More recently, a possible cooperation of COX-1 and COX-2 isoforms has been suggested in an investigation of the PGE2 pathway in a rat model of esophageal adenocarcinoma induced by gastroduodenal reflux resulting from esophagojejunostomy [63], as well as by the finding that in the same experimental model indomethacin (a dual COX-1/COX-2 inhibitor) reduced the inflammatory lesions and tumor development, whereas a selective COX-2 inhibitor (MF-tricyclic) was ineffective [64]. Here, PTGS2 is linked to neoplasm.