ABSTRACT Background: Cervical squamous cell carcinoma (SCC) remains a significant global cancer burden, with recurrence and treatment resistance creating major hurdles for long-term disease control. Antigen Kiel 67 (Ki-67), a well-established marker of cellular proliferation, and sex-determining region Y-box 2 (SOX-2), a cancer stem cell-associated marker, are less well characterized in the context of cervical SCC, particularly within our study population. Objective: To evaluate expression of SOX-2 and Ki-67 in SCC cervix and their correlation with demographic and clinicopathological factors to find their synergistic impact on disease aggressiveness. Materials and Methods: The study included 105 cases of cervical SCC over a period of 1.5 years. Clinical and demographic details were obtained from medical records. Tumors were classified into keratinizing versus non-keratinizing, and histological grading was done as per the guidelines. Immunohistochemistry (IHC) was performed for Ki-67 and SOX-2. Statistical analyses and survival outcomes were calculated. Results: Of the 105 patients, most samples underwent incisional biopsy (96%). Most patients were in the age group of 41–50 years with a median age of 54 years. The common presentations were vaginal growth and abnormal uterine bleeding. A high Ki-67 score was observed more frequently in keratinizing SCC with a higher clinical stage. Ki-67 scoring showed no significant association with clinical stage ( P = 0.42) or histological pattern ( P = 0.84), whereas histological grade showed a borderline association ( P = 0.06). SOX-2 expression was noted in 56.2% of the cases, suggesting its role in the pathogenesis of the disease. SOX-2 expression was significantly associated with histological grade ( P = 0.04), but not with clinical stage ( P = 0.44) or histological pattern ( P = 0.46). Conclusions: In conclusion, we observed a significantly better overall survival (OS) in cervical SCC patients with a low Ki-67 index. SOX-2 showed significantly higher expression in high-grade SCC, suggesting its possible role in pathogenesis. Further studies with larger sample sizes are required to validate our results.
Seth et al. (Mon,) studied this question.