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Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways

¹ Institute of Pathology, University Hospital of Essen, Essen, Germany
² Department of Obstetrics and Gynaecology, University Hospital of Essen
³ Department of Internal Medicine, Gumma Paz Gakuen College, Gumma, Japan

Correspondence to:
H A Baba
Institute of Pathology, University Hospital of Essen, D-45147 Essen, Hufelandstr 55, Germany; hideo.baba{at}medizin.uni-essen.de Background and aim: The production of prostaglandins is regulated by cyclo-oxygenases (COXs), which also have a role in tumour development and progression in various malignancies, including breast cancer. The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood. The association between expression of COX-2 and possible linked signalling pathways—namely, Akt, extracellular regulated kinases (ERK1/2), the stress-activated kinase p38 or Her-2/neu—is assessed in a series of 113 node-negative breast cancers.

Results: COX-2 was identified as an independent prognostic factor (p = 0.034) in node-negative breast cancer by survival analysis. The lack of a relationship between COX-2 expression and activated Akt, Erk1/2, p38 and Her-2/neu was indicated by statistical analysis.

Conclusions: The prognostic effect of COX-2 expression on lymph node-negative breast cancer is confirmed—COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38. Further studies are necessary for the elucidation of the signalling pathways responsible for the modification of COX-2 expression and the increased aggressiveness of breast cancers overexpressing COX-2.

Abbreviations: COX, cyclo-oxygenase; ERK, extracellular regulated kinases; FAP, familial adenomatous polyposis; FISH, fluorescent in situ hybridisation; IHC, immunohistochemistry; MAPK, mitogen-activated protein kinase; NSAID, non-steroidal anti-inflammatory drug; pAkt, phospho-Akt; pERK, phospho-ERK; PGE₂, prostaglandin E₂; pp38, phospho-p38; SSC, sodium salt citrate