# Expression of Cyclin D1, p53, and Tumor-Associated Tissue Eosinophils in Different Grades of Oral Squamous Cell Carcinoma

## TL;DR

This study examines how cyclin D1, p53, and tissue eosinophils relate to the severity of oral cancer, finding that higher cyclin D1 and p53 levels are linked to more severe tumors.

## Contribution

The study identifies cyclin D1 and p53 as potential prognostic markers and highlights TATE's role in tumor differentiation in oral SCC.

## Key findings

- Cyclin D1 and p53 expression significantly increases with higher tumor grades.
- Tumor-associated tissue eosinophils are more common in lower-grade oral SCC.
- Non-keratinizing SCC shows the highest expression of cyclin D1 and p53.

## Abstract

Background

Oral squamous cell carcinoma (SCC) is a significant health burden, particularly in developing countries. Cyclin D1 and p53 regulate cell cycle progression and apoptosis, while tumor-associated tissue eosinophilia (TATE) influences the tumor microenvironment. In this study, we aimed to assess the correlation between cyclin D1, p53, and TATE expression and tumor grade and histological subtypes in oral SCC.

Methodology

A total of 90 SCC patients were studied at the Pakistan Institute of Medical Sciences Hospital over one year. Tumors were categorized into well-differentiated, moderately differentiated, poorly differentiated, and non-keratinizing subtypes. Immunohistochemical staining for cyclin D1 and p53 was graded (0-3), while TATE was classified as grade 1 (0-10), grade 2 (11-20), and grade 3 (>20 eosinophils per high-power field). Statistical analyses were performed using SPSS version 21 (IBM Corp., Armonk, NY, USA).

Results

Cyclin D1 and p53 expression significantly increased with tumor grade (p = 0.001), whereas TATE was more prevalent in lower-grade SCC (p = 0.03). Non-keratinizing SCC showed the highest cyclin D1 (66.6%) and p53 (100%) expression, whereas 66% had grade 3 TATE.

Conclusions

Cyclin D1 and p53 are potential prognostic markers for SCC, whereas TATE may influence tumor differentiation.