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Open Access Research

Cyclin D1 and p16 expression in recurrent nasopharyngeal carcinoma

Ho-Sheng Lin12*, Gerald J Berry3, Zijie Sun4 and Willard E Fee5

Author Affiliations

1 Department of Surgery, John D. Dingell VA Medical Center, 4646 John R. Street, Detroit, MI 48201, USA

2 Department of Otolaryngology, Wayne State University, 4201 St. Antoine, 5 E University Health Center, Detroit, MI 48201, USA

3 Department of Pathology, Stanford University Medical Center, Stanford, CA 94305, USA

4 Department of Urology, Stanford University Medical Center, Stanford, CA 94305, USA

5 Department of Otolaryngology, Stanford University Medical Center, Stanford, CA 94305, USA

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World Journal of Surgical Oncology 2006, 4:62  doi:10.1186/1477-7819-4-62

Published: 5 September 2006



Cyclin D1 and p16 are involved in the regulation of G1 checkpoint and may play an important role in the tumorigenesis of nasopharyngeal carcinoma (NPC). Previous studies have examined the level of expression of cyclin D1 and p16 in primary untreated NPC but no such information is available for recurrent NPC. We set out in this study to examine the expression level of cyclin D1 and p16 in recurrent NPC that have failed previous treatment with radiation +/- chemotherapy.

Patients and methods

A total of 42 patients underwent salvage nasopharyngectomy from 1984 to 2001 for recurrent NPC after treatment failure with radiation +/- chemotherapy. Twenty-seven pathologic specimens were available for immunohistochemical study using antibodies against cyclin D1 and p16.


Positive expression of cyclin D1 was observed in 7 of 27 recurrent NPC specimens (26%) while positive p16 expression was seen in only 1 of 27 recurrent NPC (4%).


While the level of expression of cyclin D1 in recurrent NPC was similar to that of previously untreated head and neck cancer, the level of p16 expression in recurrent NPC samples was much lower than that reported for previously untreated cancer. The finding that almost all (96%) of the recurrent NPC lack expression of p16 suggested that loss of p16 may confer a survival advantage by making cancer cells more resistant to conventional treatment with radiation +/- chemotherapy. Further research is warranted to investigate the clinical use of p16 both as a prognostic marker and as a potential therapeutic target.