Document Type : Research Articles
Authors
1
Department of Pediatrics, Uttar Pradesh University of Medical Sciences, Saifai, Etawah, Uttar Pradesh, India.
2
Department of Pathology, All India Institute of Medical Sciences, Gorakhpur, India.
3
Department of Radiation Oncology, Hanuman Prasad Poddar Cancer Hospital and Research Institute, Gorakhpur, India.
4
Department of Pediatric Surgery, Uttar Pradesh University of Medical Sciences, Saifai, Etawah, Uttar Pradesh, India.
Abstract
Background: The tumor suppressor p53 and the Wnt pathway effector β-catenin represent two of the most frequently dysregulated molecular components across human malignancies. Although gallbladder cancer (GBC) predominantly affects adults, the pattern and clinicopathological correlates of p53 and β-catenin dysregulation in GBC may illuminate how these pathways behave in different biological contexts, including developmental and pediatric oncological settings, where analogous pathway alterations drive distinct tumor types. Objective: To characterize p53 and β-catenin expression patterns in gallbladder carcinoma by immunohistochemistry, correlate findings with clinicopathological parameters, and discuss in a qualified, hypothesis-generating framework the parallels and divergences between these pathway alterations and those reported in pediatric malignancies. Methods: A cross-sectional study analyzed 61 neoplastic and 49 non-neoplastic gallbladder lesions (2017–2021) using standardized immunohistochemistry for p53 (clone DO-7; Dako/Agilent, 1:100) and β-catenin (clone E247; Abcam, 1:200). Expression patterns were correlated with clinicopathological parameters using chi-square and Fisher’s exact tests. Findings were discussed in the context of published pediatric cancer literature, with explicit acknowledgment of inter-study methodological heterogeneity. Results: p53 overexpression (defined as >20% nuclear positivity) occurred in 78.2% of GBC cases versus 11.1% of benign lesions, correlating significantly with tumor grade and stage (p<0.05). Aberrant β-catenin expression (cytoplasmic/nuclear) was observed in 81.8% of malignant cases, with nuclear localization in 36.3%, correlating with poor differentiation. These patterns qualitatively parallel though are not directly quantitatively comparable to those reported in pediatric hepatoblastoma, Wilms’ tumor, and pediatric sarcomas. Conclusion: p53 and β-catenin dysregulation in GBC exhibits qualitative parallels to patterns reported in pediatric cancers, suggesting shared oncogenic pathway biology. These observations are hypothesis-generating and warrant validation through functional studies in appropriate preclinical models before therapeutic implications can be drawn.
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