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Alteration of G1/S transition regulators influences recurrences in head and neck squamous carcinomas
Author(s) -
Canzonieri Vincenzo,
Barzan Luigi,
Franchin Giovanni,
Vaccher Emanuela,
Talamini Renato,
Sulfaro Sandro,
Baldassarre Gustavo
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22723
Subject(s) - cyclin d1 , immunohistochemistry , oncology , medicine , disease , radiation therapy , cell cycle , head and neck squamous cell carcinoma , biomarker , cancer research , head and neck cancer , cancer , biology , biochemistry
Abstract Head‐Neck Squamous Cell Carcinoma (HN‐SCC) is a clinically challenging disease associated with a high mortality rate. The chemo‐radiotherapy treatments that aim to preserve the organ represent the current gold standard therapy for advanced laryngeal disease, reserving surgery only for non‐responsive or relapsed cases. Despite these aggressive approaches, local persistent or recurrent disease remains the primary cause of treatment failure but we still do not have known factors and/or markers able to predict the outcome of the disease and in particular the risk of local relapse. Here we address this point on a series of 54 cases of HN‐SCC for whom the presence of local relapse was known. Using immunohistochemistry (IHC) analysis to evaluate protein expression and localization in the recurrence free and recurrence positive samples, we studied the expression of key cell cycle regulators including p53, p16, p27, pRB, Cyclin D1, Cyclin D3, and Stathmin. Overall by analyzing seven different cell cycle regulators we can hypothesize that the alteration of G1/S regulation represents a fundamental event in the onset/progression of HN‐SCC cancers and that the associate use of Cyclin D1/p16 expression should be considered as a possible biomarker toward the identification of those patients that will probably develop a recurrent disease and thus should benefit of a more aggressive treatment. J. Cell. Physiol. 227: 233–238, 2012. © 2011 Wiley Periodicals, Inc.