BACKGROUND/AIMS: Based on the authors' data collected by comparative genomic hybridization (CGH), loss at multiple loci on whole chromosome 17 is believed to be associated with sporadic gastric cancer (GC). METHODOLOGY: In this study, previous results were extended by analyzing further loss of heterozygosity (LOH) at 15 loci along chromosome 17 in 45 sporadic GC patients using fluorescent microsatellite markers and an ABI 377 sequencer/genotyper. RESULTS: Allelic losses at all 15 markers were observed in most GC patients with the range of 11-61% LOH frequencies. Thirty-three of 45 GC patients (73%) showed LOH at least at one site, 22 at two or more sites. Ten markers were found with over 20% LOH frequencies (5 markers at 17p and 5 markers at 17q), suggesting that frequent allelic losses occur at multiple loci on chromosome 17 in GC. Three distinct regions of deletions were identified: R1 between D17S831-D17S921 at 17p12-13.3 (30cM), R2 between D17S1868-D17S787 at 17q21. 3-22 (11cM) and R3 between D17S785-D17S928 at 17q25.3 (23cM), respectively. CONCLUSIONS: The observations in this study of the three distinct deleted regions on chromosome 17 may provide some novel abnormalities of potential significance in gastric cancers, suggesting the involvement of TSGs residing in those regions in the genesis of the disease.
BACKGROUND/AIMS: Based on the authors' data collected by comparative genomic hybridization (CGH), loss at multiple loci on whole chromosome 17 is believed to be associated with sporadic gastric cancer (GC). METHODOLOGY: In this study, previous results were extended by analyzing further loss of heterozygosity (LOH) at 15 loci along chromosome 17 in 45 sporadic GC patients using fluorescent microsatellite markers and an ABI 377 sequencer/genotyper. RESULTS: Allelic losses at all 15 markers were observed in most GC patients with the range of 11-61% LOH frequencies. Thirty-three of 45 GC patients (73%) showed LOH at least at one site, 22 at two or more sites. Ten markers were found with over 20% LOH frequencies (5 markers at 17p and 5 markers at 17q), suggesting that frequent allelic losses occur at multiple loci on chromosome 17 in GC. Three distinct regions of deletions were identified: R1 between D17S831-D17S921 at 17p12-13.3 (30cM), R2 between D17S1868-D17S787 at 17q21. 3-22 (11cM) and R3 between D17S785-D17S928 at 17q25.3 (23cM), respectively. CONCLUSIONS: The observations in this study of the three distinct deleted regions on chromosome 17 may provide some novel abnormalities of potential significance in gastric cancers, suggesting the involvement of TSGs residing in those regions in the genesis of the disease.