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

It is well known that primary hepatocellular carcinoma could be derived from chronic hepatitis and liver cirrhosis in epidemiologic studies. However, it is still not clear what kinds of hepatocyte are premalignant cells. Recently we have focused on liver cell dysplasia as a possible premalignant cell, and showed localization of alpha-fetoprotein in the cytoplasma of these cells. Although the dysplastic cells were often seen in the liver of chronic active hepatitis, hepatitis B virus associated DNA polymerase activity was also significantly high in the sera from the patients with chronic active hepatitis. In this paper, we discuss the possible role of hepatitis B virus through hepatocarcinogenesis in human.
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PMID:Early lesions and development of primary hepatocellular carcinoma in man--association with hepatitis B viral infection. 7 Mar 87

Liver tissues of 180 autopsy cases of cirrhosis and hepatoma and 285 consecutive autopsy cases of other diseases were studied for liver cell dysplasia correlated with hepatitis B surface and core antigens (HBsAg and HBcAg) in liver cells and sera, and antibody to HBsAg (anti-HBs) in sera. Liver cell dysplasia was characteristic in cirrhotic livers, particularly with hepatoma. No significant difference was found in age and sex between cirrhotic cases with and without dysplasia. Rate of positive HBsAg in liver cells and sera was significantly high in cirrhotic cases with dysplasia with or without hepatoma. Massive pattern distribution of orcein-positive liver cells was statistically significant in cirrhotic livers with or without hepatoma, but morphological characteristics of orcein-positive liver cells could not be correlated in significance with dysplasia and hepatoma. HBcAg showed neither correlation with liver cell dysplasia nor hepatoma. It appears to correlate with active cirrhosis, marked liver cell degeneration and necrosis, and membranous diffuse type HBsAg in liver cells.
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PMID:Liver cell dysplasia and hepatitis B surface and core antigens in cirrhosis and hepatocellular carcinoma of autopsy cases. 21 29

Knowledge of the cellular changes that lead to hepatic neoplasia in humans is limited. Cirrhosis is a common antecedent or accompaniment of liver cell carcinoma and it seems that both its etiology and its time of duration are relevant risk factors. Many cellular changes have been observed in patients and among populations considered to be at risk. Of these, liver cell dysplasia is the most striking, and studies of its prevalence, natural history, and association with particular forms of cirrhosis suggest that it is a precancerous change. Bile duct carcinoma may follow infestation with liver flukes and duct epithelial hyperplasia is present before the development of cancer. Angiosarcoma from several causes is commonly preceded by a peculiar fibrosis, vascular changes, and Kupffer cell hyperplasia.
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PMID:Precancerous changes in the human liver. 22

Liver cell dysplasia was noted on histological examination of nontumorous liver from 24 of 50 (48%) black southern African males with hepatocellular carcinoma (HCC). Macronodular cirrhosis was present in 40 (80%). There was no statistically significant difference between the frequency of dysplasia in 50% of 40 cirrhotic and 40% of 10 noncirrhotic livers, or in 52.6% of 38 hepatitis B antigen (HBAg) positive and 33.3% of 12 HBAg negative HCC patients. HBAg positivity was present in 80% of 40 cirrhotic and in 60% of 10 noncirrhotic HCC patients. This lack of significant correlation between liver cell dysplasia, and both cirrhosis and HBAg positivity in HCC patients in contrast to findings in Uganda and the United States, suggests a different pathogenetic mechanism for dysplasia in southern Africa. Liver cell dysplasia in man appears to be analogous to preneoplastic experimentally-induced hyperplastic foci or areas.
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PMID:Liver cell dysplasia: association with hepatocellular carcinoma, cirrhosis and hepatitis B antigen carrier status. 22 74

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94

The histopathology of acute and chronic infections associated with viral hepatitis is reviewed and illustrated. Particular attention is directed to changes that help to differentiate chronic persistent from chronic active viral hepatitis. Features that help to identify the intravenous drug abuser who has hepatitis, whether acute or chronic, include the presence of particulate birefringent material (usually talc) in reticuloendothelial cells, as well as tissue eosinophilia. Ground-glass hepatocytes are characteristic of the HBAg carrier. They may be present in chronic persistent and chronic active hepatitis and in cirrhotic livers with or without hepatocellular carcinoma. Ground-glass cells which contain the surface component of the HBAg, can be stained specifically by a number of stains that include aldehyde fuchsin and orcein. The cirrhotic liver of the HBAg-seropositive patient may show liver-cell dysplasia, a premalignant change.
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PMID:Light microscopic morphology of viral hepatitis. 80 46

Hepatocellular carcinoma and obliterated hepatic bile duct were found at postmortem examination in a 4-year-old girl with arteriohepatic dysplasia (Alagille's syndrome). AFP level was extremely high. Liver cirrhosis was present on percutaneous needle biopsy 9 months before she succumbed in progressive liver failure. Episodes of repeated gastrointestinal, life-threatening hemorrhages occurred during the last 6 months of her life. Histopathologic findings of the eyes were documented at autopsy.
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PMID:Hepatocellular carcinoma associated with arteriohepatic dysplasia in a 4-year-old girl. 130 8

Liver cell dysplasia is characterized by hepatocellular foci with nuclear atypia. It is often seen in cirrhosis and may be a precursor of hepatocellular carcinoma (HCC). To determine whether liver cell dysplasia is DNA aneuploid, 72 sections of 33 cirrhotic livers from the autopsy files of The Johns Hopkins Hospital were studied, and 14 foci of dysplasia from 13 cirrhotic livers were selected. Patients ranged in age from 32 to 70 years. Histologically, there were 10 foci of low-grade dysplasia and four foci of high-grade dysplasia. Nine HCCs served as positive controls; seven autopsy livers with no morphologic or clinical evidence of primary liver disease served as negative controls. One focus of HCC and one focus of dysplasia were unsatisfactory for analysis. Flow cytometric examination demonstrated subpopulations with DNA abnormality in four of nine (44%) foci of low-grade dysplasia, of which three were aneuploid. Three of four (75%) foci of high-grade dysplasia were aneuploid. Six of eight (75%) HCCs showed DNA abnormality, of which five were aneuploid. DNA aneuploidy was not present in the seven control livers; however, one showed DNA abnormality. We conclude that liver cell dysplasia is a morphologic entity that contains DNA aneuploid cells, a feature that supports the role of liver cell dysplasia in the evolution of HCC.
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PMID:Liver cell dysplasia: a DNA aneuploid lesion with distinct morphologic features. 131 76

Liver-cell dysplasia is a well known histological entity with preneoplastic significance in experimental hepatic carcinogenesis. However, while the association of liver-cell dysplasia with hepatitis B virus can be considered as established, it is still controversial whether this lesion represents a premalignant condition in cirrhotic patients. Efforts have been made to render its morphological assessment more reliable, but no firm conclusions can be drawn from the available clinical studies, which are mainly retrospective or based on autopsy series. Preliminary results from a prospective study argue that liver-cell dysplasia is associated with an increased risk to hepatocellular carcinoma. The emergence of liver-cell dysplasia as a preneoplastic lesion in cirrhotic patients will have some impact in the future on their management, including selection for closer monitoring in early detection of hepatocellular carcinoma and for liver transplantation.
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PMID:Liver-cell dysplasia and hepatocellular carcinoma. 131 75

From January 1977 to June 1990, 1,670 patients with a liver mass or masses underwent transabdominal fine needle aspiration biopsy of the liver. Of those cases, 99 were diagnosed cytologically as "hepatocellular carcinoma" and 9 as "consistent with liver cell adenoma." Among the 99 patients with hepatocellular carcinoma, 3 were users of oral contraceptives. The nine patients with liver cell adenoma were all users of oral contraceptives. Of them, two developed foci or areas of liver cell dysplasia within the adenomas. The mean periods of oral contraceptive use among these three groups of patients were different. It appeared that patients started to develop liver cell adenoma after five years of oral contraceptive use (mean, 6.3 years). Foci or areas of liver cell dysplasia began to arise within liver cell adenomas after 8 years of oral contraceptive use (mean, 9 years), and the patients started to develop hepatocellular carcinoma after 10 years of contraceptive use (mean, 11 years). The cytologic features of liver cell dysplasia strikingly mimicked those of hepatocellular carcinoma. From this study, the foci or areas of liver cell dysplasia appear to be the missing link responsible for the transformation of liver cell adenoma to carcinoma. It is believed that liver cell adenomas are not premalignant and may undergo reversible change after withdrawal of causative agents, whereas foci or areas of liver cell dysplasia within the adenomas are irreversible, premalignant changes and may transform into hepatocellular carcinoma.
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PMID:Are oral contraceptive-associated liver cell adenomas premalignant? 131 28


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