Genomic imbalance and chromosome disorders in hepatoblastoma.
- Author:
Hong GAO
1
;
Zhi-Bo ZHANG
;
Yang-Ling OU
;
Ke-Ren ZHANG
;
Wei-Lin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Child; Child, Preschool; Chromosome Aberrations; Chromosome Deletion; Chromosomes, Human, Pair 1; genetics; Female; Hepatoblastoma; genetics; Humans; Liver Neoplasms; genetics; Loss of Heterozygosity; Male; Nucleic Acid Hybridization; methods
- From: Chinese Journal of Oncology 2006;28(12):915-919
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo establish stable techniques of comparative genomic hybridization (CGH) and apply them to elucidate the genetic characteristics of hepatoblastoma (HB), and to explore the characteristics and clinical significance of loss of heterozygosity (LOH) at 1p36 in HB.
METHODSCGH was employed to detect the genomic imbalance (DNA loss or amplification) in 20 cases of HB, and PCR-simple repeated sequence polymorphism was employed in 30 cases of HB to detect the loss of heterozygosity for 6 satellites at chromosome 1p36.
RESULTSThere were different chromosome variations for each HB. chromosome amplification was frequently seen in 1q, 2q,2p, 8q, 8p, 12q and 22q. Chromosome loss was often seen in 1p, 4q, 4p, 16q, 17p and 18q. The frequency of LOH at 6 loci on chromosome 1 was 63.3% totally (19/30), with the highest D1S199 (66.7%) and D1S450 next to it (46.7%).
CONCLUSIONThere were chromosome zones with DNA amplification or loss in hepatoblastoma. There are extensive LOH at 1p36 in hepatoblastoma. The corresponding amplification of oncogene and loss of antioncogene may take part in the development of hepatoblastoma.
