AI Article Synopsis
- - Human hepatocellular carcinomas (HCCs) develop from chronic hepatitis and cirrhosis, primarily due to viral infections like hepatitis B (HBV) and hepatitis C (HCV), though the exact mechanisms behind these processes are still unclear.
- - Chronic hepatitis promotes HCC by causing cell damage and increased cell division, leading to genetic changes in liver cells, while also creating chromosomal instability through specific proteins.
- - The research aims to shift the "hypercarcinogenic state" caused by prolonged hepatitis to a "normo- or hypocarcinogenic" state in order to prevent the development of HCC.
Article Abstract
Human hepatocellular carcinomas (HCCs) are preceded by chronic hepatitis and cirrhosis. Despite a clear viral etiology (hepatitis B virus [HBV] and hepatitis C virus [HCV] of human hepatocarcinogenesis, the mechanism is complex and the distinct molecular pathway or molecules that explain this phenomenon are not yet known. Viral hepatitis, "inflammation-mediated" hepatocarcinogenesis, greatly influences the incidence of somatic genetic events in hepatocytes, by increasing the number of target cells or the proliferation of once-hit hepatocytes, eventually leading to HCC. We propose that hepatitis virus can cause HCC by a combination of two mechanisms; (i) cell killing and stimulation of mitosis, leading to an accumulation of events necessary for transformation; and (ii) an increase in chromosomal instability mediated by induced recombinogeneic protein(s) during chronic hepatitis. These conditions may be designated as the "hypercarcinogenic state". Our goal is to change the "hypercarcinogenic state" to the "normo- or hypocarcinogenic" state and to prevent HCC development.
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| http://dx.doi.org/10.1007/s005350200149 | DOI Listing |
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