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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the clinical, prognostic, aetiological and pathological features of 41 consecutive British patients with hepatocellular carcinoma (HCC). Presenting symptoms were often vague, and patients were generally in poor condition at diagnosis, 56% being of WHO grade 2 performance score or higher. Ascites (46%) and jaundice (35%) were often present at diagnosis, and the median duration of survival from diagnosis was only 6 weeks. Only initial performance grade (p less than 0.0001) and serum bilirubin concentration (p = 0.02) significantly affected prognosis. Serum alphafoetoprotein (AFP) was positive by counter-immune electrophoresis in only 34%, but increased to 68% when radioimmunoassay was used. Cirrhosis was present in 33 patients (80%) and was most often cryptogenic (12) or alcoholic (7) in origin. Serum HBsAg was detected in 5 patients (12%) and, of the remainder tested, 21% had serological evidence of past HBV exposure. None of 8 serum HBsAg-negative tumour specimens had detectable HBV-DNA integration into the tumour cell genome. Liver-cell dysplasia was noted in 56% of patients with liver biopsies predating the diagnosis of HCC, and in 78% of biopsies taken at the time of HCC diagnosis. The commonest histological pattern was trabecular (71%). Other forms were rare; the fibrolamellar pattern was only seen in 2 patients.
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PMID:Hepatocellular carcinoma: clinical, aetiological and pathological features in British patients. 282 43

Hepatocellular carcinoma (HCC) associated with chronic hepatitis B virus (HBV) infection in Yupik Eskimos in southwestern Alaska, detected in early stages as a result of screening, appears to be more frequently associated with variants of chronic portal inflammation in the noninvolved liver than with fully developed cirrhosis, otherwise common in HBV-associated HCC from other geographic areas. Of 38 patients diagnosed with HCC since 1969, adequate tissue was available from both the tumor and nontumorous liver in 17. Of the 17 specimens, 14 had chronic portal inflammation and three had advanced cirrhosis; 12 of the 14 were from hepatitis B surface antigen carriers. These 12 cases were studied in detail to examine the features accompanying the development of HCC unobscured by cirrhotic transformation. In the noninvolved parenchyma they included hepatocytic nodules as apparent precursors to HCC and, as markers of phenotypic alterations, dysplastic hepatocytes and hepatitis B surface antigen-laden ground-glass hepatocytes. The latter were observed in eight instances and often accumulated in nodules. Parenchyma within 1 mm of the HCC exhibited increased confluent hyperplasia and frequently conspicuous necroinflammation associated with pericellular and periductular fibrosis, which contributed, in addition to fibrous connections between displaced and heavily inflamed portal tracts, to the capsule that was forming in all cases to varying degrees in the pericarcinomatous region. The HCC was uniformly trabecular and in a few specimens, a continuous transition from hyperplasia and dysplasia near the periphery of the tumor to increasing anaplasia in the center could be made out in addition to pressure effects of the HCC. The pericarcinomatous changes, including hyperplasia progressing to neoplasia and necroinflammation, are also observed in experimental models, particularly the woodchuck HCC induced by a hepadna virus related to HBV. Coordinated morphologic and molecular biologic studies on such animal models and on human HCC detected by screening, as for instance in Eskimos, neither complicated by cirrhosis, should elucidate the direction of the evolution of the HCC and the postulated promoting role of the inflammation.
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PMID:Evolution of hepatocellular carcinoma associated with chronic hepatitis B virus infection in Alaskan Eskimos. 283 72

Thirty-seven cases of cirrhosis with large liver cell dysplasia (LLCD) were evaluated by morphometric analysis and the results compared with those in 11 cases of hepatitis B surface antigen (HBsAg)-positive cirrhosis, 12 cases of cirrhosis with nodules of active regeneration, 15 cases of hepatocellular carcinomas, and 15 cases of inactive cirrhosis. The nuclear-cytoplasmic, nucleolar-cytoplasmic, and nucleolar-nuclear ratios of LLCD were significantly higher than those observed in all other nonneoplastic groups. Whereas the nuclear-cytoplasmic and nucleolar-cytoplasmic ratios of hepatocellular carcinoma cells were significantly higher than those measured in dysplastic cells, the latter had a nucleolar-nuclear ratio similar to that of neoplastic cells. These results show that, in contrast to previously accepted criteria, the nuclear-cytoplasmic ratio of LLCD is increased and that some morphometric features of LLCD are consistent with its supposed premalignant nature. The usefulness of a morphometric analysis in evaluating any group of abnormal-appearing hepatocytes is stressed.
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PMID:A morphometric study of liver cell dysplasia. 277 46

The classical morphological criteria in the diagnosis of hepatocellular carcinoma (HCC) include: (a) the similarity of tumor cells to hepatic cord cells; (b) the trabecular nature of the growth with capillary and canaliculi formation, and (c) the intravascular growth of trabecular carcinoma. These criteria apply to the most common variants of HCC but they do not suffice in all cases. That makes additional criteria and certain refinements necessary. A promising approach to the diagnosis of HCC is that based upon consideration by the pathologist of some relevant aspects of the natural history of this tumor. A panel of tests exploring the various functions and properties of liver cells should be set up. Tests for bile and fibrinogen synthesis are most important because they reflect specific and exclusive properties of the original cell line. Bile synthesis in tumor tissue is reflected by the finding of cholecholatestasis, namely bilirubinostasis and retention of copper and copper-binding proteins. The positive immunostaining for fibrinogen may appear in the form of cytoplasmic granules occurring in 50% of HCC, or in the form of fibrinogen-ground-glass (G-G) inclusions, representing a specific feature of HCC. During neoplastic transformation oncofetal proteins may reappear, alpha-fetoprotein (AFP) being very common. Despite sensitivity of AFP, this test, similar to alpha-1-antitrypsin (AAT), has very low specificity, because of the widespread occurrence of these proteins in a variety of tumors. The selection of special 'clones' such as Mallory bodies and fibrinogen-G-G is of particular value, because of the specificity of these peculiar cytoplasmic changes. Although rare, the presence of HBV antigens in tumor tissue is virtually pathognomonic for HCC. The availability of nonneoplastic liver tissue for morphological examination is of great help, because it may carry key information or markers of the development stages of HCC: cirrhosis, liver cell dysplasia, HBV antigens, congenital metabolic disorders, such as hemochromatosis and AAT deficiency. The two latter conditions represent the link with the last working hypothesis of the present study, i.e. that during neoplastic transformation hepatocytes may 'switch' their 'phenotype' thus escaping the storage phenomena, which continue to occur in nonneoplastic hepatocytes. This study provides a guideline to a dynamic approach to the diagnosis of HCC. The rationale is listed in 5 points; among them, bile production, fibrinogen synthesis, Mallory body and fibrinogen-G-G selection, HBV antigen expression can be considered at present as confident markers for the morphological diagnosis of HCC.
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PMID:Natural history of hepatocellular carcinoma as viewed by the pathologist. 283 13

In order to characterize the cytological features of highly differentiated hepatocellular carcinoma (HCC), a comparative morphometric study was made by observing 30 cases of HCCs and controls (normal, cirrhotic, and atrophic livers). Among trabecular HCCs, normotrabecular subtype (1-2 cell thick cell plate) usually showed minimal cytological atypism and was categorized as well or highly differentiated HCC. Using an image analyzer, the following 4 parameters were applied to quantitate the hepatocyte changes: mean cell size (C), mean nuclear size (N), nucleocytoplasmic (N/C) ratio and a coefficient of variance (CV = index of anisokaryosis). In normotrabecular HCCs, C was slightly but significantly reduced when compared with normal and cirrhotic livers (t-test: p less than 0.005). The value was further reduced in mid- and macrotrabecular HCCs. Normotrabecular HCCs showed almost the same N value as normal and cirrhotic livers but displayed significantly a higher N/C value than those of controls (t-test: p less than 0.001). The N/C ratio became even greater in other types of HCCs. While CV was relatively constant in other HCC groups and controls, it was extremely high in the pleomorphic type of HCC and liver cell dysplasia. The results indicated that a reduction in C and increase in N/C ratio, which appear as "nuclear crowding" in histological specimens, actually occurs in well differentiated HCC. For the histologic diagnosis of well differentiated HCC, it would be very important to examine liver specimens with these observations in mind.
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PMID:Morphometric analysis of hepatocellular carcinoma. 284 43

A series of 54 liver biopsy specimens was studied by means of the argyrophil (AgNOR) technique for nucleolar organiser region (NOR)-associated proteins. These included normal livers and livers affected by chronic active hepatitis, cirrhosis, hepatocellular carcinoma and adenoma. Four of the cases of cirrhosis showed liver cell dysplasia. The mean numbers of NOR sites in normal, cirrhotic, and carcinomatous livers were significantly different: adenoma had similar mean counts to those in chronic active hepatitis (CAH). There was no overlap between the ranges of NOR counts in normal, cirrhotic, and malignant liver specimens. Where cirrhosis and hepatocellular carcinoma were present in the same specimen, the AgNOR counts were higher in the carcinomatous than cirrhotic areas. To investigate the prospective value of the method a further seven biopsy specimens were studied; in these it had not been possible to decide on a diagnosis between normality and cirrhosis or cirrhosis and hepatocellular carcinoma. In all seven specimens a repeat biopsy or necropsy gave results as predicted by AgNOR staining. It is therefore proposed that quantitation of staining for NOR-associated proteins is a diagnostically useful method in liver disease.
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PMID:Nucleolar organiser regions in normal, cirrhotic, and carcinomatous livers. 284 58

This paper reports the study of liver cell dysplasia in cases of hepatic cirrhosis, cirrhosis associated to hepatocellular carcinoma and hepatocellular carcinoma without cirrhosis. The frequency of the lesion was higher in cases of hepatic cirrhosis and hepatocellular carcinoma associated (84.2%), compared to the other groups. The search for evidence of B virus infection (AgHbs) was positive in 72.7% of the cases with liver cell dysplasia. It is pointed out the relation of liver cell dysplasia, to hepatocellular carcinoma and B virus infection.
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PMID:[Hepatic cell dysplasia. A pre-malignant lesion related to hepatocellular carcinoma and infection by hepatitis B virus]. 284 24

We studied the expression of villin, a microfilament-associated, actin-binding protein typical of brush-border microvilli, in a variety of human carcinomas by applying immunofluorescence microscopy to frozen sections and immunoblotting methods to tissue extracts using a rabbit antiserum and a monoclonal antibody specific for villin. All of the 24 primary and metastatic colorectal adenocarcinomas tested were uniformly and strongly positive for villin, with the immunocytochemical labeling concentrated at the luminal cell margin. In poorly differentiated tumor areas, rudimentary tubules were stained. All of the six tubular adenocarcinomas of the stomach studied as well as two adenocarcinomas of the gall bladder and a hepatocellular carcinoma were also villin-positive. Villin was detectable in 12 of 14 adenocarcinomas of the pancreas; in some of these cases, its distribution was heterogeneous. Among 21 renal cell carcinomas investigated, positivity for villin was seen in nine of 13 clear cell tumors (especially those of grade II), and in all four chromophilic cell tumors; however, all four chromophobe cell tumors studied were negative. Four of 11 endometrial but none of nine ovarian carcinomas were (uniformly or focally) villin positive. Of 18 adenocarcinomas of the lung studied, one was uniformly and four focally positive for villin, while the remainder were negative. All of the other epithelial tumors studied, including 12 adenocarcinomas of the breast and seven epithelial or biphasic pleural mesotheliomas, were villin negative. Our results show that the expression of villin in intestinal epithelial cells is consistently maintained in their corresponding carcinomas, even when the organized brush-border structure has been lost. The presence of villin in some endometrial and pulmonary adenocarcinomas--in contrast to its absence in the respective normal epithelia--suggests that this protein is newly expressed during hyperplasia, dysplasia, or carcinogenesis. Determining the presence or absence of villin and its immunocytochemical staining pattern in metastatic adenocarcinomas may be of some help in determining the type and site of the primary tumor.
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PMID:Villin: a cytoskeletal protein and a differentiation marker expressed in some human adenocarcinomas. 289 90

Liver cell dysplasia (LCD) was found in 28 (60%) of 47 patients with hepatocellular carcinoma (HCC); 22 (79%) of them had associated liver cirrhosis. LCD was more frequently observed in posthepatitic cirrhosis (82%) than in the other forms. Carcinoembryonic antigen (CEA), alpha-1-antitrypsin (AAT) and alpha-fetoprotein (AFP), as demonstrated by the peroxidase-antiperoxidase method, were similarly expressed both in normal and in dysplastic cells. Hepatitis B surface antigen was found in eight cases (17%), six of which were associated with LCD. HBsAg was rarely found in dysplastic cells and frequently displayed a peculiar perinuclear pattern. The possible preneoplastic role of LCD is stressed.
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PMID:Liver cell dysplasia and hepatocellular carcinoma: a histological and immunohistochemical study. 298 89

Karyometric analysis was performed with respect to anisonucleosis, nuclear deformity and DNA content in cases of liver cell dysplasia (LCD) and hepatocellular carcinoma (HCC). Presence or absence of iron deposition in foci of LCD and HCC was also evaluated in siderotic livers. All LCDs showed marked anisonucleosis and marked increases in DNA content but slight increases in nuclear deformity. A tendency was noted in which the nuclear deformity was increased as the nuclei became larger. In contrast, HCCs showed wide ranges of anisonucleosis, nuclear deformity and DNA content. Hepatocellular carcinomas having marked anisonucleosis similar to that of LCD showed markedly increased nuclear deformity. However, unlike LCD, this increase was independent of their nuclear size. In the siderotic livers iron deposition was noted in the foci of LCD but not in the foci of HCC. These findings do not support the notion of LCD being precancerous.
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PMID:Karyometric analysis of liver cell dysplasia and hepatocellular carcinoma. Evidence against precancerous nature of liver cell dysplasia. 298 18


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