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

The development of hepatocellular carcinoma (HCC) is probably related to infection with hepatitis B virus (HBV). Hepatocytes in livers of patients with HCC have been reported to show putative preneoplastic changes such as hyperplasia, dysplasia, or adenomatous regeneration. To determine quantitatively whether these morphologic changes are associated with HBV-infected cells, the authors performed morphometry of hepatitis B surface antigen (HBsAg)-positive hepatocytes in the nontumorous portion of 10 livers with HCC and in 10 livers without HCC. The diameter of nuclei and cytoplasm of HBsAg-positive hepatocytes was measured after demonstration of HBsAg by the peroxidase-antiperoxidase method. As controls, HBsAg-negative hepatocytes in the same liver sections were measured as well as hepatocytes of 20 age-matched HBsAg-negative patients with normal liver or alcoholic cirrhosis. HBsAg-positive hepatocytes exhibited significantly larger nuclei and a higher nucleocytoplasmic ratio than control hepatocytes. In addition, HBsAg-positive cells were often arranged in foci that consisted of two cell populations: hypertrophic (enlarged nuclei and nucleocytoplasmic ratio) and hyperplastic (two-cell-thick plates of small cells with a high nucleocytoplasmic ratio). While precancerous cells have been difficult to identify, these morphologic changes are frequently associated with the development of malignant neoplasia.
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PMID:Morphometric study of hepatocytes containing hepatitis B surface antigen. 632 Jun 48

A morphological investigation was carried out to study the pathological features of liver cirrhosis caused by hepatitis C virus (HCV) infection. The materials consisted of liver specimens taken from 47 cases of anti-HCV antibody-positive liver cirrhosis (37 by surgery for hepatocellular carcinoma and 10 by autopsy), and from 21 cases of hepatitis B surface antigen-positive liver cirrhosis as the control. Liver specimens containing more than 10 regenerative nodules were examined. In addition, a histometric study was conducted to determine the degree of fibrosis and the size of regenerative nodule using a computer image-analysis system. The results showed that the histological characteristics of HCV antibody-positive liver cirrhosis are: (i) broadly expanded fibrous septa and small regenerative nodules; (ii) relatively strong inflammatory reaction and prominent lymphoid aggretation in the fibrous septum; and (iii) mild regenerative activity of the liver parenchyma, and infrequent liver cell dysplasia. These findings may facilitate better understanding of the pathology of HCV antibody-positive liver cirrhosis and more accurate pathological diagnosis by needle biopsy.
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PMID:Pathomorphological study of HCV antibody-positive liver cirrhosis. 753 51

Hepatitis B virus (HBV) DNA and its 5 antigens were studied in 225 cases of paraffin-embedded sections of human liver cirrhosis obtained by biopsy. HBxAg, pre-S1 and pre-S2 antigens were detected by immunohistochemical ABC method, HBsAg and HBcAg by PAP method. HBV DNA by in situ hybridization, and both HBV DNA and HBsAg, HBxAg or HBcAg by double labelling technique of immunohistochemistry and in situ hybridization respectively. The results showed that the positive rates were 70.0% (128/183) for HBsAg, 64.4% (85/132) for pre-S1 antigen, 61.4% (81/132) for pre-S2 antigen, 75.3% (113/150) for HBxAg, 22.4% (39/174) for HBcAg and 62.4% (58/93) for HBV DNA respectively. The double labelling positive rates were 37.3% (19/51) for both HBV DNA and HBsAg, 86.3% (44/51) for both HBV DNA and HBxAg and 39.2% (20/51) for both HBV DNA and HBcAg respectively. More than 80% of the cases with positive sections for HBV DNA and its 5 antigens were associated with liver cell dysplasia (LCD). The results of this study suggest that the occurrence and development of liver cirrhosis were closely related to chronic infection of HBV in China.
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PMID:[Expression and significance of HBV DNA and its 5 antigens in liver cirrhosis]. 778 Nov 8

The expressions of c-erbB-2 oncogene and epidermal growth factor receptor (EGFR) were investigated immunohistochemically in specimens from 184 cases of hepatitis B, cirrhosis and hepatocellular carcinoma (HCC) and 29 normal liver specimens. EGFR was expressed in 36% (48/134) of the hepatocellular carcinoma and chronic liver disorder specimens and it was immunolocalized mainly in the sinusoidal endothelial cells. No significant difference was found between EGFR expression in HCC and in benign chronic liver disorders. These results indicate that EGFR may have some role in the proliferation of the sinusoidal epithelial cells in chronic liver disease. Low level c-erbB-2 expression was observed in 5/29 (17%) of normal liver specimens. In chronic hepatitis B and liver cirrhosis, its expression was found in all specimens. c-erbB-2 protein was immunolocalized mainly in small polygonal liver cells (SPLCs) and hepatocytes in small-cell dysplasia (SCD) and in ductular metaplasia (DM); c-erbB-2 expression in HCC cells was found to be weaker than in SPLCs, the hepatocytes in SCD and in DM. These results indicate that activated c-erbB-2 oncogene may have a role in human HCC genesis through promoting the development of SCD from SPLC proliferation and the progression of SCD. The close relation between the expression of c-erbB-2 and HBxAg imply that the activation of c-erbB-2 in human liver tissues may be related to HBV X gene.
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PMID:[Expression of c-erbB-2 protein and EGF receptor in hepatitis B, cirrhosis and hepatocellular carcinoma]. 778 35

The effect of high cadmium levels in the diet on development of primary hepatocellular carcinomas (PHC) in transgenic mice expressing hepatitis B surface antigen (high expressing lineage 50-4) was determined to test the hypothesis that the incidence of PHC in areas of the world with endemic hepatitis B infections is related to the amount of cadmium in the diet. Groups of transgenic 50-4 mice and non-transgenic litter-mates consumed a diet containing high (5 micrograms/g) or low (< 0.05 micrograms/g) cadmium concentrations ad libitum for up to 20 months. Grossly visible and microscopic changes in the livers were examined at different time points after initiation of the cadmium feeding (3, 6, 9, 14-15 and 18-20 months). Although there was no difference in the incidence of tumors in 50-4 male or female mice fed high or low cadmium diets, male mice fed with high cadmium had more poorly differentiated liver tumors than did low-cadmium fed male mice. These observations suggest that dietary cadmium levels do not affect the number of tumors, but may affect progression of the carcinogenic process leading to development of more poorly differentiated tumors. In addition, after uniform liver dysplasia at 6-13 months in all 50-4 mice, 'remodeling' of large areas of the liver with formation of normal appearing liver cords, admixed with dysplastic and nodular areas, was noted in both male and female aged 50-4 transgenic mice.
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PMID:Dietary cadmium may enhance the progression of hepatocellular tumors in hepatitis B transgenic mice. 792 3

Mutant tumor-suppressor gene p53 is reported in over 50% of hepatocellular carcinomas (HCC). We studied 60 HCC, 30 with large cell liver cell dysplasia (LCD), suggested to be a preneoplastic change progressing to HCC, in the adjacent non-neoplastic liver. Immunohistochemistry was performed for the presence of mutant p53 and hepatitis B surface (HBs) and core (HBc) antigens, using a labeled streptavidin-biotin technique with monoclonal (1/20) and polyclonal (1/40) anti-p53 and with anti-HBs (prediluted) and anti-HBc (1/400). Twenty-nine (48%) HCC were p53 immunopositive, with both antibodies in 9, 17 with monoclonal p53 only, and 3 with polyclonal p53 only. p53 immunoreactivity was present in 3 of 19 (16%) non-neoplastic livers, 4 of 20 (20%) cirrhotic livers, and one of 30 (3%) LCD. HBs and HBc, respectively, were present in 0% and 5% non-neoplastic livers, 20% and 10% cirrhotic livers, 7% and 10% LCD, and 3% and 5% HCC. None of the p53-positive HCC had HBV markers in adjacent liver. This frequency (48%) of p53 in HCC is similar to that in other countries. The data suggest a role for p53 mutations in hepatocarcinogenesis, even in the absence of HBV infection, apparently not progressing through LCD but occurring as a late event.
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PMID:Immunohistochemical p53 in hepatocellular carcinoma and liver cell dysplasia. 793 18

Large cell liver cell dysplasia (LCD), a suggested preneoplastic change progressing to hepatocellular carcinoma, has been reported associated with alpha-1-antitrypsin deficiency which in some countries has an increased frequency of hepatocellular carcinoma. We examined the nonneoplastic liver from 13 alpha-1-antitrypsin deficiency patients for LCD and, using a labeled streptavidin-biotin technique, for immunohistochemical markers: AAT (1/200), hepatitis B surface (HBsAg, prediluted) and core (HBcAg, 1/400) antigens, and monoclonal (1/20) and polyclonal (1/40) mutant p53, a tumor suppressor gene. There were eight males and five females ranging from 2 mo to 76 yr (mean 40 yr). Nine livers showed cirrhosis, one chronic persistent hepatitis, one portal fibrosis, and two cholestatic hepatitis (in the two infants). The nine cases with LCD included five males and four females of mean age 46 yr (range, 17-71), eight with cirrhosis and one with portal fibrosis. Only one liver with LCD and cirrhosis had HBcAg in cirrhotic and dysplastic cells. No patient had developed hepatocellular carcinoma. All 13 livers were immunonegative for HBsAg and mutant p53, and immunopositive for AAT present in normal, cirrhotic, and dysplastic liver cells. Thus, LCD was identified in 82% of adult alpha-1-antitrypsin deficiency livers (69% including infantile patients), 89% with cirrhosis, and none with malignancy. HB expression was rarely present; serology for HB and/or hepatitis C was positive in 46% adults. Immunoreactive AAT was present in dysplastic cells. p53 gene mutations do not appear to have a role in the pathogenesis of LCD in alpha-1-antitrypsin deficiency.
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PMID:Liver cell dysplasia in alpha-1-antitrypsin deficiency. 815 50

To test the hypothesis that increased proliferative capacity of cells in a liver remnant is a risk factor for tumor recurrence in patients who have undergone liver resection for hepatocellular carcinoma, DNA flow-cytometric measurement and cell-cycle analysis of the nontumor parts of resected hepatocellular carcinomas (tumor size < 5 cm) were performed. The disease-free survival rates 1, 2, 3 and 4 yr after surgery were 64%, 58%, 43%, and 36%, respectively. Proliferative capacity (fractions of synthetic, postsynthetic and mitotic phases) of the nontumor parts, irrespective of liver pathology, was higher than that of normal liver and statistically lower than that of tumor parts from resected hepatocellular carcinoma specimens. Livers with chronic active hepatitis (+) and with hepatocyte dysplasia (-) had significantly lower proliferative activity than did those with chronic active hepatitis (-) and with hepatocyte dysplasia (+), respectively [corrected]. We saw no significant difference in proliferative capacity between patients with and without cirrhosis. Disease-free-survival analysis showed that the presence of liver pathology (hepatitis B infection, cirrhosis, chronic active hepatitis and hepatocyte dysplasia) was not the factor linked to tumor recurrence in the liver remnant and that a marked increase in proliferative capacity (> or = 18%), regardless of liver pathology, was the risk factor linked to tumor recurrence after liver resection. We conclude that there is some degree of increased proliferative capacity in the nontumor parts of resected hepatocellular carcinomas and that a marked increase in the proliferative capacity (> or = 18%) of the nontumor part is a significant risk factor in predicting tumor recurrence in the liver remnant after liver resection.
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PMID:Can determination of the proliferative capacity of the nontumor portion predict the risk of tumor recurrence in the liver remnant after resection of human hepatocellular carcinoma? 839 30

On the basis of the successful establishment of an animal model in tree shrews experimentally infected with human hepatitis B virus (HBV), a study on the hepatocarcinogenic effects of HBV and/or aflatoxin B1 (AFB1) was conducted. The results showed that the incidence of hepatocellular carcinoma (HCC) was significantly higher in the animals both infected with HBV and exposed to AFB1 (52.94%) than in those solely infected with HBV (11.11%) or exposed to AFB1 (12.50%). No HCC of precancerous lesions were found in the controls that were neither HBV-infected nor AFB-1 exposed. Precancerous lesions, including liver cell dysplasia and enzyme-altered hyperplastic hepatocyte foci, were observed before the occurrence of HCC, and the frequency of their appearance correlated well with the incidence of HCC. HBV DNA and the protein it encodes were detected in the cancer cells and/or the surrounding hepatocytes. Integration of HBV DNA into the host liver genome was found during hepatocarcinogenesis among the animals infected by HBV. These results suggest that exposure to HBV and AFB1 may play a synergistic role in the development of HCC, and support the viewpoint of an aetiological relationship between HBV and HCC.
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PMID:Human hepatitis B virus and hepatocellular carcinoma. II. Experimental induction of hepatocellular carcinoma in tree shrews exposed to hepatitis B virus and aflatoxin B1. 860 52

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The majority of patients who develop HCC have underlying cirrhosis, which suggests that cirrhosis itself represents a preneoplastic condition. Nevertheless, whereas patients with cirrhosis of any origin are at increased risk of developing HCC, those with chronic hepatitis B or C infection seem to be at greatest risk. Patients with cirrhosis resulting from chronic alcohol use, hemochromatosis, autoimmune hepatitis, or alpha-1 antitrypsin deficiency have less risk of developing this cancer, and some hepatic diseases, such as primary biliary cirrhosis and Wilson's disease, do not predispose affected persons to an appreciable risk of developing HCC. Certain histological features, such as liver cell dysplasia and macroregenerative nodules, may represent preneoplastic alterations of hepatocytes, but these changes do not seem to be a necessary step in the evolution of liver cancer. The pathogenesis of HCC is unclear, but seems to involve several steps. Hepatitis B virus infection may result in the malignant transformation of hepatocytes by some directly oncogenic mechanism, whereas other necroinflammatory conditions probably predispose to the development of HCC through the introduction of genetic alterations coupled with a reduction of genetic repair functions. Screening patients at risk for the development of HCC using alpha fetoprotein measurements and ultrasonography is widely practiced despite inconclusive evidence of efficacy. If screening is performed, the program used should be tailored to the perceived risk for a particular patient.
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PMID:Preneoplastic conditions of the liver. 870 61


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