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Analysis of p16 INK4A expression of oral squamous cell carcinomas in Taiwan: Prognostic correlation without relevance to betel quid consumption
Author(s) -
Chen YaWei,
Kao ShouYen,
Yang MuhHwa
Publication year - 2012
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.23067
Subject(s) - medicine , immunohistochemistry , oncology , incidence (geometry) , cancer , basal cell , lymph node metastasis , correlation , biomarker , metastasis , pathology , biology , biochemistry , physics , geometry , mathematics , optics
Objectives In this study, we examined the role of p16 INK4A , a surrogate biomarker of HPV‐related head and neck cancers with better prognosis, in an endemic area of betel quid (BQ)‐related oral squamous cell carcinoma (OSCC). Methods p16 INK4A immunohistochemistry was examined in 165 OSCCs, statistical analyses were performed to elucidate the correlation between p16 INK4A expression and BQ habits/pathologic features, and the prognostic impact of p16 INK4A and different parameters were analyzed. Results The incidence of p16 INK4A expression was similar between BQ chewers and non‐chewers. p16 INK4A expression was significantly associated with nodal metastasis ( P = 0.005). There was a trend suggesting that the loss of p16 INK4A expression was more frequent in higher T stages, however, this was found only in patients without lymph node metastasis ( P = 0.059). A poorer prognosis and a higher risk of tumor recurrence were found in OSCCs without p16 INK4A expression. (The HR for cancer‐specific mortality and cancer recurrence was 3.55 and 1.89, respectively.) Conclusion Although it has been suggested that BQ chewers had a greater tendency toward tumor recurrence and poor outcome, our data demonstrated that p16 INK4A expression is unrelated to BQ habit and that p16 INK4A downregulation is a strong predictor for OSCC progression, recurrence and survival in Taiwan. J. Surg. Oncol. 2012; 106:149–154. © 2012 Wiley Periodicals, Inc.