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Histol Histopathol. 2013 Sep;28(9):1175-84. Epub 2013 Apr 10.

Beta-catenin and survivin expression in keratocystic odontogenic tumor (KCOT). A comparative immunohistochemical study in primary, recurrent and nevoid basal cell carcinoma syndrome (NBCCS)-associated lesions.

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  • 1Department of Medical and Surgical Science. II Dental Unit - University of Catania, Catania, Italy.



To determine the epithelial expression of β-catenin and survivin in sporadic (primary, and recurrent) and nevoid basal cell carcinoma syndrome (NBCCS) keratocystic odontogenic tumour (KCOT) in order to assess activation of the β-catenin pathway and evidence of apoptotic inhibition, processes that may contribute to the known differences in their biological behaviour.


Sections from 40 cases of KCOT (19 sporadic/primary; 9 sporadic/recurrent and 12 NBCCS-associated) were immunohistochemically stained for β-catenin and survivin. The extent and intensity of immunoreactivity within the lining epithelium was assessed, using semi-quantitative scales, independently by two pathologists who were blinded to the clinical-pathological data. Data were analysed using Kruskal-Wallis test and, for pair-wise comparisons, Mann-Whitney test with Bonferroni correction.


All cystic epithelial linings stained for β-catenin and survivin but there were differences in the pattern and intensity of staining among KCOT types. Sporadic primary KCOT showed weaker staining for β-catenin (P=0.0003) and survivin (P<0.0048) that was restricted to the basal and para-basal layers only, compared to sporadic recurrent and NBCCS-associated KCOT, which showed expression throughout all epithelial layers. There were no differences in β-catenin expression among recurrent and NBCCS-associated KCOT, whereas the intensity of survivin staining was higher in NBCCS-KCOT (P=0.0003). Nuclear staining for β-catenin was found exclusively in recurrent (5/9 cases) and NBCCS-associated (4/12 cases) KCOT.


The data demonstrate β-catenin delocalization and survivin over-expression in recurrent sporadic and NBCCS-associated KCOT suggesting that these pathways related to apoptotic inhibition have a role in KCOT growth and recurrence.

[PubMed - indexed for MEDLINE]
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