Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the surgical results of hepatectomy for hepatocellular carcinoma in relation to hepatitis virus status in Taiwan, 252 patients (196 men and 56 women; March 1992 to August 1998) were reviewed. The patients were divided into four groups: 30 patients (11.9%) seronegative for both hepatitis B surface antigen (HBsAg) and antihepatitis C antibody (HCVAb) (N-HCC group); 133 patients (52.8%) seropositive for HBsAg and seronegative for HCVAb (B-HCC group); 66 patients (26.2%) seronegative for HBsAg and seropositive for HCVAb (C-HCC group); and 23 patients (9.1%) seropositive for both HBsAg and HCVAb (BC-HCC group). Patients in group C-HCC were older (p = 0.001) and had a higher incidence of diabetes mellitus (p = 0.004). Also, they had a higher indocyanine green retention rate at 15 minutes (p = 0.021), longer international normalization ratio for the prothrombin time (p = 0.049), and smaller tumor (p = 0.006). Postoperative complications and hospital mortality were significantly higher in patients in the C-HCC and BC-HCC groups (p = 0.046, 0.021). All patients were followed 12 to 76 months after hepatectomy (mean 23.5 +/- 16.3 months). The 1-, 3-, and 5-year overall cumulative survival rates of the 252 patients in this series were 80%, 54.3%, and 34.2%, respectively. The cumulative intrahepatic recurrence rates were 46.5%, 64.9%, and 72.9% at 1, 3, and 5 years, respectively. The mean disease-free survival time was longest in group C-HCC and shortest in group BC-HCC (p = 0.020). The overall survival time and cumulative survival rates in the four groups were not significantly different (p = 0.146).
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PMID:Surgical results in patients with hepatitis virus-related hepatocellular carcinoma in Taiwan. 1205 31

The present study was designed to examine the distribution of hepatitis B virus (HBV) genotypes among patients at various stages of chronic liver disease type B in Okinawa Prefecture, Japan, where the prevalence of hepatitis B surface antigen is the highest in Japan despite the lowest mortality rate from primary liver cancer. Serum samples from 227 HBV carriers were determined for HBV genotype by polymerase chain reaction (PCR)-restriction fragment length polymorphism. Five of 227 sera were negative for HBV DNA by nested PCR and were excluded from the genotype analysis. Genotype B was predominant in asymptomatic carriers (45/67, 67%), whereas genotype C was predominant in chronic liver disease: 49% (50/103) in patients with chronic hepatitis, 63% (20/32) in patients with cirrhosis, and 60% (12/20) in patients with hepatocellular carcinoma. The distribution of genotype B decreased with increasing liver disease severity. However, this tendency was seen among patients aged less than 50 years old, whereas the prevalence of genotype B was similar among carriers with various liver diseases who were older than age 50. In conclusion, HBV genotype B was prevalent and less frequent among patients with advanced liver disease, particularly in patients aged less than 50 years. These findings suggest that the preponderance of genotype B is responsible for the low mortality rate of primary liver cancer associated with HBV seen in Okinawa Prefecture, despite having the highest HBV carrier rate in Japanese.
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PMID:Preponderance of hepatitis B virus genotype B contributes to a better prognosis of chronic HBV infection in Okinawa, Japan. 1211 93

More than 2 billion people in the world are infected with the hepatitis B virus, of whom 280 million are chronic carriers. This virus is responsible for up to 80% of primary hepatic cancer, which is one of three main causes of cancer deaths in east and southeast Asia as well as Africa. Mainly young people are at risk of getting infected and becoming chronic carriers. 70-90% of infants who are infected at birth will become chronic carriers. The virus is transmitted via body fluids, especially blood. It can be transmitted among children and from mother to child during the perinatal period. The vaccination program against hepatitis B is an important tool for preventing its spread. Vaccines contain the viral surface antigen (HBsAG) and are produced from plasma by recombinant DNA techniques. If it is administered properly, a 95% rate of immunization against hepatitis B is achieved. Over the years, more than 40 million doses have been administered. A complete regimen of three doses produces excellent seroconversion rates. The minimum time required between doses is 4 weeks, but a longer interval is preferable between the second and third doses. Since the probability of perinatal infection is low, the first dose may be administered from the sixth week in conjunction with the first dose of diphtheria-pertussis-tetanus (DPT) vaccine. The subsequent doses should coincide with the administration of other vaccines. The hepatitis B vaccine could be administered simultaneously with measles, DPT, poliomyelitis, and BCG vaccines. Complete immunization against hepatitis B costs $2.80 for three doses--an amount that could decline in the coming years.
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PMID:[Hepatitis B vaccine: a new force against pandemic diseases]. 1217 51

To investigate the infection of HCV and the expression of HCV antigen (HCAg) in HCC, immunohistochemical protocol was performed on tumorous liver tissues from 40 patients with HCC to detect HCAg and hepatitis B virus surface antigen (HBsAg) simultaneously. The results showed that the positive rates for HCAg and HBsAg were 17.5% (7/40) and 70% (28/40) respectively. HBsAg and HCAg were simultaneously detected in six of 40 cases and only one case had HCAg positive alone in the liver tumorous tissue. The positive signals were localized in diffuse cytoplasm of hepatocytes and the positively stained cells were mainly distributed in local pattern. The results suggested that HCV infection did exist in some cases of HCC, so HCV might be a viral risk factor in addition to HBV in the genesis of HCC in China.
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PMID:[Immunohistochemical detection of hepatitis C virus antigen from hepatocellular carcinoma]. 1221 37

Risk factors associated with hepatocellular carcinoma (HCC) are well documented, but the synergisms between these risk factors are not well examined. We conducted a hospital-based, case-control study among 115 HCC patients and 230 non-liver cancer controls. Cases and controls were pathologically diagnosed at The University of Texas M. D. Anderson Cancer Center and were matched by 5-year age groups, sex, and year of diagnosis. Information on risk factors was collected by personal interview and medical records review. Blood samples were tested for the presence of antibodies to hepatitis C virus antigen (anti-HCV), hepatitis B surface antigen (HBsAg), and antibodies to hepatitis B core antigen (anti-HBc). Conditional logistic regression was used to determine odds ratios (ORs) by the maximum likelihood method. Multivariate ORs and 95% confidence intervals (CIs) were 15.3 (4.3-54.4), 12.6 (2.5-63.1), 4.5 (1.4-14.8), and 4.3 (1.9-9.9) for anti-HCV, HBsAg, heavy alcohol consumption (>/=80 mL ethanol/d), and diabetes mellitus, respectively. Synergistic interactions on the additive model were observed between heavy alcohol consumption and chronic hepatitis virus infection (OR, 53.9; 95% CI, 7.0-415.7) and diabetes mellitus (OR, 9.9; 95% CI, 2.5-39.3). Independent of the effect of HCV, HBV, and diabetes mellitus, heavy alcohol consumption contributes to the majority of HCC cases (32%), whereas 22%, 16%, and 20% were explained by HCV, HBV, and diabetes mellitus, respectively. In conclusion, the significant synergy between heavy alcohol consumption, hepatitis virus infection, and diabetes mellitus may suggest a common pathway for hepatocarcinogenesis. Exploring the underlying mechanisms for such synergisms may indicate new HCC prevention strategies in high-risk individuals.
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PMID:Risk factors for hepatocellular carcinoma: synergism of alcohol with viral hepatitis and diabetes mellitus. 1239 12

Dietary exposure to aflatoxins is one of the major risk factors for hepatocellular carcinoma. Individual susceptibility to aflatoxin-induced hepatocarcinogenesis may be modulated by both genetic and environmental factors affecting metabolism. A cross-sectional study was performed to evaluate determinants of the formation of aflatoxin covalently bound to albumin (AFB1-albumin adducts). A total of 474 subjects who were free of liver cancer and cirrhosis and were initially selected as controls for previous case-control studies of aflatoxin-induced hepatocarcinogenesis in Taiwan, were employed in this study. Aflatoxin-albumin adducts were determined by competitive enzyme-linked immunosorbent assay, hepatitis B surface antigen and antibodies to hepatitis C virus by enzyme immunoassay, as well as genotypes of glutathione S-transferase M1-1 and T1-1 by polymerase chain reaction. The detection rate of AFB1-albumin adducts was significantly higher in males (42.5%) than in females (21.6%) (multivariate-adjusted odds ratio=2.6, 95% confidence interval=1.4-5.0). The formation of detectable albumin adducts was moderately higher in hepatitis B surface antigen carriers (42.8%) than in non-carriers (36.6%) (multivariate-adjusted odds ratio=1.4, 95% confidence interval=1.0-2.1). In addition, the detection rate of AFB1-albumin adducts tended to increase with the increasing number of null genotypes of glutathione S-transferase M1-1 and glutathione S-transferase T1-1. In conclusion, this cross-sectional study has assessed the relative contributions of environmental exposure and host susceptibility factors in the formation of AFB1-albumin adducts in a well characterised Chinese adult population. This study further emphasises the necessity to reduce aflatoxin exposure in people living in an area endemic for chronic hepatitis B virus infection.
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PMID:Determinants of formation of aflatoxin-albumin adducts: a seven-township study in Taiwan. 1243 85

Vinyl-chloride monomer (VCM), a human carcinogen, has caused angiosarcoma of the liver. Recent studies have shown that VCM exposure is associated with hepatocellular cancer. In Taiwanese studies, the majority of VCM-exposed workers with liver cancer had history of hepatitis B virus (HBV) infection. To determine the role of HBV on the development of liver cancer in the VCM-exposed workers, we conducted a case-control study from a previously established polyvinyl chloride (PVC) cohort consisting of 4096 male workers from six PVC polymerization plants. A total of 18 patients with liver cancer, and 68 control subjects matched for age and specific plant of employment were selected. Detailed history of the participants that included alcohol consumption status, cigarette use, occupation, and family history of chronic liver disease were obtained using an interviewer-administered questionnaire. When the HBV surface antigen (HBsAg)-negative subjects without history of tank-cleaning were used as the reference, the HBsAg-negative subjects with history of tank-cleaning demonstrated a 4.0-fold greater risk of liver cancer (95% confidence interval: 95% CI = 0.2-69.1). The HBsAg carriers without history of tank-cleaning revealed a 25.7-fold greater risk of liver cancer (95% CI = 2.9-229.4). Whereas the HBsAg carriers with history of tank-cleaning revealed the greatest risk (matched odds ratio (ORm) 396.0, 95% CI = 22.6 -infinity) of developing liver cancer among subjects with different VCM-exposure status and HBsAg status categories. Further analysis showed the interaction term was significant (P < .01). Therefore, our results suggest an interaction between occupational VCM exposure and HBV infection for the development of liver cancer.
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PMID:Interaction of vinyl chloride monomer exposure and hepatitis B viral infection on liver cancer. 1270 41

Each of the risk factors for human liver cancer (aflatoxin exposure, hepatitis B virus-associated liver injury, p53 loss, p53ser249 mutation, and male sex) also increases the incidence of hepatocellular carcinoma (HCC) in mouse models of hepatocarcinogenesis. Neonatal mice, partially hepatectomized adult mice, and p53-deficient mice each have a higher hepatocyte proliferation rate, are less able to detoxify AFB1, and form more DNA adducts than do normal wild-type controls. However, transgenic hepatitis B surface antigen mice, expressing hepatitis B surface antigen under control of the albumin promoter (alb/psx), are able to detoxify AFB1 at the same level as do wild-type mice. Thus, AFB1-induced HCC development in neonatal mice and p53+/- mice may be due to "immature" carcinogen metabolism, whereas increased HCC in transgenic hepatitis B virus mice may be due to promotion effects of increased proliferation. Future studies will explore the effects of modifying factors on the development of HCC.
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PMID:Mouse models to study the interaction of risk factors for human liver cancer. 1463 66

Occult hepatitis B is defined by the presence of hepatitis B viral (HBV) DNA in the serum or liver in persons lacking hepatitis B surface antigen (HBsAg) in the serum. A high prevalence of occult HBV has been reported in hepatocellular carcinoma (HCC) from Asia, but little information is available on the prevalence of occult HBV in HCC from regions with a low prevalence of typical chronic hepatitis B infection. In a retrospective study, 19 cases of primary liver cancer were investigated for the presence of occult HBV DNA by amplification of the surface, core, and X gene. In addition, HBV copy numbers were quantitated by real time polymerase chain reaction, genotyped, and samples tested for covalently closed circular HBV DNA, which is a marker of active viral replication. Occult HBV was found in three of 19 cases (16%). Genotyping was successful in two cases, both of which were genotype A. HBV DNA copy numbers were low, all less than 10 copies/microg liver DNA. No closed circular HBV DNA was detected. Thus, in this study occult HBV was of genotype A and was found in a low percentage of cases of HCC and was associated with low tissue HBV DNA copy numbers and no detectable evidence for viral replication.
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PMID:Occult hepatitis B viral DNA in liver carcinomas from a region with a low prevalence of chronic hepatitis B infection. 1523 Aug 51

Chronic infection of the hepatitis B virus (HBV) is one of the causes leading to liver cancer. The 3.2kb genome of HBV encodes four proteins: core antigen, surface antigen, a DNA polymerase and the X protein (HBx). The biological functions of HBx are not fully understood. It has been shown that HBx is a potent trans-activator, which activates transcription of many cellular and viral promoters indirectly via protein-protein interactions. These transactivating activities of HBx may contribute to the development of hepatocellular carcinoma. In this paper a truncated mini-HBx(-Cys) (18-142) protein, where the cysteines had been either deleted or substituted by serines, was constructed by site-directed mutagenesis and overexpressed as a 6xHis fusion protein in Escherichia coli. The 6xHis-mini-HBx(-Cys) protein was isolated from inclusion bodies, purified by Ni-affinity chromatography under denaturing conditions and refolded by sequential dialysis. The structure of the 6xHis-mini-HBx(-Cys) protein was analyzed by circular dichroism, fluorescence and one-dimensional NMR spectroscopic assays. The data presented here suggest that HBx is unstructured but has a propensity to gain secondary structure under specific experimental conditions. Its conformational flexibility might partially explain its functional complexity, namely its capacity to interact with a wide array of signaling proteins, transcriptional regulators and nucleic acids.
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PMID:Expression and spectroscopic analysis of a mutant hepatitis B virus onco-protein HBx without cysteine residues. 1584 20


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