Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias

• Verfasst von: Nasser, Wasim [VerfasserIn]
• Verfasst von: Flechtenmacher, Christa [VerfasserIn]
• Verfasst von: Holzinger, Dana [VerfasserIn]
• Verfasst von: Hofele, Christof [VerfasserIn]
• Verfasst von: Bosch, Franz X. [VerfasserIn]
• Titel: Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias
• Verf.angabe: Wasim Nasser, Christa Flechtenmacher, Dana Holzinger, Christof Hofele, Franz X. Bosch
• E-Jahr: 2011
• Jahr: 25 March 2011
• Umfang: 7 S.
• Fussnoten: Im Titel ist "INK4a" hochgestellt ; Gesehen am 21.09.2022
• Titel Quelle: Enthalten in: Journal of oral pathology & medicine
• Ort Quelle: Oxford [u.a.] : Wiley-Blackwell, 1972
• Jahr Quelle: 2011
• Band/Heft Quelle: 40(2011), 8, Seite 629-635
• ISSN Quelle: 1600-0714
• DOI: doi:10.1111/j.1600-0714.2011.01026.x
• Datenträger: Online-Ressource
• Sprache: eng
• Bibliogr. Hinweis: Erscheint auch als : Druck-Ausgabe: Nasser, Wasim, 1978 - : Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias. - 2011
• Sach-SW: combined protein biomarkers
• Sach-SW: leukoplakia without dysplasia
• Sach-SW: oral leukoplakia
• Sach-SW: potential malignant progression
• K10plus-PPN: 1817177567

Abstract

J Oral Pathol Med (2011) 40: 629-635 Background: The risk of malignant progression of oral leukoplakia with and without dysplasia is unpredictable. Materials and methods: Leukoplakias without dysplasia of 35 patients, leukoplakias with dysplasia of 4 patients, and similar lesions obtained from tumor patients were retrospectively examined by immunohistochemistry for the expression of the proteins pRb, p53, p16INK4a, Cyclin D1 and Ki-67. The predictive power of combined aberrant expression patterns for the progression of leukoplakias without dysplasia was examined. Results: Increased expression of p53, Ki-67 and Cyclin D1, and loss of p16INK4a occurred in 45.9%, 38.9%, 29.4% and 32.4% of the leukoplakias without dysplasia, respectively. All alterations increased with progression but had poor positive predictive value. However, the combined p53/p16INK4a/Ki-67 aberration occurred in only three (9%) cases, of which two patients (66.7%) experienced progression to dysplasia and carcinoma in situ. The combined p53/p16INK4a/Ki-67 alteration had a negative predictive value (NPV) and sensitivity of 100%, specificity of 97% and positive predictive value (PPV) of 67%. By contrast, the combined p53/p16INK4a/Cyclin D1 alteration had 97% NPV and sensitivity of 50%, specificity of 90% and only 25% PPV. Loss of pRb and concomitant overexpression of p16INK4a were not observed arguing against an involvement of HPV in oral leukoplakia. Conclusions: We propose the combined p53/p16INK4a/Ki-67 alteration as a basic marker to define high risk leukoplakia patients. Lesions not showing this alteration appear to be harmless. Future studies should validate these findings and search for proteins which can further improve the PPV of the proposed basic marker.