1992Journal of Gastroenterology and HepatologyRequires access

Loss of heterozygosity on chromosome 16 in hepatocellular carcinoma

K Sakai, Hikaru Nagahara, Kohji Abe, Hiroshi Obata

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Abstract

In order to understand the molecular genetics of human hepatocellular carcinoma (HCC) a common chromosomal abnormality in HCC was examined using restriction fragment length polymorphism (RFLP) analysis. Sixty-eight HCC specimens were examined for loss of heterozygosity at 11 different chromosomal arms including 1p, 5p, 11p, 11q, 13q, 14q, 15q, 16p, 16q, 18q, and 19q. Losses were not detected on chromosome 1, 5, 14, 15 or 19, and the frequencies of losses were low (11-19%) for chromosomes 11, 13 and 18. In contrast, loss of heterozygosity was frequently observed for three different loci on chromosome 16, the HBA locus at 16p13.3 (22%), the MT2 locus at 16q21-22.1 (15%) and the HP locus at 16q22.1-22.2 (39%). There was no remarkable difference in the frequencies of loss of heterozygosity at these loci among HBV related HCC, HCV related HCC and neither virus (NBNC) related HCC. Thus, the results indicate that at least three different genetic abnormalities in chromosome 16 are commonly observed in various HCC, and that this chromosome may have some important role(s) in recessive genetic changes which generate this tumour.

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What this paper is about

In order to understand the molecular genetics of human hepatocellular carcinoma (HCC) a common chromosomal abnormality in HCC was examined using restriction fragment length polymorphism (RFLP) analysis. Sixty-eight HCC specimens were examined for loss of heterozygosity at 11 different chromosomal arms including 1p, 5p, 11p, 11q, 13q, 14q, 15q, 16p, 16q, 18q, and 19q. Losses were not detected on chromosome 1, 5, 14, 15 or 19, and the frequencies of losses were low (11-19%) for chromosomes 11, 13 and 18. In contrast, loss of heterozygosity was frequently observed for three different loci on chromosome 16, the HBA locus at 16p13.3 (22%), the MT2 locus at 16q21-22.1 (15%) and the HP locus at 16q22.1-22.2 (39%). There was no remarkable difference in the frequencies of loss of heterozygosity at these loci among HBV related HCC, HCV related HCC and neither virus (NBNC) related HCC. Thus, the results indicate that at least three different genetic abnormalities in chromosome 16 are commonly observed in various HCC, and that this chromosome may have some important role(s) in recessive genetic changes which generate this tumour.

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Available abstract

In order to understand the molecular genetics of human hepatocellular carcinoma (HCC) a common chromosomal abnormality in HCC was examined using restriction fragment length polymorphism (RFLP) analysis. Sixty-eight HCC specimens were examined for loss of heterozygosity at 11 different chromosomal arms including 1p, 5p, 11p, 11q, 13q, 14q, 15q, 16p, 16q, 18q, and 19q. Losses were not detected on chromosome 1, 5, 14, 15 or 19, and the frequencies of losses were low (11-19%) for chromosomes 11, 13 and 18. In contrast, loss of heterozygosity was frequently observed for three different loci on chromosome 16, the HBA locus at 16p13.3 (22%), the MT2 locus at 16q21-22.1 (15%) and the HP locus at 16q22.1-22.2 (39%). There was no remarkable difference in the frequencies of loss of heterozygosity at these loci among HBV related HCC, HCV related HCC and neither virus (NBNC) related HCC. Thus, the results indicate that at least three different genetic abnormalities in chromosome 16 are commonly observed in various HCC, and that this chromosome may have some important role(s) in recessive genetic changes which generate this tumour.

Key concepts: Loss of heterozygosity, Medicine, Hepatocellular carcinoma, Oncology, Chromosome, Internal medicine, Cancer research, Genetics

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