Chromosomal analysis of hepatic adenoma and focal nodular hyperplasia by comparative genomic hybridization
Article first published online: 22 MAY 2002
Copyright © 2002 Wiley-Liss, Inc.
Genes, Chromosomes and Cancer
Volume 35, Issue 2, pages 138–143, October 2002
How to Cite
Chen, Y.-J., Chen, P.-J., Lee, M.-C., Yeh, S.-H., Hsu, M.-T. and Lin, C.-H. (2002), Chromosomal analysis of hepatic adenoma and focal nodular hyperplasia by comparative genomic hybridization. Genes Chromosom. Cancer, 35: 138–143. doi: 10.1002/gcc.10103
- Issue published online: 26 AUG 2002
- Article first published online: 22 MAY 2002
- Manuscript Accepted: 7 MAR 2002
- Manuscript Received: 27 AUG 2001
- National Health Research Institute. Grant Number: NHRI-EX90-8927SP
- Frontier Medical Genomic Program of National Science Council. Grant Number: NSC 89-2318-B-010-014-M51
- Chien-Tien Hsu Cancer Research Foundation
- Program for Promoting Academic Excellence of Universities from the Ministry of Education, Taiwan. Grant Number: 89-B-FA22-2-4
Hepatic adenoma (HA) and focal nodular hyperplasia (FNH) are two common non-malignant tumors of the liver. Genomic analysis on these benign lesions may shed light on the genetic mechanism underlying liver carcinogenesis. We used comparative genomic hybridization (CGH) to evaluate genomic changes in eight cases of HA and six cases of FNH, obtained by surgical procedures; the resulting chromosomal aberration profiles were analyzed together with their pathological and clinical manifestations. We found consistent chromosomal lesions associated with both non-malignant hepatic tumors. The overall genomic abnormalities in HA and FNH were much less obvious than those in hepatocellular carcinoma (HCC). Among these limited changes, frequent gains were located on chromosomal arms 1q (50%), 17q (50%), 1p (38%), and 11q (38%) in HA, and on 11q (50%), 9q (33%), 17q (33%), and 22q (33%) in FNH. Gains outnumbered losses, and HA contained more CGH abnormalities than did FNH. Interestingly, CGH alteration hotspots found in HA, but not in FNH, appeared largely to coincide with common genomic lesions of cancerous HCC, suggesting an interesting relationship along the tumorigenesis pathway of HA and HCC. © 2002 Wiley-Liss, Inc.