Activation-Induced Cytidine Deaminase Expression in Gastric Cancer

• Published in: Tumor biology Vol. 28; no. 6; pp. 333 - 339
• Main Authors: Kim, Chang Jae, Song, Jae Hwi, Cho, Yong Gu, Cao, Zhang, Kim, Su Young, Nam, Suk Woo, Lee, Jung Young, Park, Won Sang
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Springer Nature B.V 01.01.2007
• Subjects: Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Cell Nucleus - metabolism; Cytidine Deaminase - genetics; Cytidine Deaminase - metabolism; DNA Primers; Gastric Mucosa - enzymology; Gastric Mucosa - pathology; Helicobacter Infections - enzymology; Helicobacter Infections - virology; Helicobacter pylori; Helicobacter pylori - genetics; Humans; Immunoenzyme Techniques; Lymph Nodes - enzymology; Lymph Nodes - pathology; Lymphatic Metastasis; Mutation - genetics; Polymerase Chain Reaction; Polymorphism, Single-Stranded Conformational; Research Article; Stomach Neoplasms - metabolism; Stomach Neoplasms - pathology; Tumor Suppressor Protein p53 - metabolism; Activation-induced cytidine deaminase; Mutations; AID expression; Helicobacter pylori; Gastric cancer; p53
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1159/000124239

Helicobacter pylori increases the risk of gastric cancer development and triggers aberrant expression of activation-induced cytidine deaminase (AID). The goal of the present study was to investigate whether AID expression is involved in the development or progression of gastric cancer and the nuclear expression of p53 protein in cancer cells. We examined the expression pattern of the AID and p53 proteins in 186 gastric adenocarcinomas by immunohistochemistry. In order to investigate the molecular mechanism of AID expression, we also searched for mutations in the AID gene by single-strand conformational polymorphism and sequencing methods. In 186 sporadic gastric cancers, AID expression was detected in the 73 corresponding normal gastric mucosa and in 50 gastric cancers. Statistically, the expression of AID protein was not associated with clinicopathological parameters, including tumor size, location, differentiation and lymph node metastasis (p > 0.05). Interestingly, a significant association was observed between AID and the nuclear expression of p53 (p = 0.0094). Mutational analysis revealed no mutation in the AID gene in the gastric cancers. These results suggest that aberrant expression of the AID protein may contribute to the development of gastric cancers and induce p53 nuclear expression.