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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic liver diseases, in particular chronic HBV and HCV infections, frequently progress to liver cirrhosis and HCC. The molecular events underlying hepatocarcinogenesis are not yet well defined. It appears likely, however, that HCCs result from a stepwise carcinogenesis: due to chronic liver disease there is liver cell necrosis, inflammation and regeneration with a high mitotic rate of liver cells. In this setting, chromosomal DNA rearrangements occur which may result in the activation of cellular oncogenes or inactivation of tumor suppressor genes. Viral genes or gene products as well as cofactors, such as alcohol or aflatoxins, may make a specific contribution to these molecular events. Apart from the molecular aspects of hepatocarcinogenesis, for clinical practice the implementation of measures to prevent or treat chronic liver diseases should reduce the incidence of HCCs, one the most frequent malignancies in some areas of the world.
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PMID:[Hepatocellular carcinoma: molecular biology aspects]. 784 55

A number of biochemical events accompany the development of chronic liver disease and its evolution into hepatic cancer. Low plasma zinc and high plasma copper levels have been observed in individuals with advanced hepatocellular liver disease. Moreover, many investigators have demonstrated an increase in serum estradiol levels in individuals with chronic liver disease and hepatocellular carcinoma (HCC). In the present study, the relationship between these biochemical events and HCC was investigated in an animal model. Specifically, carbon tetrachloride (CCL4) was administered intragastrically to 20 female Sprague Dawley rats for 30 weeks. All 20 animals developed cirrhosis. Six (30%) developed HCC. Significantly higher serum estradiol, zinc and copper levels were observed in the rats developing HCC as compared with those with cirrhosis alone (P < or = 0.05, 0.01 and 0.001, respectively). A trend toward increased serum levels of progesterone, ALT and total bilirubin (0.1 > or = P < or = 0.05) was found in the animals developing HCC. No differences in serum testosterone and alkaline phosphatase levels were noted between animals with and without HCC. These studies demonstrate that in animals with experimental CCL4-induced cirrhosis and HCC serum levels of estradiol, zinc and copper are increased, as is the case in man.
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PMID:CCL4-induced liver cirrhosis and hepatocellular carcinoma in rats: relationship to plasma zinc, copper and estradiol levels. 795 73

We studied the presence of Hepatitis C Virus (HCV) antibodies in a defined Malaysian population and examined the association, if any, between HCV and the Hepatitis B Virus (HBV), using sensitive recombinant DNA second generation Enzyme Immunoassay (EIA) test kits. This sero-prevalence study comprised 1,434 sera from eleven distinct groups comprising intravenous drug users (IVDU), haemophiliacs, male homosexuals, female prostitutes, healthy blood donors, staff of dialysis unit and laboratory personnel, chronic renal failure patients undergoing dialysis (CRFD), patients with liver cirrhosis, chronic active hepatitis, chronic persistent hepatitis and primary liver cancer. Except in laboratory personnel and dialysis staff, HCV antibodies were detected in each group of patients ranging from 3% in blood donors to 85% in IVDU. The main modes of HCV transmission identified were parenteral drug use, transfusion and/or dialysis related. The HBV was found to be the major viral etiological agent in 75% of chronic liver disease (CLD); while in 10% of cases both HCV and HBV were detected. HCV was implicated as the sole viral agent in only a small proportion (1.5%) of patients with chronic liver disease.
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PMID:Hepatitis C--the Malaysian story. 826 52

The hypothesis that adult infection with the hepatitis B virus in the United States leads to a carrier state with a high risk of primary liver cancer was tested in two ways: (a) a cohort mortality study of U.S. Army veterans given yellow fever vaccine contaminated with hepatitis B virus in 1942 and controls and (b) a case-control study comparing veterans with hepatocellular carcinoma in Veterans Affairs hospitals with matched controls with respect to receipt of contaminated vaccine in 1942. Three groups totaling 69,988 men were the subjects of the cohort study: group 1 comprised men hospitalized with hepatitis in 1942, group 2 comprised men subclinically infected in 1942 and group 3 comprised controls who entered service after the contaminated vaccine was discontinued. Hepatocellular carcinoma cases (n = 24) and control subjects (n = 63) derived from Veterans Affairs hospital discharge files were the subjects of the case-control study. Group comparisons of death rates from liver cancer were refined by expert review of records to select hepatocellular carcinoma from among all causes of death so diagnosed in the cohort study. Slightly excess mortality was found for hepatocellular carcinoma in group 2 (subclinical hepatitis B) but not for group 1 (overt hepatitis B) compared with group 3 (controls) (p = 0.08). Mortality from nonalcoholic chronic liver disease was less in group 2 than in group 3. In the case-control study, the relative risk for hepatocellular carcinoma conferred by receipt of contaminated vaccine was estimated as 3.3 (p = 0.06). We conclude from the cohort study that immunocompetent adult males rarely become carriers after hepatitis B virus infection, probably far less often than the frequently assumed rate of 5% to 10%. The small excess liver cancer mortality seen in the cohort study and the results of the case-control study are consistent, nevertheless, with the now well-established etiological role of hepatitis B virus infection in liver cancer.
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PMID:Mortality follow-up of the 1942 epidemic of hepatitis B in the U.S. Army. 840 52

Technetium 99m diethylenetriaminepentaacetic acid-galactosyl human serum albumin is a newly developed analog ligand to asialoglycoprotein receptor, which is a hepatic cell surface receptor specific for galactose-terminated glycoproteins. Hepatic functional imaging, which yields estimates of asialoglycoprotein receptor concentration, was performed after intravenous injection of 3 mg technetium 99m diethylenetriaminepentaacetic acid-galactosyl human serum albumin. A total of 75 human subjects were studied: 6 controls without liver diseases, 51 patients with chronic liver diseases and 18 patients with acute liver diseases. In chronic liver disease the asialoglycoprotein receptor concentration significantly correlated with the clinical severity based on the criteria of the Liver Cancer Study Group of Japan (rs = -0.890, p = 0.0001). Good correlations between the asialoglycoprotein receptor concentration and conventional liver function tests were also observed. In acute liver disease the asialoglycoprotein receptor concentration correlated well with the normotest (r = 0.796, p = 0.0001), prothrombin time (r = 0.701, p = 0.0002) and total serum bilirubin (r = -0.642, p = 0.0007). We conclude that the parameter, asialoglycoprotein receptor concentration, obtained from the kinetic analysis of technetium 99m diethylenetriaminepentaacetic acid-galactosyl human serum albumin time-activity data, is a sensitive measure of functioning hepatocyte mass in acute and chronic liver disease.
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PMID:Quantitative assessment of hepatocellular function through in vivo radioreceptor imaging with technetium 99m galactosyl human serum albumin. 849 49

The availability of the anti-HCV assay has confirmed most of the suspicions and predictions regarding the epidemiology of NANB hepatitis virus made before the discovery of HCV. It is now clear that HCV is responsible for the majority of cases of post-transfusion and sporadic NANB hepatitis, as well as of most cases of unidentified chronic liver disease. It seems plausible that HCV may act as a negative co-factor in other chronic liver diseases, especially those caused by alcohol, other hepatitis viruses, and so-called 'autoimmune hepatitis'. The issue of perinatal and sexual transmission of HCV has not yet been clarified, and further studies are urgently needed. Finally, the high prevalence of anti-HCV detected in HCC suggests that HCV is a major co-factor in the development of HCC and again raises the issue of viral persistence and neoplastic transformation, an issue that for HBV has not yet been elucidated.
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PMID:Epidemiology of hepatitis C virus infection. 850 43

Viral hepatitis has a high prevalence in East Asia and is an important problem. Identification of the individual hepatitis viruses. A-E, has enabled researches to investigate the epidemiology and pathogenesis of viral hepatitis and its sequelae, and possible means of prevention. Because of improvement in hygiene in East Asia in recent decades, hepatitis A virus infection has decreased markedly. However, this has resulted in the younger population being susceptible to hepatitis A. Fortunately, effective active immunization for hepatitis A has become available. Hepatitis B is still rampant, especially in the southern part of East Asia where chronic infection is common. Patients who are chronic hepatitis B virus carriers are reservoirs for the virus and have a much higher risk of chronic liver disease and hepatocellular carcinoma (HGC). Currently, hepatitis B infection is being brought under control in East Asia through mass immunization. Serologic and molecular epidemiologic studies have also revealed that Hepatitis C is prevalent in the region. Hepatitis C virus also contributes to the development of cirrhosis and HCC. No effect immunization is currently available, and hepatitis C can only be controlled by preventative measures. The epidemiology and pathogenesis of viral hepatitis is discussed in this review, including new viral hepatitis agents possibly responsible for non-A-E hepatitis.
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PMID:Viral hepatitis in East Asia. 864 98

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

Although carrier rates for the HBsAg as well as the prevalence of HBV-associated chronic liver disease (CALD) are known to be high in Nigeria, not much is known about the role of the hepatitis C (HCV) and D (HDV) viruses. We undertook a prospective serological study of a cohort of 50 new patients and attending a Nigerian teaching hospital for various forms of histologically characterised chronic liver disease. Forty-five patients (90%) had antibodies to HBcAg (anti-HBcAb). Thirty one patients (62%) were HBsAg-positive, out of whom 15 were HbeAg-positive. Two (4%) of the HbsAg-positive patients, both suffering from liver cancer, were also hepatitis D antigen positive. Similarly, two (4%) patients were positive for anti-HCV antibodies. There were no cases of co-infection by the HBV and HCV. This study suggests that while the HBV is the major aetiological agent of chronic liver disease in Nigeria, the HDV is not an important aggravating factor save in a small number of patients. The HCV is probably not yet an important cause of chronic liver disease but this situation might change when HBV infection is controlled.
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PMID:Hepatitis B virus markers, hepatitis D virus antigen and hepatitis C virus antibodies in Nigerian patients with chronic liver disease. 890 63

Interferon is the only treatment shown to be effective on hepatitis C in controlled trials. The response to treatment is generally assessed in terms of a return to normal transaminase activity, but also negative PCR testing for viral RNA and histopathological examination of the liver. At a dose of 3 MU three times a week for 6 months, 25% of patients have a persistent return to normal transaminase activity, 25% relapse when interferon is withdrawn, and the remaining 50% have persistently high levels at the end of treatment and are considered resistant. The rate of persistent responses increases to 40% when treatment is extended to one year. Viral RNA becomes undetectable in the serum of 80% of these responders. Most also have a histological improvement, but so do a number of patients who relapse or who are resistant. In the longer term, interferon could prevent the onset of liver cancer in patients with viral C cirrhosis. Interferon is generally well tolerated at the doses currently used, most side effects (hematologic, neuropsychiatric and thyroid disorders) resolving when treatment is stopped. The following factors are clearly predictive of the response to interferon : young age, short time since onset, absence of cirrhosis, lower-level viremia, and infection by HCV genotypes other than 1b. Interferon is markedly less effective in immunodeficient patients (transplant, HIV infection, etc.). Several add-on treatments have been tried, but ribavirin appears to be the most promising, both during initial interferon therapy and for patients who relapse or are resistant to a first course. Interferon therapy of the acute phase of hepatitis C significantly reduces the risk of chronic liver disease. There is no vaccine against HCV infection.
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PMID:[Prevention and treatment of hepatitis C]. 899 9


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