EXPRESSION AT TUMOUR BUDDING SITES IN COLORECTAL ADENOCARCINOMAS: TRANSLATING MORPHOLOGIC SCORE INTO CLINICALLY USEFUL RESULTS

Abstract

Background: Tumour budding is recognized as an independent prognostic factor in colorectal adenocarcinoma. Increased nuclear expression of β-catenin at tumour budding sites has been implicated in the epithelial-mesenchymal transition. This study evaluated the pathogenetic role of tumour budding through nuclear β-catenin expression and examined its correlation with lymphovascular invasion in colorectal adenocarcinoma.

Material and Methods: This prospective and retrospective study included biopsy-proven colorectal carcinoma cases diagnosed over a two-year period at the Institute of Pathology, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai. Of 199 colorectal adenocarcinomas (NOS), 60 randomly selected cases were included for detailed clinicopathological evaluation. Tumour budding was graded at the invasive front using conventional hematoxylin and eosin staining according to the ITBCC 2016 guidelines and by β-catenin immunohistochemistry. β-Catenin expression was analyzed and correlated with histopathological parameters.

Results: The highest incidence of colorectal carcinoma occurred in patients aged 51–60 years. Females constituted 55% of cases, and proximal tumours accounted for 51.7%. Tumours measuring <5 cm comprised 53.3% of cases, while 53.3% were Stage II. Lymphovascular invasion was absent in 71.7% of cases. By conventional hematoxylin and eosin assessment, 55% of cases demonstrated intermediate tumour budding (B2, 5–9 buds). High tumour budding (B3, >10 buds) was observed in patients aged 51–60 years, and all 14 B3 cases (100%) were moderately differentiated adenocarcinomas. Using β-catenin immunohistochemistry, 43.3% of cases were categorized as intermediate tumour budding (B2). Membranous β-catenin expression was observed in 61.7% of cases, whereas nuclear β-catenin expression was observed in 11.7%. No significant improvement in tumour budding detection was achieved using β-catenin immunohistochemistry compared with conventional hematoxylin and eosin evaluation.

Conclusions: Tumour budding can be assessed using both conventional hematoxylin and eosin staining and β-catenin immunohistochemistry. High tumour budding may provide additional prognostic information; however, no statistically significant association with lymphovascular invasion was demonstrated in this study. However, β-catenin immunohistochemistry did not significantly improve the detection of tumour budding over conventional histopathological assessment.