Expression of cell cycle control proteins in normal epithelium, premalignant and malignant lesions of oral cavity

Shintani, Satoru; Mihara, Mariko; Nakahara, Yuji; Kiyota, Akihisa; Ueyama, Yoshiya; Matsumura, Tomohiro; Wong, David T.W

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Volume 38, Issue 3 , Pages 235-243, April 2002

Expression of cell cycle control proteins in normal epithelium, premalignant and malignant lesions of oral cavity

Satoru Shintani
- Department of Oral and Maxillofacial Surgery, Ehime University School of Medicine, Ehime, Japan
- Corresponding author. Tel.: +81-89-960-5393; fax: +81-89-960-5396
Mariko Mihara
- Department of Oral and Maxillofacial Surgery II, Okayama University Dental School, Okayama, Japan
Yuji Nakahara
- Department of Oral and Maxillofacial Surgery, Ehime University School of Medicine, Ehime, Japan
Akihisa Kiyota
- Department of Oral and Maxillofacial Surgery II, Okayama University Dental School, Okayama, Japan
Yoshiya Ueyama
- Department of Oral and Maxillofacial Surgery II, Okayama University Dental School, Okayama, Japan
Tomohiro Matsumura
- Department of Oral and Maxillofacial Surgery II, Okayama University Dental School, Okayama, Japan
David T.W Wong
- Laboratory of Molecular Pathology, Division of Oral Pathology, Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, Boston, USA

Received 22 February 2001; accepted 29 March 2001.

Abstract

In this study, we examined the expression of cyclins, cyclin dependent kinase (CDKs) and CDK inhibitors by immunohistochemical analysis in 20 normal mucosa, 42 epithelial dysplasia (ED), and 117 oral squamous cell carcinoma. Neither Cyclin D1 nor CDK2 were detectable in normal tissue and ED. Their presence, however, was detectable in squamous cell carcinoma (SCCs) (Cyclin D1, 35.9%; CDK2, 66.7%). Cyclin E was detectable in 57.1% of severe ED and 62.8% of SCCs. For the CDK inhibitors, these proteins were detectable in all normal mucosa and most of the mild and moderate ED. For severe ED, expression of these proteins was not observed in some cases (p12^DOC−1, 14.3%; p16^INK4A, 28.6%; p27^KIP1, 7.1%). For SCCs, the expression of p12^DOC−1 was lost in 71.8%, p16^INK4A in 69.2% and p27^KIP1 in 35.9%. These results suggest that elevated expression of cyclin D1, cyclin E, CDK2 and loss of p12^DOC−1, p16^INK4A and p27^KIP1 may contribute to the multistep nature of oral carcinogenesis.

Keywords: Cyclin, Cyclin dependent kinase, Cyclin dependent kinase inhibitor, Oral cancer