Recently, mammalian heparanase was cloned, and its probable function in tum
or progression was reported. However, its expression in human clinical canc
ers has not been fully studied. Thus we determined the heparanase mRNA expr
ession in 30 esophageal cancer cell lines and 144 clinical samples includin
g 38 esophageal squamous cell carcinomas, 71 gastric adenocarcinomas, and 3
5 colorectal adenocarcinomas. The fresh surgical specimens of cancer tissue
(T) and its paired normal tissue (N) were used. The heparanase mRNA was ev
aluated by reverse transcriptase-polymerase chain reaction, and the T/N exp
ression ratio was determined in clinical cases. All 30 esophageal cancer ce
ll lines expressed heparanase mRNA. The T/N ratio was determined as high (g
reater than or equal to1.3), equal (0.8-1.2) or low (less than or equal to0
.7) in each clinical case. In cases of esophageal cancer, 7 showed high, 10
equal and 21 low expression. In cases of colorectal cancer, 3 showed high,
16 equal and 16 low expression. On the other hand, 42 showed high, 22 equa
l and 7 low expression in cases of gastric cancer. The frequency of high ex
pression cases was greater in gastric cancer than in esophageal or colorect
al cancers (p < 0.05). There were no differences in clinicopathologic facto
rs including prognosis between high and low expression cases of each cancer
. Our mRNA study of heparanase indicated that its expression status was dif
ferent among gastrointestinal cancers. The clinical and pathological impact
was low compared to other proteinases, although further studies are recomm
ended for final conclusion.