Carcinogenesis, Vol. 20, No. 11, 2083-2088,
November 1999
© 1999 Oxford University Press
Cancer Biology |
Gain of chromosomes 15 and 19 is frequent in both mouse hepatocellular carcinoma cell lines and primary tumors, but loss of chromosomes 4 and 12 is detected only in the cell lines
Department of Pathology, Asahikawa Medical College, 4-5-3-11 Nishikagura, Asahikawa 078-8510 and
1 Department of Developmental Biology and Oncology, Division of Molecular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan
Chromosomal alterations were investigated in hepatocellular carcinoma cell lines, primary tumors and liver epithelial cell lines derived from normal livers of C57BL/6JxC3H/HeJ F1 and C3H/HeJxC57BL/6J F1 mice. In the primary tumors, non-random gain of chromosomes 15 and 19 was found in seven and five of 14 hepatocellular carcinomas, respectively. On the other hand, in the cases of both liver epithelial and hepatocellular carcinoma cell lines, frequent changes were loss of chromosomes 4 (4/9 cell lines) and 12 (3/9) as well as gain of chromosomes 15 (5/9) and 19 (4/9). These results indicate that the chromosomal gain is associated with both in vivo carcinogenesis and establishment of cell lines, while the loss is specific for the latter. PCR analysis using polymorphic microsatellite DNA markers revealed that the loss of chromosome 12 as well as chromosome 4 was much more frequent for the C57BL/6J hepatocarcinogenesis-resistant rather than the susceptible C3H/HeJ strain.
Abbreviations: B6, C57BL6/J; B6C3F1, C57BL6/JxC3H/HeJ F1; C3H, C3H/HeJ; C3B6F1, C3H/HeJxC57BL/6J F1; DEN, diethylnitrosamine; HCC, hepatocellular carcinoma; LE, liver epithelial; LOH, loss of heterozygosity.
2 To whom correspondence should be addressedEmail: ogawak{at}asahikawa-med.ac.jp
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