ENHANCED EXPRESSION OF TRANSFORMING GROWTH FACTOR BETA ONE (TGF-β1) DURING PROGRESSION OF ORAL EPITHELIAL DYSPLASIA TO CARCINOMA

Document Type : Original Article

Authors

1 Lecturer, Department of Oral Pathology, Faculty of Dentistry, Tanta University, Egypt

2 Associate Professor, Department of Oral Pathology, Faculty of Dentistry Tanta University, Egypt

Abstract

Objective:  transforming  growth  factors  (TGFs),  the  pro-inflammatory cytokines  play  an important role in malignancy. This study was aimed to evaluate immunohistochemically the expression of TGF-β1 protein in epithelial dysplasia (ED), carcinoma in situ (CIS) and oral squamous cell carcinoma (OSCC) in order to elucidate its role in oral carcinogenesis.
 
Material and methods: 30 cases of OSCC was investigated including well, moderately and poorly differentiated OSCC (10 cases each) that contained normal epithelium, ED and foci of CIS. They were subjected to immunohistochemistry using antibodies against TGF-β1.
Results: the expression of TGF-β1 was increased in intensity and distribution in different stages of ED and OSCC when compared to normal mucosa. In ED, TGF-β1 intensity score was weak (1+) in 8 cases (26.6%), moderate (2+) in 20 cases (66.6%) and strong (3+) in 2 cases (6.6%). In CIS, the intensity score of TGF-ß1 was weak (1+) in 3 cases (10%), moderate (2+) in 17 cases (56.6%) and strong (3+) in 10 cases (33.3%). TGF-β1 expression was markedly enhanced in both OSCC cells and stromal cells. TGF-β1 score of intensity was weak (1+) in 2 cases (20%) of well differentiated and in 1 case (10%) of moderately and poorly differentiated OSCC. TGF-β1 score of intensity was moderate (2+) in 3 cases (30%) of well differentiated and moderately differentiated, and in 1 case (10%) of poorly differentiated. On the other hand, the expression score of TGF-β1 was strongly positive (3+) in 5 (50%), 6 (60%) and 8 (80%) cases of well, moderately and poorly differentiated OSCC respectively.
 
Conclusion: enhanced expression of TGF-β1 could be responsible for transformation of oral premalignant lesions to OSCC as well as more aggressive tumor growth, metastasis and resistance to treatment.
 

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