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)

In West Malaysia, hepatocellular carcinoma (HCC) is common in the Chinese and in the members of the Senoi aboriginal tribe, two racial groups with diametrically opposite life-styles. Certain fundamental differences exist between the liver tumors in the two races. In the Senoi, the tumor occurs in a younger age group and there is a greater male preponderance than in the Chinese. There is also a very close relationship between hepatitis B virus infection, chronic active hepatitis, cirrhosis, liver cell dysplasia, and HCC in the Senoi and the tumors generally present as multiple nodules studding both lobes of the liver. In the Chinese, although a relationship between hepatitis B virus infection, HCC, and cirrhosis exists, this association is not as strong as in the Senoi and the tumors are generally large and solitary. The data suggest that, although the hepatitis B virus is probably an important oncogenic agent in both racial groups, there may be a difference in the pathogenesis of HCC in the two races.
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PMID:Race-related morphologic variations in hepatocellular carcinoma. 299 Jun 66

In 70 patients with hepatocellular carcinoma without history of antineoplastic chemotherapeutic drugs, anabolic and contraceptive steroids, representative sections of nonneoplastic liver tissue were examined for the presence of etiological markers. Hepatitis B surface antigen-positive hepatocytes were found in 16 (22.8%), alpha-1-antitrypsin globules in 3 (4.2%), Mallory bodies in 9 (12.8%), acicular inclusions in 1 (1.4%), diffuse giant mitochondria in 2 (2.8%), copper-binding protein in 25 (35.7%), greater amount of hemosiderin in 9 (12.8%) cases. Thorotrast was not detected. One or more markers were seen in 38 (54.3%) cases, most frequently in association with liver cell dysplasia and alcoholism. The presence of hepatitis B surface antigen in livers with dysplastic foci was highly significant as compared to organs showing no dysplasia. Only the mentioned antigen and the alpha-1-antitrypsin globules were found to indicate the etiology of the underlying liver lesion. The value of the other markers was found inconsistent in etiological diagnosis.
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PMID:The etiology of underlying liver lesions in 70 autopsied cases of hepatocellular carcinoma. 299 28

An assessment was made of the frequency of liver cell dysplasia and the mean age of each group in 56 normal, 13 cirrhotic, and 50 hepatocellular carcinoma (HCC) patients, 40 with cirrhosis, from southern Africa. Dysplasia increased from 7.1% in normal subjects to 38.5% in cirrhotic, 40% in noncirrhotic HCC, and 52.5% in cirrhotic HCC patients, three statistically similar frequencies. Average patient ages were as follows: patients with normal livers, 37.3 years; with cirrhosis, 42.4 years; with noncirrhotic HCC, 36.5 years; and with cirrhotic HCC, 34 years, the mean age with dysplasia being lower than that of the whole group. With no increase in frequency of dysplasia from cirrhosis to HCC with cirrhosis, with a similar high frequency in HCC without cirrhosis, and with a mean age of all HCC patients 8 years less than that of cirrhotics and 3 years less than normals, chronologic evolutionary progression from cirrhosis to dysplasia to HCC in southern Africa cannot be demonstrated.
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PMID:Liver cell dysplasia in normal, cirrhotic, and hepatocellular carcinoma patients. 300 93

This report documents the occurrence of hepatocellular carcinoma in a 36-year-old man with arteriohepatic dysplasia and a noncirrhotic liver. This case represents one of the oldest patients reported to have arteriohepatic dysplasia and the first with the development of a hepatocellular carcinoma, of which I am aware. Although this tumor has been reported with other familial cholestatic syndromes, the absence of an underlying cirrhosis is of particular interest.
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PMID:Hepatocellular carcinoma associated with arteriohepatic dysplasia. 300 58

Liver cell dysplasia (LCD) is a premalignant cytologic change of hepatocytes that has been statistically linked to cirrhosis, hepatocellular carcinoma (HCC), and chronic liver disease related to hepatitis B virus. The relationship of LCD to non-A, non-B (NANB) hepatitis is currently unknown. We studied liver biopsy and surgical resection specimens from 36 patients with NANB hepatitis, and identified LCD in 17 (42.5%) of 40 specimens, most often associated with cirrhosis. Dysplasia was present in individual hepatocytes, in clusters, and in a distinctive "spreading" pattern of hepatocytes about central veins. Three patients had HCC with a predominant giant cell pattern, as well as LCD. These findings suggest that LCD and HCC should be included among the potential pathologic sequelae of NANB hepatitis.
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PMID:Liver cell dysplasia and hepatocellular carcinoma in non-A, non-B hepatitis. 302 14

Expression of the ras oncogene p21 product by hepatocytes of cirrhotic liver with hepatocellular carcinoma (HCC) was examined immunohistochemically using mouse monoclonal antibody RAP-5. At the concentration of antibody used, histologically normal liver tissues were negative for p21 antigen, whereas hepatocytes of cirrhotic nodules from 80 of 92 HCC patients (87.4%), and 10 of 32 patients without HCC (59.4%) were positive. This difference was statistically significant (p less than 0.05). The incidence of p21 expression by hepatocytes was significantly higher in macronodular cirrhotic patients than in those with micronodular cirrhosis (p less than 0.05) and tended to be higher in those positive for hepatic hepatitis B virus markers than in those that were negative (p less than 0.1). All 16 patients with liver cell dysplasia, and 17 of 18 with adenomatous hyperplasias showed increased expression of p21 antigen. In HCC it was detected on tumor cells of 63 of 101 patients (62.4%). Characteristically, its expression in well-differentiated HCC was mild and uniformly diffuse, and in moderately differentiated tumors was markedly heterogeneous in both intensity and distribution, whereas no expression was observed in cells of poorly differentiated HCC. These observations suggest that elevated ras p21 antigen expression is important in the development of both cirrhotic nodules and HCC, but that after tumor development, its sustained elevation is no longer necessary for cell proliferation and progression through the grades of anaplasia.
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PMID:Immunohistochemical detection of ras oncogene p21 product in liver cirrhosis and hepatocellular carcinoma. 303 55

The cirrhosis and hepatocellular carcinoma associated with alpha 1-antitrypsin deficiency has been exclusively reported with the PI Z allele. We present a 63-yr-old white man with emphysema, cirrhosis, and hepatocellular carcinoma. The latter occurred on a background of diffusely distributed hepatocellular dysplasia. Serum protein electrophoresis suggested a deficiency of alpha 1-antitrypsin quantitated at 13% of normal. PI phenotyping showed that he had only the rare PI Mmalton allele, previously associated only with severe lung disease. Family studies demonstrated the distribution of this rare allele. The liver at autopsy displayed well-differentiated hepatocellular carcinoma in addition to alpha 1-antitrypsin deposits in normal, dysplastic, and malignant cells.
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PMID:Diffuse hepatocellular dysplasia and carcinoma associated with the Mmalton variant of alpha 1-antitrypsin. 303 14

Morphometrical analysis of different types of liver cells was performed in cases of chronic active hepatitis (CAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). The area and a form factor (form AR) of nuclei and cytoplasms were determined, and the nucleo-cytoplasmic ratio (N/C) was calculated in normal hepatocytes, HBsAg-positive cells, large dysplastic cells, cancer cells and in a liver cell population identifiable as "small dysplastic cells" (small cells). The nucleo-cytoplasmic ratio of the small cells and of the neoplastic cells was roughly the same and the highest. Large dysplastic cells showed a small nucleo-cytoplasmic ratio, almost comparable with that of normal hepatocytes and similar to that of HBsAg-positive cells. Since cellular precursors of liver cancer are expected to have a nucleo-cytoplasmic ratio similar to that of neoplastic cells, our morphometrical evaluation indicates small cells as the true precancerous cells; liver cell dysplasia (large dysplastic cells), as described by Anthony et al., should not be considered as a true preneoplastic change.
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PMID:Morphological precursors of hepatocellular carcinoma: a morphometrical analysis. 303 18

In a consecutive autopsy series of 95 males, parenchymal hyperplastic nodules of clear cells occurred in 11.6% and liver cell dysplasia (LCD) in 7.4%. These two possible preneoplastic lesions never occurred together. Of the men, 50.5% had been alcoholics or had drunk more than an average of 80 g of alcohol daily, and 65.3% had been smokers, as established by interviewing a family member or a close friend of the deceased. Hyperplastic nodules of clear cells were found in association with liver cirrhosis (p less than 0.005), liver enlargement (p less than 0.025), and heavy alcohol consumption (p less than 0.05), and tended (n.s.) to be associated with smoking. The largest nodules of clear cells were found in nodular regenerative hyperplasia of the liver in a male who had used testosterone. In another case focal nodular hyperplasia coexisted. Hyperplastic nodules showed no association with the occurrence of cavernous hemangioma or benign bile duct tumors. Males with hyperplastic nodules of clear cells were significantly (p less than 0.01) younger (average 49.3 years) than those with LCD (average 61.1 years). Males with LCD were slightly (p less than 0.05) older, tended to have a small-sized liver, but were otherwise comparable with males without precursor lesions. The present results indicate that both hyperplastic nodules and liver cell dysplasia are common findings in male autopsy series comprising alcoholics and smokers. Hyperplastic nodules were associated with some of the predisposing factors of primary hepatocellular carcinoma.
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PMID:Preneoplastic lesions of human liver. 357 Jan 37

In a family encompassing three generations, six of 11 evaluated members have two or three elements of a triad comprising adrenocortical micronodular dysplasia, mucocutaneous lentigines, and cardiac myxomas. Evaluation of the adrenals in affected members revealed characteristic pathologic lesions of micronodular adrenal hyperplasia and corticotropin-independent steroidogenesis that correlated with age, suggesting a progressive lesion that begins in early childhood. Since all subjects with micronodular hyperplasia and/or cardiac myxomas also had mucocutaneous lentigines, the skin lesions were markers for affected subjects. This family is one of the larger reported with this syndrome. Of special note was the finding of rare visceral tumors in affected family members, including melanocytic schwannomas and a fibrolamellar hepatoma, signaling another feature of the syndrome. Since 60% of this family encompassing three contiguous generations were affected, the syndrome appears to be inherited as an autosomal or X-linked dominant gene.
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PMID:Adrenocortical micronodular dysplasia, cardiac myxomas, lentigines, and spindle cell tumors. Report of a kindred. 382 21


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