Gastric adenocarcinoma is one of the most common malignancies in the world,
and yet little is known about its molecular process of development and pro
gression. Recent studies have suggested that ingestion of nonsteroid antiin
flammatory drugs reduces the risk of colon cancer, presumably by inhibiting
the cyclooxygenase (COX) enzyme. COX-2, one isoform of the COX enzyme, is
the rate-limiting enzyme in prostaglandin synthesis, and the function of th
is enzyme is thought to relate to inflammatory processes and carcinogenesis
. To understand the role of COX enzyme in gastric cancer, we measured COX-2
expression in 104 human gastric carcinoma tissues by immunohistochemical a
nalysis. We obtained tissue specimens from 104 surgically resected gastric
adenocarcinoma patients. We performed immunohistochemical stain for human C
OX-2 with polyclonal antibody in gastric carcinoma. After curative resectio
n and extensive lymph node dissection, all patients received adjuvant chemo
therapy containing 5-fluorouracil, Expression of COX-2 showed cytoplasmic s
taining, not only in cancer cells but also in precancerous lesions such as
metaplastic and adenomatous cells. We confirmed up-regulation of COX-2 in g
astric cancer tissues compared with normal paired mucosa using Western blot
analysis. There was no correlation between clinicopathological characteris
tics of gastric cancer patients and intensity of COX-2 protein expression.
This study indicates that COX-2 protein overexpression may contribute to an
early event of gastric cancer development, and it further suggests that se
lective inhibition of COX-2 may provide a chemopreventive effect against ga
stric carcinogenesis.