Background: Helicobacter Pylori (H. Pylori) has been known as the strongest risk factor in developing gastric carcinoma (GC) through a cascade of epithelial changes that leads to precancerous lesions which predispose to gastric carcinoma. Aim of the work: This study was designed to investigate the expression of P53 , SOX2 and SOX9 in H. Pylori chronic gastritis , pre-cancerous gastric lesions and gastric carcinoma .
Method: Fifty seven cases of chronic gastritis were selected (37 cases of chronic superficial gastritis without intestinal metaplasia(IM) and 20 cases showed intestinal metaplasia), 18 cases of dysplasia and 30 cases of gastric carcinoma beside 6 normal gastric endoscopic biopsies . Giemsa stains used to detect H pylori colonies. Immunohistochemical technique was applied to detect P53, SOX2 and SOX9 expression and correlate them with clinopathological finding.
Results: Both P53 and SOX9 expression was statistically increased from normal gastric mucosa through chronic superficial gastritis, intestinal metaplasia , dysplastic cases and GC . In the contrast, SOX2 expression was observed in (9.5%) of GC, compared with (83.3%) of normal mucosa.
Among H pylori infected cases , P53 expression was found in 53.8% of chronic superficial gastritis, 81.2% of metaplasia , 88.8% of dysplasia and 80% of GC (p0.05). SOX2 was significantly inversely correlated with the grade of the tumor, LN metastasis and distant metastasis.
A positive significant was found between P53 and SOX9 in chronic superficial gastritis , IM , Dysplasia and carcinoma cases in relation to H pylori infection .
Conclusion : It was elucidated that 1- - H. pylori infection can strength and contribute in SOX9 and P53 mutation , considering H. pylori a risk factor for gastric carcinogenesis. 2- It was concluded that SOX2 is able to repress SOX9 and /or P53 expression, which might be one of the molecular mechanisms involved to maintain normal gastric differentiation 3- SOX9 overexpression and SOX2 suppression that occurs in H pylori infection could lead to intestinal metaplasia . |
