Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of estrogens and testosterone were measured in 25 male patients with hepatocellular carcinoma and associated cirrhosis of the liver and in another 25 male patients with cirrhosis only. The two groups were statistically comparable in terms of age distribution, duration of liver disease, incidence of alcohol abuse, incidence of hepatitis B surface antigenemia, and grade of hepatic dysfunction. Estrone was significantly elevated in both groups of patients. Estradiol concentrations were above normal in 10 patients with hepatocellular carcinoma and in 11 with cirrhosis only. All patients had normal concentrations of estriol. There were no statistical differences between the two groups in either individual or total estrogen levels (estrone 0.05 less than p less than 0.1). Eight of the patients with hepatocellular carcinoma and 5 of the cirrhotics had lower testosterone levels than normal, but this difference was not significant. However, the estrone to testosterone ratios were significantly higher in the hepatocellular carcinoma group than in the cirrhosis group (p less than 0.05). The present study seems to indicate that hyperestrogenemia commonly seen in male patients with liver cirrhosis may play some role in hepatic carcinogenesis of cirrhotic livers. Further studies are needed to determine if the estrone to testosterone ratio is implicated in hepatocarcinogenesis in cirrhotic men.
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PMID:Serum levels of estrogens and testosterone in cirrhotic men with and without hepatocellular carcinoma. 298 53

The lipotropes (choline, methionine, folate, and vitamin B12) have a rich history, with many fluctuations in scientific effort and popularity, covering the past 6 decades. A thin thread of common interest in 1-carbon metabolism and a small band of dedicated individuals have kept this area of biology alive. Today, the lipotropes are enjoying a resurgence of interest and effort with promise for significant contributions to some of our most serious chronic diseases. Between 1920, when Banting and Best initiated a work that led to the discovery of insulin, and 1982-83, when investigators working in 3 laboratories announced that lipotrope deficiency alone could result in liver cancer in rodents, many have used this model to study nutritional problems and, more recently, carcinogenesis. Lipotropes are important to lipid metabolism and to synthesis and maintenance of cellular membranes. When weanling rats were fed a diet low in lipotropes, within a few days the liver accumulated lipid, first in the centrilobular zone and later throughout the entire lobule and lobe. If the diet was continued for a longer period, the liver underwent fibrosis and cirrhosis with some rats ultimately developing hepatocellular carcinoma. Although lipotrope deficiency can result in liver cancer, all hepatocarcinogens tested thus far were enhanced in their activity by diets low in lipotropes. Important changes associated with lipotrope deficiency included membrane damage, decreased serum very low density lipoprotein and drug metabolizing enzymes, decreases in S-adenosylmethionine and in methylation of cytosine, increases in cellular peroxidation products and free radicals, decreased immunocompetence, and a markedly shortened lag time for chemical induction of liver cancer in animals. The overall effect of lipotrope deficiency is an increase in the susceptibility to cancer in animals; the exact mechanisms are unclear.
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PMID:Lipotropic factors and oncogenesis. 303 98

The cancers consistently associated with ingestion of alcohol, the head and neck cancers, are also associated with tobacco use and arise from epithelia that are in direct contact with both agents. Tobacco smoking-related cancers at sites not directly in contact with alcoholic beverages, that is, lung, bladder, and perhaps pancreas, do not consistently show a relationship to alcohol consumption, although lung and pancreatic tumors are associated in some studies. Liver cancer was thought to be strongly related to alcohol consumption on epidemiological grounds and because of its relationship to cirrhosis. As knowledge of the viral etiology of some cirrhoses has evolved and as methods to detect viruses have developed, the significant association between hepatitis B virus and hepatocellular carcinoma has become clear. Alcohol and hepatitis B virus may interact in the etiology of the disease and have important separate roles as well. There are epidemiologic and experimental data showing that malnutrition (resulting from poor food choice), economic deprivation, or alcoholism contributes to the risk for head, neck, and liver cancers. Colon cancers occur about equally in men and women, are found in well-nourished populations, and are not associated with tobacco smoking. Rectal cancers show a preponderance of cases in men but are frequently found in women as well and are not thought to be associated with smoking or malnutrition. The association between colorectal cancers and alcohol consumption, when it is found, apparently occurs at even relatively low alcohol intakes and is often stronger for consumption of beer than of other beverages. Nutritional and metabolic mechanisms proposed for the influence of alcohol on carcinogenesis are supported by studies in human subjects and laboratory animals. Animal models are needed in which effects of ethanol on carcinogenesis can be consistently demonstrated and which can then be used to examine mechanisms.
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PMID:Alcohol and cancer. 303 1

The biological characteristics of hepatocellular cancer vary appreciably in different parts of the world, but especially between regions with very high and low incidences of the tumour. Hepatocellular cancer is multifactorial in origin, and the pattern of its aetiological associations differs between populations at high and low risk. In Africans and Chinese, who have the highest incidences of hepatocellular cancer, the hepatitis B virus is the most important causal association. The viral carrier state is acquired during early childhood, and carries a relative risk for the development of the tumour of over 200. Integration of hepatitis B virus DNA probably acts as a genotoxic initiator in the multistep process of hepatocarcinogenesis, although the precise mechanisms involved have not been determined. Aflatoxin ingestion may also have an aetiological role in high incidence regions, probably as a genotoxic or epigenetic promoter to hepatitis B virus-initiated carcinogenesis. In low risk populations cirrhosis is the most important causal association of hepatocellular cancer. The cirrhosis is often the result of alcohol abuse, but the tumour may complicate all aetiological forms of this disease. Whether neoplasia is an inevitable consequence of the hyperplasia of cirrhosis, or the increased hepatocyte turnover rate acts as a promoter is not known. Hepatitis B virus infection plays a lesser part, and aflatoxin no part at all.
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PMID:The development of hepatocellular cancer in humans. 304 Feb 42

We investigated insulin-like growth factor II (IGF-II) mRNA in three groups of human liver samples including primary liver cancers, benign liver tumors and cirrhosis; indeed these pathological conditions would allow us to distinguish between different steps in liver carcinogenesis. A 40- to 100-fold increase in IGF-II mRNA was shown in 9/40 of the liver cancer samples as compared to normal adult liver. RNA blot analysis using both IGF-II cDNA and oligonucleotide probes showed the reexpression of two fetal (6 and 5 kilobases) IGF-II transcripts in primary liver cancers and in some cirrhotic adjacent tissues; these included all the samples with enhanced IGF-II expression. By contrast the adult (5.3 kilobases) IGF-II transcript was identified in most of the benign liver tumors and liver cirrhosis; in addition, in some of these samples, the 5-kilobase fetal transcript was also detected. The increase of IGF-II mRNA in some liver cancers is consistent with an autocrine mechanism conferring a selective growth advantage to tumorous liver cells. Furthermore, these results indicate a differential expression of IGF-II transcripts in nonmalignant hepatocyte proliferation (benign liver tumors and cirrhosis) as compared to liver cancer. Finally this study suggests that, in liver cirrhosis and in some benign liver tumors, premalignant proliferative states might be identified by the presence of IGF-II fetal transcripts.
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PMID:Differential expression of insulin-like growth factor II mRNA in human primary liver cancers, benign liver tumors, and liver cirrhosis. 318 92

During investigations of the evolution of experimental laboratory infections of woodchucks (Marmota monax) with the woodchuck hepatitis virus (WHV), eight hepatocellular carcinomas (HCC) were observed, six in newborns and two in young adult animals, all within 17-36 months after infection. The absence of an external cocarcinogenic effect in the well-monitored woodchucks indicates the carcinogenicity of WHV and suggests the same for the genetically and biologically similar human hepatitis B virus (HBV). Laboratory infections of woodchucks with two strains of WHV, not reported here in detail, resembled human and chimpanzee HBV infections histologically and serologically. In these studies, eight woodchucks became carriers of surface antigen of WHV for greater than 1 year. All eight woodchucks developed HCC, indicating a 100% risk of HCC in experimentally infected chronic WHV antigen carriers, which is analogous to the high risk of HCC in human hepatitis B surface antigen carriers. Histologically, the absence of cirrhosis in the examined pericarcinomatous tissue permits recognition of gradual transition from normal parenchyma to neoplastic nodules to HCC of rising anaplasia, indicating a continuum of increasingly more malignant neoplastic stages, as known for chemical carcinogenesis. The HCC developed in carrier woodchucks infected as newborns with only minor, if any, hepatitic changes but is associated with antigen-carrying hepatocytes and sometimes with hyperplastic nodules. This stage was preceded in infected adults by an early, acute, weeks-long hepatitis coinciding with the appearance of surface antigen. These findings are also analogous to typical HBV infection in human newborns and young adults, respectively. At the time of HCC development in all animals with adequate histologic material, an acute recent necroinflammation appeared around the tumor, associated with abnormal hematopoietic cells around and within the tumor. A promoting role in carcinogenesis of this necroinflammation of yet unestablished pathogenesis is being postulated, to be confirmed by determination of the status of the WHV DNA in the HCC and by prospective histologic study of the inflammatory reaction.
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PMID:Hepatocarcinogenicity of the woodchuck hepatitis virus. 346 14

Technical BHC and the alpha, beta, gamma and delta isomers of BHC are carcinogenic for the liver of mice and rats. Mice given the isomers of BHC developed carcinomas and hyperplastic nodules of the liver as early as 24 weeks. Several strains of mice (dd, ICR-JLC, CL1, DDY, IRC, DBA/Z, C3H/HEN, C57BL/6 were susceptible. Male mice were more susceptible to hepatic carcinogenesis than female mice and they appeared to be more susceptible to alpha-BHC. The incidence of neoplasms of the liver was increased when beta-, gamma-, or delta-BHC were each given together with alpha-BHC. PCB-5 promoted the induction of hepatic neoplasms when administered with beta-BHC. Technical BHC and its isomers are carcinogenic for the liver of male and female Wistar rats. Beta-BHC is carcinogenic for the liver of Osborne-Mendel male rats. Osborne-Mendel rats receiving delta-BHC developed cirrhosis of the liver, portal vein thrombosis, and focal necrosis of the skeletal muscle. Male rats ingesting technical BHC or the beta or delta isomers also had atrophic testes.
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PMID:Carcinogenicity of benzene hexachloride and its isomers. 616 79

In Japan, most cases of primary hepatocellular carcinoma are associated with liver cirrhosis. Therefore, we must carefully consider the occurrence of hepatocellular carcinoma in cases where liver cirrhosis can be diagnosed. Among 333 patients with liver cirrhosis in whom the clinical course was observed for at least one year after initial diagnosis in the author's clinic, primary hepatocellular carcinoma developed in 20 patients. In this paper, the author intends to elucidate the clinicopathological aspects of these 20 patients with primary hepatocellular carcinoma to delineate clinical features of primary hepatocellular carcinoma in its early stage and to find a clue to carcinogenesis in the cirrhotic liver.
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PMID:Clinicopathological aspects of primary hepatocellular carcinoma occurring in patients with liver cirrhosis. 619 Feb 71

The relationship between hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC), with or without cirrhosis, was assessed immunopathologically through the detection of tissue hepatitis B surface antigen (HBsAg) on paraffin sections of 284 biopsy and surgical specimens of HCC, which were performed from 1970 to 1979, by the indirect immunoperoxidase technique. In 190 cases with nontumorous liver tissue available for histologic and etiologic analyses, cirrhosis was identified in 69.8% (37 of 53) in needle biopsy, 67.4% (31/46) in wedge, and 30.8% (28/91) in the resection or lobectomy group. HBsAg was detected in the nontumorous liver parenchyma in 85.7% in the whole series, and 90.6% in the cirrhotic cases (96.8% in wedge and 100% in resection cases). The HBsAg positivity in the noncirrhotic cases of the resection group was 84.1% (53/63), whereas the 10 negative cases in this group were all noncirrhotic. This clearly demonstrates a strong association of HBsAg and HCC in both cirrhotic and noncirrhotic patients in Taiwan, particularly in the cirrhotic group, as evidenced by the high prevalence of HBsAg in wedge and resection series. On the other hand, the etiology in the HBsAg-negative and noncirrhotic group, which also had a less evident male predominance (male:female = 3.3:1 versus 6-19.5:1) and significantly less liver cell dysplasia than HBsAg-positive or cirrhotic groups, remains to be explained. In 223 cases where tumor tissue met the minimal requirement for analysis, HBsAg was demonstrated in 27 cases (12.1%) in the tumor cells (15% in the resection group). This investigation indicates an important etiologic role of HBV in hepatocellular carcinogenesis, and the development of HCC does not depend on the coexistence of cirrhosis in Taiwan.
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PMID:Hepatitis-B surface antigen and hepatocellular carcinoma in Taiwan. With special reference to types and localization of HBsAg in the tumor cells. 631 75

Hepatocellular carcinoma (HCC) is among the 10 most common tumors in the world. However, incidence is not evenly distributed across the world. In many instances, the proximate cause for the tumor can be identified. Chronic hepatitis B infection is probably the most common cause, followed by chronic hepatitis C. Other important causes are alcoholic liver disease, hemochromatosis, alpha 1-antitrypsin deficiency, and other chronic liver diseases. Although proximate causes may be identifiable, pathogenesis remains uncertain. Factors that may be important include the presence of Aflatoxin B1 in food, genetic changes induced by the hepatitis B virus, and repeated rounds of necrosis and regeneration, also induced by hepatitis viruses. The genes involved and the mutations necessary for hepatic carcinogenesis are unknown, with the sole exception of the p53 gene, which is probably a late phenomenon. Screening for HCC is widely practiced despite the lack of evidence of improved survival. The screening tests used include alphafetoprotein levels and ultrasonography. Screening can identify small tumors; however, survival may not be improved, because the presence of cirrhosis may limit the number of patients who can undergo resections; recurrences or second primary tumors are common; and the presence of chronic liver disease means that survival may be limited anyway. There are many different forms of therapy available; unfortunately, most have not been compared in randomized controlled trials. Surgery remains the therapy of choice if feasible. All other therapy is palliative, including chemotherapy, chemoembolization, hepatic artery embolization, various forms of radiotherapy, and various forms of ablative therapy.
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PMID:Hepatocellular carcinoma. 753 16


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