PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) AND P53 IN EPITHELIAL DYSPLASIA AND SQUAMOUS-CELL CARCINOMA OF ORAL-MUCOSA - A MARKER FOR POOR TUMOR DIFFERENTIATION, INCREASING NUCLEAR ATYPIA AND INVASIVENESS

Citation
Ha. Lan et al., PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) AND P53 IN EPITHELIAL DYSPLASIA AND SQUAMOUS-CELL CARCINOMA OF ORAL-MUCOSA - A MARKER FOR POOR TUMOR DIFFERENTIATION, INCREASING NUCLEAR ATYPIA AND INVASIVENESS, Anticancer research, 16(5B), 1996, pp. 3059-3065
Citations number
39
Categorie Soggetti
Oncology
Journal title
ISSN journal
02507005
Volume
16
Issue
5B
Year of publication
1996
Pages
3059 - 3065
Database
ISI
SICI code
0250-7005(1996)16:5B<3059:PCNA(A>2.0.ZU;2-7
Abstract
The immunohistochemical expression of proliferating cell nuclear antig en (PCNA) and p53 was investigated in 9 cases of epithelial dysplasia and 38 cases of squamous cell carcinoma of the oral cavity. The intens ity of immunoreactivity for each marker was assessed casing a semiquan titative grading system, and was correlated with tumor differentiation , nuclear atypia and the patterns of invasive margins in the underlyin g connective tissue. PCNA expression in dysplastic epithelium was obse rved in the suprabasal and lower spinous layers; and the labeling grad e and intensity of staining increased along with the degree of cellula r atypia. In 2 cases of dysplasia, weak positive immunoreactivity for p53 could be seen in a few isolated cells of the basal layer: In squam ous cell carcinoma, PCNA expression was correlated with the degree of tumor differentiation and nuclear atypia in well and moderately differ entiated carcinoma, but not with the invasive pattern of tumor growth. Immunoreactivity for p53 was positive in 30 cases and showed a distri bution pattern very similar to PCNA but with fewer positive cells. Thr ee distinct categories of expression for PCNA and p53 were observed, a mong therm a combination of intense reactivity for both markers was in dicative of poor differentiation, higher nuclear atypia and more invas ive growth of tumor cells.