Integration of hepatitis B virus and alteration of the 1p36 region found in cancerous tissue of primary hepatocellular carcinoma with viral replication evidenced only in noncancerous, cirrhotic tissue
✍ Scribed by Daniela Simon; Brian I. Carr
- Book ID
- 102854223
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 706 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
We have studied the genetic profile of the host genome and hepatitis B virus (HEW) in HBV-associated primary hepatocellular carcinoma (HCC). Comparative analyses of HCC cell line Hep 40 and the original biopsy specimens showed the episomal and replicating form of HBV only in the biopsy specimen from nontumor (NT) cirrhotic liver tissue, where a molecular change in the lp36 region was detected (NT tissue showed a normal 46XY karyotype). In contrast, only integrated HBV was detected in HCC tumor (T) tissue and Hep 40 cells. Two HBV integration sites were identical in HCC tissue and the hyperdiploid Hep 40 cell line, where genetic alteration in the lp36 region was identified. These data indicate that viral replication is ongoing only in NT cirrhotic-hyperplastic, chromosomally normal tissue with evidence for genetic instability. Only the tumor cell with altered genotype has virus integrated. (HEPATOLOGY 1995;22:1393-1398.)
Hepatocellular carcinoma (HCC) is a leading cause of cancer death worldwide and is strongly associated with chronic carriage of hepatitis B virus (HBV).',' There are currently an estimated 250 million acutely or chronically infected people in the world. Up to 10% of individuals initially infected with HBV become chronic carriers, a state that can lead to liver injury, cirrhosis, and HCC. However, no direct transforming activity has been demonstrated for any HBV gene product, nor is there evidence for an HBV-encoded oncogene, for an HBV integration mechanism that activates or represses any particular cellular gene, or for the forma-Abbreviations: HCC, hepatocellular carcinoma; HBV, hepatitis B virus; PB, peripheral blood; NT, nontumor; T, tumor; EBV, Epstein-Barn virus; LOH, loss of heterozygosity.
From the 'Medical College of Pennsylvania, Philadelphia, P A and the 'University of Pittsburgh,