Activation-Induced Cytidine Deaminase Expression In Colorectal Cancer

Activation-induced cytidine deaminase (AID) produces immune-diversity by inducing somatic hypermutations and class-switch recombinations in human immunoglobulin genes. This role of AID in causing genomic mutations, also can potentially cause somatic mutations in various host genes of non-lymphoid tissues, and contribute to tumorigenesis. The goal of the present study was to investigate whether AID expression was involved in the development or progression of colorectal cancer, and the nuclear expression of p53 protein in cancer cells. We examined the pattern of expression of AID and p53 proteins in 71 colorectal adenomas and 122 sporadic colorectal cancers by immunohistochemistry. AID and p53 expression was detected in 57 (46.7%) and 78 (63.9%) out of 122 colorectal cancers, respectively. Statistically, the expression of the AID protein was not associated with the 5-year survival or clinical and pathological parameters, including tumor stage, location, size, and lymph node metastasis (P > 0.05). However, the expression of the AID protein was associated with tumor differentiation (P = 0.004). In addition, a significant association was observed between AID and the nuclear expression of p53 in colorectal cancers (P = 0.0357). Only 3 (4.2%) of the 71 colorectal adenomas showed immunopostivity for AID, resulting in a significant difference between total colorectal cancers and adenomas (P < 0.001). The p53 expression was detected in 7 (9.9%) out of 71 colorectal adenomas. Statistically, AID protein was not associated with the degree of dysplasia and the nuclear expression of p53 in colorectal adenomas (P > 0.05). These results suggest that aberrant expression of the AID protein might play a role in the development of colorectal cancers.