Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative genomic hybridization

Citation
Xy. Guan et al., Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative genomic hybridization, GENE CHROM, 29(2), 2000, pp. 110-116
Citations number
28
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
GENES CHROMOSOMES & CANCER
ISSN journal
10452257 → ACNP
Volume
29
Issue
2
Year of publication
2000
Pages
110 - 116
Database
ISI
SICI code
1045-2257(200010)29:2<110:RCAIHC>2.0.ZU;2-X
Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignancies world wide and has a very poor prognosis. Fifty primary HCC cases have been analy zed in the present study to explore the association between genomic alterat ion in primary HCC and clinical features. Several recurrent chromosomal abn ormalities were identified in this study. The most frequently detected chro mosomal gains involved chromosome arms Iq (33/50 cases, 66%), 8q (24/50 cas es, 48%), and 20q (10/50 cases, 20%). High-copy-number amplifications invol ving Iq (4 cases), 8q (3 cases), and 20q (3 cases) were detected, and a min imum overlapping amplified region at 1q12-q22 was identified. The most freq uently detected loss of chromosomal material involved 16q (35/50 cases, 70% ), 17p (26/50 cases, 52%), 19p (21/50 cases, 42%), 4q (20/50 cases, 40%), 1 p(18/50 cases, 36%), 8p(16/50 cases, 32%), and 22q (14/50 cases, 28%). The associations between genomic alterations detected in the present study and clinical features including clinical stage, tumor size, HBV infection, chro nic liver disease, and liver cirrhosis were explored. Our CGH results sugge st that the gain of 20q and deletion of 8p are late genetic alterations in HCC, because the incidence of these alterations was obviously increased in the advanced clinical stages. Another finding showed that loss of 8p and ga in of 8q and 20q are associated with tumor size. The recurrent gain and los s of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in HCC development and progression. (C) 2000 Wiley-Liss, Inc.