The major purpose of this study was to evaluate the association of Hel
icobacter pylori and diffuse type gastric cancer (DGC) clinicopatholog
ically (study 1). The second aim was to investigate genetic difference
s of H. pylori in patients with DGC and intestinal type cancer (IGC) (
study 2). The prevalence of H. pylori and the types of histopathologic
al changes were evaluated in resected early gastric cancer (DGC; 25 pa
tients, IGC; 25 patients). Genetic differences of H. pylori in DGC pat
ients (n = 19) and IGC patients (n = 22) were analyzed by polymerase c
hain reaction (PCR) methods in terms of restriction fragment length po
lymorphism patterns of the ureB gene and cagA gene positive rates. All
patients had evidence of H. pylori infection in the resected stomach,
but the positive rate for H. pylori in the area surrounding cancer wa
s 52% (in DGC; 56%, IGC; 48%). But in 40.0% of DGC cases (10/25), muco
sal atrophy and intestinal metaplasia were rarely seen in the area sur
rounding cancer and the positive rate of H. pylori was 80.0% (8/10), i
n contrast, in 60.0% of IGC cases (15/25), atrophy and metaplasia were
progressed and positive rate of H. pylori was 26.7% (4/15) in the are
a. UreB gene products from 89.5% of DGC cases (17/19) were unable to b
e digested by Spe I. 31.8% of products from IGC cases (7/22) were also
unable to be digested by Spe I? but the positive rate of cagA gene in
this group was higher than other groups. The high prevalence of H. py
lori infection in DGC patients suggests that H. pylori plays a role in
the pathogenesis of DGC, but in the stomach with DGC, it is considere
d atrophy and intestinal metaplasia are not so implicated in H. pylori
, compared with IGC. A genetic specificity of H. pylori in DGC and IGC
was indicated by the results, suggesting that H. pylori may play diff
erent roles in the pathogenesis of DGC and IGC.