Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τρίτη 9 Οκτωβρίου 2018

Asymmetrical proliferative pattern loss linked to cyclin D1 overexpression in adjacent non-tumour epithelium in oral squamous cell carcinoma

Publication date: Available online 9 October 2018

Source: Archives of Oral Biology

Author(s): Pablo Ramos-García, Miguel Ángel González-Moles, Ángela Ayén, Lucía González-Ruiz, Isabel Ruiz-Ávila, Daniel Lenouvel, José Antonio Gil-Montoya, Manuel Bravo

Abstract
Objective

To evaluate cyclin D1 overexpression in oral squamous cell carcinomas and adjacent non-tumour epithelium as a biomarker of premalignant fields and a risk factor for multiple tumour development.

Design

We studied cyclin D1 expression in 54 patients with 68 oral squamous cell carcinomas plus adjacent non-tumour epithelia characterized as close (n = 58) or distant (n = 41) from the invasion point. Randomized 40x fields were evaluated (4 in tumour tissue and 1 each in close and distant non-tumour epithelium). Expression in non-tumour epithelium was evaluated in basal, parabasal, middle-third and upper-third compartments.

Results

Cyclin D1 overexpression was found in both carcinomas and non-tumour epithelia. Nuclear expression in basal and parabasal layers of distant epithelium was significantly increased in patients with multiple tumours (p < 0.001). A significant association between cyclin D1 overexpression in different epithelial layers was found in both close and distant epithelia. A significant association was found between nuclear expressions of cyclin D1 and Ki-67 in the basal layer of distant epithelium (p = 0.02).

Conclusions

Cyclin D1 overexpression is an early event in oral carcinogenesis linked to loss of the physiological asymmetrical proliferation pattern. Cyclin D1 overexpression in basal and parabasal layers of epithelia distant from the invasion point may act as a potential marker of premalignant fields and multiple tumour development.



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