The molecular mechanism of gastric tumourigenesis has not yet been cla
rified, although investigators have postulated that differentiated ade
nocarcinoma may arise from pre-existing adenoma, similarly to the colo
rectal adenoma-carcinoma sequence. An allelotype analysis has been per
formed to identify chromosomal regions which are frequently deleted in
gastric tumours and to examine the significance of the adenoma-carcin
oma sequence in gastric tumiourigenesis. Forty-five gastric tumours, 2
0 adenomas, and 25 differentiated adenocarcinomas were examined for lo
ss of heterozygosity (LOH) using 39 microsatellite markers covering ea
ch non-acrocentric chromosome arm. Frequent LOH in the adenocarcinomas
was observed on chromosomes 2q (33 per cent), 4p (33 per cent), 5q (5
0 per cent), 6p (33 per cent), 7q (43 per cent), 11q (36 per cent), 14
q (38 per cent), 17p (45 per cent), 18q (36 per cent), and 21q (40 per
cent). In contrast, the incidence of LOH in adenomas did not exceed 1
0 per cent at any of the loci examined. In addition to the p53 gene on
17p and the DCC gene on 18q, which are known to be frequently deleted
in differentiated adenocarcinomas of the stomach, other unknown tumou
r suppressor genes on the above-mentioned chromosomes may also be inac
tivated. These observations suggest that the adenoma-carcinoma sequenc
e is not a major pathway in gastric tumourigenesis.