Analysis of Genomic Imbalances in Korean Gastric Carcinoma Using Comparative Genomic Hybridization.
- Author:
Soo Yeun PARK
1
;
Hye Jin HWANG
;
Chan Joo LEE
;
Sun Hwa PARK
Author Information
1. Department of Anatomy, College of Medicine, Ewha Womans University, Korea.
- Publication Type:Original Article
- Keywords:
Comparative genomic hybridization (CGH);
Gastric cancers;
Chromosome aberrations
- MeSH:
Asian Continental Ancestry Group;
Carcinogenesis;
Chromosome Aberrations;
Comparative Genomic Hybridization*;
Diagnosis;
DNA;
Genes, Tumor Suppressor;
Genome;
Humans;
Korea;
Mass Screening;
Neoplasm Metastasis;
Nucleic Acid Hybridization;
Oncogenes;
Prognosis;
Stomach Neoplasms
- From:Korean Journal of Anatomy
2004;37(6):539-547
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Chromosomal abnormalities, which are valuable markers for diagnosis and prognosis of cancer, provide useful clues in characterizing cancer at molecular level. Gastric cancer is the major cause of cancer deaths in Asian countries, including Korea. Genetic changes during the progression and metastasis of gastric cancer remain unclear. Recently, technique of degenerate oligonucleotide primed (DOP) PCR-comparative genomic hybridization (CGH) permits genetic imbalances screening of the entire genome using only small amounts of tumor DNA. In non-metastatic gastric cancers the common sites of copy number increases were detected at 8q (64%), 4p12-q24 (64%), 5p13-q23 (64%), 13q21-q32 (64%), 6q11-q21 (55%), 7q(50%), 14q11.2-q21 (45%), 3q11-q13.3 (41%), and 2q23-q32 (41%). In metastatic gastric cancers, the frequent sites of gains were detected at 8p21-qter (60%), 5 (54%), 20 (42%), 6pter-q24 (51%), 1q21-qter (46%), 3p14-qter (46%), 22q (46%), and 4 (43%). Deletion or chromosomal loss was found to be less frequent in this study. The frequent sites of copy number decreases were detected at 1p34-pter (23%), 16q23-q24 (18%), and 19q13 (18%) in non-metastatic gastric cancers. In metastatic gastric cancers, chromosome losses were detected at X (37%), 1p33-pter (37%), and 16p (23%). The recurrent gains and losses of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in the tumorigenesis of gastric cancer.
