Genetic Alterations in Primary Gastric Carcinomas Correlated with Clinicopathological Variables by Array Comparative Genomic Hybridization.
10.3346/jkms.2006.21.4.656
- Author:
Ji Un KANG
1
;
Jason Jongho KANG
;
Kye Chul KWON
;
Jong Woo PARK
;
Tae Eun JEONG
;
Seung Mu NOH
;
Sun Hoe KOO
Author Information
1. Department of Clinical Pathology, Chungnam National University Hospital, Daejeon, Korea. shkoo@cnuh.co.kr
- Publication Type:Original Article ; Comparative Study ; Research Support, Non-U.S. Gov't
- Keywords:
Mutation;
Genetic Alteration;
Stomach Neoplasms;
Chromosome-based comparative genomic hybridization;
Gene Dosage;
Copy-Number Gain;
Copy-Number Loss
- MeSH:
Stomach Neoplasms/genetics/*pathology;
Reverse Transcriptase Polymerase Chain Reaction/methods;
Receptors, Thyrotropin/genetics;
Nucleic Acid Hybridization/*methods;
Neoplasm Staging;
Middle Aged;
Male;
MafB Transcription Factor/genetics;
Lymphatic Metastasis/genetics;
Humans;
Genome, Human/genetics;
Gene Expression Regulation, Neoplastic;
Female;
Chromosomes, Human, Pair 20/genetics;
Chromosomes, Human, Pair 14/genetics;
*Chromosome Aberrations;
Aged, 80 and over;
Aged;
Adult
- From:Journal of Korean Medical Science
2006;21(4):656-665
- CountryRepublic of Korea
- Language:English
-
Abstract:
Genetic alterations have been recognized as an important event in the carcinogenesis of gastric cancer (GC). We conducted high resolution bacterial artificial chromosome array-comparative genomic hybridization, to elucidate in more detail the genomic alterations, and to establish a pattern of DNA copy number changes with distinct clinical variables in GC. Our results showed some correlations between novel amplified or deleted regions and clinical status. Copy-number gains were frequently detected at 1p, 5p, 7q, 8q, 11p, 16p, 20p and 20q, and losses at 1p, 2q, 4q, 5q, 7q, 9p, 14q, and 18q. Losses at 4q23, 9p23, 14q31.1, or 18q21.1 as well as a gain at 20q12 were correlated with tumor-node-metastasis tumor stage. Losses at 9p23 or 14q31.1 were associated with lymph node status. Metastasis was determined to be related to losses at 4q23 or 4q28.2, as well as losses at 4q15.2, 4q21.21, 4q 28.2, or 14q31.1, with differentiation. One of the notable aspects of this study was that the losses at 4q or 14q could be employed in the evaluation of the metastatic status of GC. Our results should provide a potential resource for the molecular cytogenetic events in GC, and should also provide clues in the hunt for genes associated with GC.
