Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Long-Evans with a cinnamon-like color (LEC) rat is a mutant of the Long-Evans strain that develops hereditary hepatitis and hepatoma with ageing. Age-related changes in the mRNA expression of DNA methyltransferase (DNA MTase) were examined in livers of LEC rats using Long Evans with an agouti color (LEA) rats as controls. A dramatic increase in the expression of this mRNA was observed in LEC rats at 20 weeks when acute hepatitis appeared. Their high mRNA levels were maintained until 52 weeks of age. The mRNA expression as well as DNA MTase activities were found to be higher in cancer lesions than in adjacent normal tissue. These increases may be related to liver regeneration and to early events in cellular transformation of LEC rats.
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PMID:Expression of DNA methyltransferase in LEC rats during hepatocarcinogenesis. 847 22

Hepatocellular carcinoma (HCC) usually develops on the basis of chronic hepatitis and liver cirrhosis, where inactivation of several tumor suppressor genes (TSGs) takes place via methylation of the promoter. Interestingly, these methylation events are more prevalent in a background liver at high risk of HCC than one at low risk. Abnormal methylation is also observed in precancerous nodules such as dysplastic nodules and adenomas, suggesting that epigenetic alteration is an early event for HCC carcinogenesis. It is possible that infection with the hepatitis virus induces alteration of methylation at promoters of TSGs. Some studies suggested that viral proteins interfere with DNA methyltransferase in chronic hepatitis B. Induction of epigenetic alteration in chronic hepatitis C might, however, might be a consequence of oxidative stress. In addition, we proposed age should be taken into consideration for HCC development via epigenetic pathways. Further investigations are required to understand the mechanism of inducing epigenetic instability during hepatocarcinogenesis.
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PMID:Impact of hepatitis virus and aging on DNA methylation in human hepatocarcinogenesis. 2023 2

Alterations in DNA methylation, which are associated with DNA methyltransferase abnormalities and result in silencing of tumor-related genes and chromosomal instability, are involved even in precancerous changes in various organs. DNA methylation alterations also account for the histological heterogeneity and clinicopathological diversity of human cancers. Therefore, we have analyzed DNA methylation on a genome-wide scale in clinical tissue samples. Our approach using the bacterial artificial chromosome array-based methylated CpG island amplification method has revealed that DNA methylation alterations correlated with the future development of more malignant cancers are already accumulated at the precancerous stage in the kidney, liver and urinary tract. DNA methylation profiles at precancerous stages are basically inherited by the corresponding cancers developing in individual patients. Such DNA methylation alterations may confer vulnerability to further genetic and epigenetic alterations, generate more malignant cancers, and thus determine patient outcome. On the basis of bacterial artificial chromosome array-based methylated CpG island amplification data, indicators for carcinogenetic risk estimation have been established using liver tissue specimens from patients with hepatitis virus infection, chronic hepatitis and liver cirrhosis or histologically normal urothelia, and for prognostication using biopsy or surgically resected specimens from patients with renal cell carcinoma, hepatocellular carcinoma and urothelial carcinoma. Such genome-wide DNA methylation profiling has now firmly established the clinical relevance of translational epigenetics.
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PMID:DNA methylation profiles in precancerous tissue and cancers: carcinogenetic risk estimation and prognostication based on DNA methylation status. 2212 5