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High CDC20 expression is associated with poor prognosis in oral squamous cell carcinoma

Objectives Human Cell Division Cycle 20 (CDC20) homolog is a crucial target of the spindle assembly checkpoint. It is an activator of the Anaphase‐Promoting Complex/Cyclosome (APC/C) which promotes anaphase onset and mitotic exit through the ubiquitination of securin and cyclin B1. Overexpression of...

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Published in:Journal of oral pathology & medicine 2014-03, Vol.43 (3), p.225-231
Main Authors: Moura, Inês M. B., Delgado, Maria L., Silva, Patrícia M. A., Lopes, Carlos A., do Amaral, José B., Monteiro, Luís S., Bousbaa, Hassan
Format: Article
Language:English
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Summary:Objectives Human Cell Division Cycle 20 (CDC20) homolog is a crucial target of the spindle assembly checkpoint. It is an activator of the Anaphase‐Promoting Complex/Cyclosome (APC/C) which promotes anaphase onset and mitotic exit through the ubiquitination of securin and cyclin B1. Overexpression of CDC20 was previously reported in oral squamous cell carcinoma (OSCC). Here, we propose to explore the clinicopathological significance of CDC20 overexpression and its potential use as a prognostic marker in OSCC. Methods Using tissue microarray technology, we analyzed CDC20 expression in 65 primary OSCC tissues by immunohistochemistry. Statistical analysis was performed to evaluate the clinicopathological and prognostic significance of CDC20 expression in OSCC. Results Of the 65 cases of patients with OSCC studied, 37 (56.9%) showed high CDC20 protein expression. No clinicopathological features were correlated with CDC20 expression. Importantly, in univariable analysis, OSCC patients with higher CDC20 protein expression showed significantly shorter cancer‐specific survival rate (P = 0.018). Multivariable analysis identified high CDC20 expression as an independent prognostic factor (P = 0.032). Conclusion High CDC20 expression is associated with poor prognosis in OSCC and may be used to identify high‐risk OSCC patients and may serve as a therapeutic target.
ISSN:0904-2512
1600-0714
DOI:10.1111/jop.12115