses in plasma pools such as parvovirus B19 or hepatitis A virus (HAV), and/or the introduction of a nanofiltration step during the purification process, when possible, may greatly contribute to their safety. The emergence of a new form of the Creutzfeldt-Jakob disease (nvCJD) introduces a new series of questions about the safety of blood products that, although the risks appear limited, are not yet resolved.
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PMID:[Viruses and unconventional transmissible agents: update on transmission via blood ]. 1091 17

Despite sustained improvement of donor selection and serologic screening assays, there still remains a small but significant transfusion risk for each of the major viral agents (hepatitis B virus [HBV], hepatitis C virus [HCV], human immunodeficiency virus [HIV] and human T-cell leukemia virus [HTLV]). The risk is due to the failure of the screening tests to detect all the infected blood donations and in particular those which are recently infected in the pre-seroconversion window phase of infection, and the asymptomatic immunosilent chronic carriers who never develop antibodies. Another source of risk relates to variant strains of known viruses that are not detected by the current assays. The last potential risk involves the failure to detect infected blood samples because of inaccurate performances of the test process. In order to reduce this residual risk, the French health authorities requested the progressive introduction of nucleic acid technology (NAT) in blood screening so as to be generalised to all blood centres in the course of year 2000. Multicentric studies are underway to identify the most suitable techniques for the French network.
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PMID:[Screening for viral genomes in blood transfusion]. 1091 18

Interferons display a wide range of antiviral, antiproliferative, and immunomodulatory activities on a variety of cell types and have been used to treat many diseases including hairy-cell leukemia and hepatitis B and C and have also been applied to other therapeutic areas. To improve the pharmacological properties of interferon (IFN) alpha-2b, a long-acting pegylated form (PEG-IFN) has been developed [PEG, monomethoxy poly(ethylene glycol) with average molecular mass of 12 000 Da]. PEG-IFN is a mixture of pegylated proteins with differing sites of PEG attachment. To identify the major positional isomer in the pegylated material [PEG-IFN(His-34)], NMR studies were conducted on a subtilisin-digested N-acetylated peptide of the major positional isomer [PEG-IFN(His-34)dig], synthetic peptide analogues containing His-34, as well as unmodified IFN and PEG-IFN(His-34). Our studies reveal a novel interferon-polymer attachment site as a histidine-linked interferon conjugate. We show that the major component of PEG-IFN is pegylated in the imidazole side chain of histidine-34. Chemical shift data suggest that pegylation occurs mainly at the N(delta)(1) position in the imidazole side chain of this residue. This positional isomer, PEG-IFN(His-34), comprises approximately 47% of the total pegylated species when PEG-IFN is synthesized under the current experimental conditions at pH 6.5 with an electrophilic derivative of PEG, succinimidyl carbonate PEG. The reversibility of the histidine modification was examined. The PEG-imidazole adduct in the intact protein, PEG-IFN(His-34), is labile but much more stable than in the peptide, PEG-IFN(His-34)dig. Apparently, the tertiary structure of the intact protein protects the His(34)-imidazole ring from depegylation.
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PMID:Identification of the major positional isomer of pegylated interferon alpha-2b. 1097 46


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