Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Karyometrical analysis was performed in order to characterize histologically the precancerous condition of cirrhotic livers. The following parameters of hepatocytic nuclei were estimated in 29 normal and 35 cirrhotic livers: Nvo, the number of nuclei in a unit volume of hepatic tissue; D, the mean of nuclear diameters; s. the standard deviation of nuclear diameters (the degree of anisokaryosis); and N/C, the nucleocytoplasmic volume ratio. Results indicate: (1) In normal livers, Nvo is inversely correlated with age (r = 0.53, p less than 0.01), D and s are positively correlated with age (r = 0.68, p less than 0.01, and r = 0.75, p less than 0.01, respectively) and N/C is almost constant regardless of age. (2) Each of the parameters is independent of age in cirrhotic livers. (3) Nvo and N/C are larger, and D and s are smaller in cirrhotic livers with hepatocellular carcinoma than in those without carcinoma (p less than 0.05). From these results, it is concluded that the parenchyma of cirrhotic livers with hepatocellular carcinoma, which is in strongly precancerous conditions, can be characterized by hyperplasia of small hepatic cells rather than by liver cell dysplasia which is defined by marked anisokaryosis and nuclear pleomorphism.
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PMID:Hyperplasia of small hepatic cells in the precancerous condition of cirrhotic livers. 630 Nov 3

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

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

The morphology of liver cirrhosis and the incidence of hepatocellular carcinoma (HCC) in HBsAg-positive alcoholics (17 cases) were examined and compared with those of HBsAg-negative alcoholics (31 cases) and HBsAg-positive non-alcoholics (59 cases). These materials were obtained from our autopsy cases during the last 9 years. About 70% of the 17 showed macronodular cirrhosis, in which periportal and portal lymphoid cell infiltration and liver cell dysplasia were often present, as seen in HBsAg positive non-alcoholics. Furthermore, the liver weight and age distribution at autopsy in HBsAg-positive alcoholics were similar to those of HBsAg-positive non-alcoholics and different from those of HBsAg-negative alcoholics. The association rate of HCC was very high in HBsAg-positive alcoholics (64.7%), similar to that in HBsAg-positive non-alcoholics (67.8%), while the rate in HBsAg-negative alcoholics was low (22.6%). It therefore seems likely that in HBsAg-positive alcoholics concomitant HB virus infection has a major effect on the development of cirrhosis, especially a macronodular type, and on HCC formation.
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PMID:Morphology of cirrhosis and occurrence of hepatocellular carcinoma in alcoholics with and without HBsAg and in non-alcoholic HBsAg-positive patients. A comparative autopsy study. 632 10

Male and female BALB/c mice were treated orally with 5 mg/kg body weight of methyltestosterone for 10 months. Age-matched control animals received no steroid treatment. The livers of all animals were examined by standard histopathological methods. Hepatocellular dysplasia was found in livers of all treated mice, but not in control animals. The extent and severity of this dysplasia showed a sex difference. Most of the male mice (55/78) developed severe dysplasia and in 23/78 the dysplasia was only moderate; the corresponding numbers for female mice were: mild, 15/71; moderate, 48/71 and severe dysplasia, 8/71. Microscopic hepatocytic nodules were found in 6/78 males and 7/71 females. Hepatocellular carcinoma was seen in one male mouse. These findings indicate that methyltestosterone appears to act as a weak total hepatocarcinogen under the experimental conditions used.
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PMID:The effects of long-term administration of methyltestosterone on the development of liver lesions in BALB/c mice. 674 51

One hundred and twenty-four infants admitted to hospitals in Norway between 1955 and 1974 during the first 3 months of life with cholestatic jaundice were studied retrospectively. Sixty-four infants had had extrahepatic atresia of the biliary tree and 60 had had intrahepatic cholestasis. This gives an incidence of about 1:9000 live births for cholestasis. In 4 of the 64 infants with extra-hepatic atresia a bile duct-to-bowel anastomosis had been performed but this was successful in only 2. Sixty of these infants had died by their 2nd birthday. Twenty-six of the infants with intrahepatic cholestasis had died by 1978 and the most common causes of death were cholestasis complicated by infection, bleeding, or hepatoma. The survivors aged between 4 and 23 years were followed up in 1978. In about two-thirds of them aetiological factors--such as alpha-1-antitrypsin deficiency, arteriohepatic dysplasia, cholestasis with lymphoedema--and other familial or genetic factors, or infections were found. Four of the 34 survivors are known to have cirrhosis. Twenty patients had biochemical abnormalities, and 12 had normal liver function tests. Two patients could not be examined. Of the 19 patients with familial or genetic aetiological factors, 4 had cirrhosis, 14 had biochemical abnormalities, and only 5 had normal liver function tests. Of 11 survivors with idiopathic disease or septicaemia, none had cirrhosis and only 4 had abnormal liver function tests.
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PMID:Cholestatic jaundice in infancy. The importance of familial and genetic factors in aetiology and prognosis. 727 1

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

The clinicopathological findings of eight children with hepatic adenoma in the absence of cirrhosis are presented. The lesions ranged in diameter from 0.1 to 14.5 cm. Associated disorders were Fanconi's anemia, type I glycogen storage disease. Hurler's disease, and severe combined immunodeficiency with ADA deficiency. The remaining three children had adenoma without known associated disorders. In the children with glycogenosis and Hurler's disease the adenomas were multiple. Significant dysplasia occurred in the two children with Fanconi's anemia; however, the lesions behaved in a benign fashion--one with regression of the tumor after cessation of androgen therapy and the other with nonrecurrence after complete resection. Proliferating cell nuclear antigen (PCNA) labeling index (LI) of the adenoma arising in patients with Fanconi's anemia was significantly greater than the PCNA-LI of adenoma in the other children (mean 4.1% versus 0.9% of nuclei), approaching the lower end of the spectrum for reported hepatocellular carcinoma cases. We emphasize that the worrisome pathology that may occur in hepatic adenoma in children, particularly with Fanconi's anemia, does not necessarily predict malignant behavior. The association of hepatic adenoma with Hurler's disease or severe combined immunodeficiency has not been reported previously.
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PMID:Hepatic adenoma in the pediatric age group. Clinicopathological observations and assessment of cell proliferative activity. 757 76

Hepatitis C can cause a range of hepatic histopathology. The virus may cause an acute hepatitis indistinguishable from any other acute viral hepatitis, but it is more likely to be associated with steatosis, bile duct injury, and portal lymphoid aggregates. Chronic infection with hepatitis C can range from mild nonspecific changes, presumably representing a hepatitis C carrier state, to end-stage liver disease with cirrhosis and hepatocellular carcinoma. Between these are chronic hepatitis of varying severity. Steatosis, portal lymphoid aggregates, and bile duct injury, while not specific, are very characteristic of chronic hepatitis C. Reputed precursors of hepatocellular carcinoma, including liver cell dysplasia and adenomatous hyperplasia, frequently follow the development of cirrhosis and are presumed to predispose to the development of malignancy. New techniques for localizing the virus in liver tissue will undoubtedly lead to greater understanding of the pathogenesis of hepatitis C-related diseases.
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PMID:Histopathology of hepatitis C virus infection. 759 46

We examined 41 consecutive cirrhotic liver explants from French patients for the presence of nodules of adenomatous hyperplasia (AH) and then analyzed these lesions, together with underlying cirrhosis (C) and associated hepatocellular carcinoma (HCC), for various histological parameters, cellular density, and proliferative activity. Thirty-five AHs were identified in 10 livers (prevalence, 24%); seven of 10 were HCV positive. Hepatocellular carcinoma was more frequent in patients with AH than in patients without. The AHs consisted of 17 ordinary (OAH) and 18 atypical (AAH) adenomatous hyperplasia lesions. There was a malignant focus in five of the 18 AAHs. Wide areas of large liver cell dysplasia were frequent in OAH but never found in AAH. Obvious steatosis was frequent in HCC but exceptional in AAH and absent in OAH. There was a significant increase in cellular density in AAH and HCC as compared with C and OAH. Proliferative cell nuclear antigen immunostaining similarly showed an increase in proliferation from OAH or C to AAH and HCC. These data suggest that, in Europe as in Japan, one pathway of hepatocarcinogenesis is a multistep process in which AAH should be considered as a premalignant lesion very close to grade I HCC, while OAH seems to correspond to a regenerative nodule with limited proliferative ability.
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PMID:Adenomatous hyperplasia in cirrhotic livers: histological evaluation, cellular density, and proliferative activity of 35 macronodular lesions in the cirrhotic explants of 10 adult French patients. 861 68


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