Seventy-six gastric carcinomas were analyzed with regard to whether or
how microsatellite instability was associated with the development of
the carcinoma. Microsatellite instability occurred as a late genetic
alteration, with an incidence significantly higher in the advanced sta
ge (17 of 51) than in the early stage (3 of 25; P < 0.05). Chromosomal
losses on 5q and 17p, detected by polymerase chain reaction-restricti
on fragment length polymorphism, more frequently accompanied microsate
llite instability (9 of 15 and 8 of 11, respectively), compared with c
arcinomas which lacked instability (5 of 28 and 9 of 30, respectively;
P < 0.01 and P < 0.05, respectively). Epstein-Barr virus was observed
in only 8 of 76 carcinomas, none of which was associated with microsa
tellite instability. No significant correlation,vas found between inst
ability and the familial tendency to develop gastric carcinomas. Our r
esults suggest that microsatellite instability might play a role in th
e progression of gastric carcinomas but not in Epstein-Barr virus-asso
ciated gastric carcinomas.