Source:http://linkedlifedata.com/resource/pubmed/id/12969185
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2003-9-12
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| pubmed:abstractText |
To test the hypothesis that hepatitis C virus (HCV) might induce hepatocyte proliferation directly, thereby predisposing HCV carriers to cirrhosis and hepatocellular carcinoma, we have used a new method to identify proliferating hepatocytes, employing a novel monoclonal antibody to minichromosome maintenance (Mcm) proteins, essential components of the pre-replication complex. Antibody to Ki-67, a conventional marker of cell division, was also studied. Eighty-seven patients with chronic HCV infection and a broad spectrum of histological change were studied. Proliferation was observed rarely in hepatocytes from normal liver from healthy controls (always less than 0.01%). However, proliferating hepatocytes were detected in all HCV-infected patients and the proportion of hepatocytes expressing Mcm-2 (3-40%) always exceeded that expressing Ki-67 (1-14%) and correlated positively with increasing stage of fibrosis (P = 0.0001) and viral replication (P = 0.0004). There were weaker but significant associations between the proportion of hepatocytes expressing Mcm-2 and inflammatory indices including interface hepatitis, portal tract inflammation, lobular inflammation and steatosis. There was no association between the proportion of hepatocytes expressing Mcm-2 and age, gender or past alcohol consumption, but there was a weak association with current consumption of alcohol (P = 0.0067). The proportion of Ki-67 hepatocytes did not correlate with any clinical, laboratory or histological parameter. Mcm-2 was also detected in bile duct cells, sinusoidal lining cells and infiltrating lymphocytes, but at low frequency. These data indicate first, that Mcm-2 is a more sensitive marker of hepatocyte proliferation than Ki-67, second that many hepatocytes in chronic HCV infection have entered the cell cycle and third, suggest that interference with the hepatocyte cell cycle might be an alternative approach to therapy.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1352-0504
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
10
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
345-50
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading |
pubmed-meshheading:12969185-Adult,
pubmed-meshheading:12969185-Aged,
pubmed-meshheading:12969185-Aged, 80 and over,
pubmed-meshheading:12969185-Alcohol Drinking,
pubmed-meshheading:12969185-Biological Markers,
pubmed-meshheading:12969185-Biopsy,
pubmed-meshheading:12969185-Cell Division,
pubmed-meshheading:12969185-Disease Progression,
pubmed-meshheading:12969185-Female,
pubmed-meshheading:12969185-Hepatitis C, Chronic,
pubmed-meshheading:12969185-Hepatocytes,
pubmed-meshheading:12969185-Humans,
pubmed-meshheading:12969185-Ki-67 Antigen,
pubmed-meshheading:12969185-Liver Cirrhosis,
pubmed-meshheading:12969185-Male,
pubmed-meshheading:12969185-Middle Aged,
pubmed-meshheading:12969185-Nuclear Proteins,
pubmed-meshheading:12969185-Virus Replication
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| pubmed:year |
2003
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| pubmed:articleTitle |
Improved detection of hepatocyte proliferation using antibody to the pre-replication complex: an association with hepatic fibrosis and viral replication in chronic hepatitis C virus infection.
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| pubmed:affiliation |
Department of Histopathology, Addenbrooke's Hospital, Cambridge, UK.
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| pubmed:publicationType |
Journal Article
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