Deletions in human chromosome arms 11p and 13q in primary hepatocellular carcinomas (original) (raw)
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1988
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Cytogenetics and Cell Genetics
Research Articles| May 09 2008
Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY
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Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY
Search for other works by this author on:
Cytogenetics and Cell Genetics (1988) 48 (2): 72–78.
Abstract
Normal liver and hepatocellular carcinoma (HCC) genotypes were compared at loci on most of the human chromosomes with probes that detect restriction fragment length polymorphisms. Six of fourteen tumors exhibited loss of heterozygosity of one or more markers on 11 p. Ten patients were informative for loci on 13q, and 5 of these 10 exhibited loss of heterozygosity for one or more of the 13q markers. Altogether, 9 of the 14 patients showed loss of a polymorphic allele for one or more loci on either 11p or 13q. A survey of loci on 16 additional chromosomes indicated that the deletions were not due to a general loss of heterozygosity in HCCs. Quantitative densitometry showed that each of the 10 deletions resulted in hemizygosity (no reduplication) of the remaining allele in tumor tissue. In contrast to hereditary embryonal tumors, in which reduplication of the remaining chromosome is the rule, simple deletion appears to be the primary mechanism responsible for the loss of heterozygosity in these adult, nonhereditary HCCs. These data show that HCCs arising in hepatitis B virus carriers are a genetically heterogeneous group of tumors, some of which may arise through 13q alterations, some through 11p alterations, some with both chromosomes altered, and some with both intact.
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© 1988 S. Karger AG, Basel
1988
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