AI Article Synopsis
- The study investigated hepatocellular carcinoma (HCC) in woodchucks infected with the woodchuck hepatitis virus (WHV) and the role of cellular oncogenes in tumor development.
- Enhanced expression and alterations of the c-myc oncogene were found in some HCC cases, with transcript sizes varying significantly and expression levels much higher than normal liver tissue.
- The research revealed unique rearrangements of the c-myc gene, similar to those seen in human cancers like Burkitt's lymphoma and acute leukaemias, while confirming that WHV did not directly cause these alterations.
Article Abstract
Hepatocellularcarcinoma (HCC) that occur in woodchucks chronically infected with woodchuck hepatitis virus (WHV) were screened for activation of cellular oncogenes. Enhanced expression and allelic alterations of the c-myc oncogene were found in three HCC out of nine. Variations in the size of the c-myc transcripts, ranging from 2.0 kilobases (kb) to 5.6 kb, as well as in the level of c-myc gene expression, 5-50-fold higher than in adjacent liver tissues, were observed among the three HCC. Rearrangements of the c-myc locus were either upstream of the gene or within the first intron. Cloning and sequencing of the break-point region from one of the three tumours showed that the c-myc gene was truncated and joined to a unique cellular sequence of unknown function. WHV DNA was not integrated near the c-myc coding exons, excluding a direct role of the virus in c-myc activation. The novel type of rearrangement and activation of the c-myc gene, reported here in liver tumours of hepatitis virus infected animals, appears strikingly similar to those resulting from chromosomal translocations in human Burkitt's lymphomas, acute B- and T-cell leukaemias and mouse plasmacytomas.
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| http://dx.doi.org/10.1038/324276a0 | DOI Listing |
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