Immunohistochemical Analysis of SOX2, Ki67, and p53 Expression in the Progression of Barrett’s Esophagus to Esophageal Adenocarcinoma
Background: Barrett’s esophagus (BE) is a premalignant condition that progresses to esophageal adenocarcinoma (EAC) through a sequence of dysplastic changes. The molecular alterations involved in this transition remain incompletely understood. This study evaluates the expression of SOX2, Ki67, and p53 across different stages of BE progression using immunohistochemistry.
Methods: A retrospective analysis was performed on 90 formalin-fixed paraffin-embedded (FFPE) tissue samples from patients categorized into six groups: normal esophageal squamous epithelium (n=15), reflux disease (n=15), non-dysplastic BE (n=15), low-grade dysplasia (LGD, n=15), high-grade dysplasia (HGD, n=15), and esophageal adenocarcinoma (EAC, n=15). Immunohistochemical staining for SOX2, Ki67, and p53 was conducted. Staining intensity and percentage of positive cells were assessed semi-quantitatively. Statistical analysis was performed using ANOVA and Spearman’s correlation tests.
Results: SOX2 expression was significantly reduced with disease progression (p < 0.001), with strong expression in normal esophageal epithelium (58.3 ± 4.8%) and near-total loss in EAC. Ki67 expression increased significantly in dysplastic and neoplastic tissues (p < 0.001), with the highest levels observed in HGD (38.3 ± 4.8%). p53 nuclear accumulation was minimal in normal and non-dysplastic BE, but increased significantly in HGD (35.0 ± 11.2%) and peaked in EAC (53.3 ± 9.7%) (p < 0.001), suggesting TP53 mutation involvement in malignant transformation.
Conclusion: The findings suggest that SOX2 downregulation is an early event in BE, facilitating intestinal metaplasia, while Ki67 and p53 overexpression are associated with dysplasia progression. These biomarkers may serve as useful indicators for identifying high-risk BE patients requiring closer surveillance and early intervention strategies.
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