COX-2 indices were significantly higher in gastric carcinoma tissues with deep invasion; indices for pT1, pT2, pT3, and pT4 carcinomas were 0.8 +/- 0.3, 2.8 +/- 0.5, 4.3 +/- 1.0, and 8.8 +/- 5.5, respectively (P < 0.05).
COX-2 expression was comparable in gastric stump carcinomas and conventional gastric carcinomas and localized primarily to the cytoplasm of the neoplastic cells.
COX-2 gene product was evaluated immunohistochemically in 30 healthy persons, in 22 patients with dysplastic lesions without previous or concomitant carcinomas, and in 29 patients with oral carcinomas.
COX-2 expression was evaluated through immunohistochemical and mRNA analysis in carcinomas, adenomas, and healthy mucosa from six patients carrying germ line biallelic MYH mutations.
COX-2 was expressed in DCAMKL1-positive tuft cells in Cdx2- and DCAMKL1-transgenic mouse stomachs, whereas the Sox9 transcription factor was ubiquitously expressed in gastric carcinomas, including COX-2-positive cells.
COX-2 expression induces carcinogenesis and is thought to be an adverse prognostic factor in gastric carcinomas while the prognostic value of DNA mismatch repair (MMR) is still controversial.
Active caspase-3, ssDNA, p53, Bax and COX-2 were more frequently observed among high grade and higher stage (> or =T2) carcinomas compared with low grade and lower stage (T1) tumours.
All these results suggest that knockdown of COX-2 expression can lead to potent antitumor activity and chemosensitizing activity to taxanes in human laryngeal carcinomas.
By immunohistochemistry, we assessed COX-2 expression in 24 hyperplastic polyps, 7 sessile serrated polyp/adenomas (SSA), 5 mixed polyps with SSA and adenoma, 27 traditional serrated adenomas, 515 non-serrated adenomas (tubular adenoma, tubulovillous adenoma and villous adenoma), 33 adenomas with intramucosal carcinomas, 96 adenocarcinomas with serration (corkscrew gland) and 111 adenocarcinomas without serration.
Clinical trials of COX-2 inhibitors have provided the "proof of principle" that inhibition of this enzyme can prevent the formation of colonic adenomas and potentially carcinomas, however concerns regarding the potential toxicity of these drugs have limited their use as a chemopreventative strategy.
Gastric carcinoma tissues release high level of prostaglandin E2 (PGE2) when compared to non-neoplastic mucosa, and cyclooxygenase-2 (COX-2), which is the rate-limiting enzyme in prostaglandin (PG) biosynthesis, is often overexpressed in gastric carcinomas and during gastric carcinogenesis.
HuR and COX-2 protein expression were studied by immunohistochemistry of normal colon mucosa (N=20), adenomas (N=112), carcinomas (N=9) from patients with FAP, and 141 sporadic colorectal adenocarcinomas (Dukes B and C).
In addition, PPARgamma protein was not detected in all of the eight carcinomas in which COX-2 protein was detected, suggesting that expression of PPARgamma and COX-2 was in a reciprocal relationship.