BACKGROUND. The cyclooxygenase (COX) enzyme catalyzes the formation of pros
taglandins, which can affect cell proliferation and alter the response of t
he immune system to malignant cells. The inducible form of COX, COX-2, has
been shown to be important in carcinogenesis.
METHODS, The authors studied COX-1 and -2 expression in 20 tumors of the lu
ng, colon, and breast (60 total) by using commercially available monoclonal
and polyclonal antibodies on formalin fixed, paraffin embedded tissue. Our
evaluation also included seven carcinoma-associated colonic adenomas and 1
0 mammary ductal carcinomas in situ (DCIS). Quantitation of immunoreactivit
y was accomplished using an immunohistochemical scoring system that approxi
mates the use of image analysis-based systems.
RESULTS. Ninety percent of lung tumors (squamous cell carcinomas and adenoc
arcinomas), 71% of colon adenocarcinomas and 56% of breast tumors (DCIS and
infiltrating ductal and lobular carcinomas) expressed COX-2 at a moderate
to strong level, which was significantly different from the negligible expr
ession in distant nonneoplastic epithelium (controls; P < 0.0001). Poorly d
ifferentiated histologic features were correlated with low COX-2 expression
overall, especially in colon carcinomas. Among breast carcinomas, DCIS was
more likely to: express COX-2 than invasive carcinomas. Adenomatous coloni
c epithelium showed moderate COX-2 expression, as did adjacent nonneoplasti
c epithelium. COX-1 immunoreactivity was essentially weak to moderate in al
l tissues evaluated.
CONCLUSIONS. COX-2 expression is upregulated in well and moderately differe
ntiated carcinomas of the lung, colon, and breast whereas COX-1 appears to
be constitutively expressed at low levels. A possible COX-2 paracrine effec
t is suggested by moderate immunoreactivity in adjacent nonneoplastic epith
elium. Cancer 2000;89:2637-45. (C) 2000 American Cancer Society.