COX-2 overexpression in canine tumors: potential therapeutic targets in oncology
E.P. Spugnini1, A. Porrello2, G. Citro1 and A. Baldi1,3
1SAFU Department, Center for Experimental Research, Regina Elena Cancer Institute, Rome, italy, 2Molecular Oncogenesis Laboratory, Department of Experimental Oncology, Regina Elena Cancer institute, Rome, Italy and 3Department of Biochemistry, Section of Pathology, Second University of Naples, Naples, Italy
Offprint requests to: Dr. Enrico Spugnini, SAFU Department, Regina Elena Cancer Institute, Via delle Messi d’Oro 156, 00158 Rome, Italy. e-mail: enrico.spugnini@tiscali.it
Summary. Cyclooxygenases catalyze the initial, rate-limiting steps of prostaglandin synthesis from arachidonic acid. Two isoforms of this enzyme exist in mammalian and avian species: COX-1 and COX-2. COX-1 is constitutively expressed and is the major isoform of gastrointestinal tissue. COX-2 is induced in response to inflammatory stimuli. COX-2 has been implicated in carcinogenesis of several neoplasms. Furthermore, COX-2 over-expression has been noted in many solid tumours and has been correlated with a worse prognosis in colorectal cancer, non-small-cell lung cancer, mesothelioma and gastric cancer. In this review, the most recent findings on the mechanisms by which COX-2 promote tumorigenesis are discussed, with particular emphasis on the studies involving spontaneous canine neoplasms. Histol Histopathol 20, 1309-1312 (2005)
Key words: COX-2, Canine tumors, Chemotherapy
DOI: 10.14670/HH-20.1309