Gastric carcinomas can develop as part of the hereditary nonpolyposis colon cancer (HNPCC) syndrome {1130, 922}. They are intestinal type cancers, without an association with H. pylori infection; most exhibit microsatellite instability (MSI) {4} with a trend that is opposite to that found in tumours arising in young patients {1739}.

Gastrointestional polyposis syndromes

Gastric carcinomas also occur in patients with gastrointestinal polyposis syndromes including FAP and Peutz-Jeghers syndrome.

Overall, gastric carcinoma is rare in these settings, and the exact contribution of the polyposis and underlying germline alterations of APC and LKB1/STK11 to cancer development is unclear.

Blood group A

The blood group A phenotype associates with gastric carcinomas {27, 649}. H. pylori adhere to the Lewisb blood group antigen and the latter may be an important host factor facilitating this chronic infection {244} and subsequent cancer risk.

Molecular genetics

Loss of heterozygosity studies and comparative genomic hybridization (CGH) analyses have identified several loci with significant allelic loss, indicating possible tumour suppressor genes important in gastric carcinoma. Common target(s) of loss or gain include chromosomal regions 3p, 4, 5q, (30 to 40% at or near APCs locus) {1656, 1577}, 6q {255}, 9p, 17p (over 60 percent at TP53's locus) {1656}, 18q (over 60 percent at DCC's locus) {1981}, and 20q {1287, 449, 2192}. Similar LOH losses at 11p15 occur in proximal and distal carcinomas, suggesting common paths of develop-

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