Expression of cell cycle control proteins in normal epithelium, premalignant and malignant lesions of oral cavity
| Autor: | David T.W. Wong, Yuji Nakahara, Mariko Mihara, Satoru Shintani, Tomohiro Matsumura, Akihisa Kiyota, Yoshiya Ueyama |
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| Rok vydání: | 2002 |
| Předmět: |
Cancer Research
Cyclin E Cyclin D Blotting Western Cyclin B Cell Cycle Proteins Protein Serine-Threonine Kinases Epithelium Cyclin D1 Cyclin-dependent kinase Biomarkers Tumor CDC2-CDC28 Kinases Humans neoplasms Cyclin-Dependent Kinase Inhibitor p16 Cyclin biology Tumor Suppressor Proteins Cyclin-Dependent Kinase 2 Intracellular Signaling Peptides and Proteins Mouth Mucosa Cell cycle Immunohistochemistry Cyclin-Dependent Kinases stomatognathic diseases Oncology Epidermoid carcinoma Carcinoma Squamous Cell biology.protein Cancer research Mouth Neoplasms biological phenomena cell phenomena and immunity Oral Surgery Carrier Proteins Precancerous Conditions Cyclin-Dependent Kinase Inhibitor p27 |
| Zdroj: | Oral Oncology. 38:235-243 |
| ISSN: | 1368-8375 |
| DOI: | 10.1016/s1368-8375(01)00048-3 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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