Potential relevance of cyclooxygenase-2 expression in keratocystic odontogenic tumours - an immunohistochemical study

• Type: Article in International Scientific Journal
• Date: 2011

Authors

Mendes, RA (Author) Other; Carvalho, JFC (Author) Other; van der Waal, I (Author) Other

Journal

Title: Journal of Oral Pathology & Medicine

Vol. 40

Pages: 497-503

ISSN: 0904-2512

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 10 Citations

Scopus - 11 Citations

Other information

Authenticus ID: P-002-Q7E

DOI: 10.1111/j.1600-0714.2010.00997.x

Abstract (EN): There is increasing evidence that overexpression of cyclooxygenase-2 (COX-2) plays an important role in tumour growth and spread of tumours by interfering with cell proliferation, cellular adhesion, immune surveillance, apoptosis, and angiogenesis. COX-2 levels are increased in various tumours. In this study, the expression of COX-2 in 116 specimens of keratocystic odontogenic tumours (KCOT) has been analyzed. KCOT is a benign neoplasm of odontogenic origin with an occasionally aggressive behavior leading to high recurrence rates. Formalin-fixed, paraffin-embedded blocks were sectioned and used for hematoxylin-eosin (H&E) staining and incubated with an anti-COX-2 monoclonal antibody for immunohistochemical examination. Detection of the COX-2 antibody was performed with the EnVision kit. Cellular staining pattern for COX-2 was cytoplasmatic, and the staining intensities were semi-quantitatively evaluated as follows: negative (-), mild (+/-) or strong (+). Mild to strong expression of COX-2 was observed in 83 (71.6%) cases; 34 (29.3%) of which were mild positive and 49 (42.2%) were strong positive. COX-2 stain was detected mainly in the epithelial lining. The expression of COX-2 in KCOT and the current knowledge of the role played by COX-2 in tumorigenesis further strengthen the current concept that the KCOT should be regarded as a neoplasm. Furthermore, the multitude of markers known to be overexpressed in KCOTs is suggestive of what could be called a 'network addiction' pattern, rather than a pathological mechanism dependant on a specific activated/suppressed gene, thus explaining its aggressive behavior. J Oral Pathol Med (2011) 40: 497-503

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 7