Abstract 1161: The relationship between the 14-3-3zeta expression pattern and the clinicopathological variables of the 192 gastric cancer patients.

Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Gastric cancer remains one of the most common malignant diseases, despite its steady declining trend worldwide. Overall, gastric cancer mortality is estimated to be 700000 cases annually (10.4% of all cancer related death), ranking second only after lung cancer. 14-3-3zeta, a member of 14-3-3 proteins, have important roles in a wide range of biological processes through the interactions with >100 key proteins, such as FOXO3a, Bad and CCND1. Recent studies have revealed that up-regulation of 14-3-3zeta contribute to the transformation phenotype of breast and lung cancer. However, the relevance of 14-3-3zeta expression in gastric carcinogenesis remained poorly understood. In this study, we aimed to clarify the clinicopathological significance of 14-3-3zeta expression in patients with gastric cancer. A total of 192 gastric cancer specimens were obtained from patients undergoing curative surgery at Oita University Hospital. The expression levels of 14-3-3zeta were investigated by immunohistochemistry. The relationship between the 14-3-3zeta expression pattern and the clinicopathological variables of the gastric cancer patients were analyzed. 14-3-3zeta was strongly expressed in 102of the 192 cases. Strong expression of 14-3-3zeta was correlated with Lymph node metastasis, Histological subtype and Tumor stage (Fisher's exact test, p<0.05). These results suggest that up-regulation of 14-3-3zeta is associated with the clinically malignant features of gastric cancer. Citation Format: Tetsuya Aizawa, Yoshiyuki Tsukamoto, Masatsugu Moriyama, Tsuyoshi Noguchi. The relationship between the 14-3-3zeta expression pattern and the clinicopathological variables of the 192 gastric cancer patients. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1161. doi:10.1158/1538-7445.AM2013-1161