Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinicopathologic relevance of the hepatic expression of Lewis Y (Le(y)), a carbohydrate antigen, and its plasma levels was studied in benign and malignant liver diseases. Tissue and plasma antigens, respectively, were determined with an avidin-biotin-peroxidase complex method and a radioimmunoassay using monoclonal antibody AH6. Normal liver cells and bile ductules did not express Le(y). In the inflammatory tissues, the liver cells and proliferated bile ductules expressed Le(y). The strongest expression by the liver cells was observed in chronic active hepatitis with severe activity and that by the ductules in liver cirrhosis. Only 1 of 16 hepatocellular carcinomas expressed Le(y). The plasma levels of Le(y) increased significantly but nonspecifically in chronic persistent hepatitis, chronic active hepatitis, liver cirrhosis, and hepatocellular carcinomas. It was concluded that (1) Le(y) is an inflammation-associated but not a cancer-associated antigen; (2) the more the tissue damage advances, the more the antigen is expressed; and (3) hepatic and plasma Le(y) are, however, nonspecific markers of necroinflammatory liver diseases.
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PMID:Hepatic neoexpression and increased plasma levels of Lewis Y, a carbohydrate antigen, in chronic inflammatory liver diseases. 804 85

Infection of Hepatitis B Virus (HBV) is a risk factor of chronic active hepatitis (CAH), hepatic cirrhosis and hepatocellular carcinoma (HCC). Infection of HBV may develop to HCC without antecedent hepatic cirrhosis. Pathogenesis of HBV causing malignant changes has not been fully understood. HBx, a protein of HBV, is an activator of transcription process involved in hepatocarcinogenesis. Most of human cancer associated with mutation of p53, a Tumor Suppressor Genes, a protein serves as cellular protection for growth and cell division, which is one of predisposition factor of hepatocarcinoma. Some studies indicate the correlation between mutation / inactivation of p53 and HBV protein x (HBx) in hepatocarcinogenesis. In that process, HBx will suppress p53 function, which will lead to ineffective liver cell division and resulting in HCC.
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PMID:Hepatocarcinogenesis in viral Hepatitis B infection: the role of HBx and p53. 1695 33