Introduction: Sox genes encode a family of high-mobility group transcription factors that play critical roles in organogenesis. Sox2 is suggested to be one of stemness factors that render the reprogramming capability of adult cells into germ-line-competent induced pluripotent stem cells. Sox2 might be associated with cancer stem cells that are the only cells with unlimited proliferation potential and with the capability of driving tumor progression. Recently, a number of studies have reported the correlation between Sox transcription factors and human cancers. Since little is known about the efficacy of Sox2 as a potential biomarker for gastric cancer, we investigated the significance of Sox2 expression in human gastric cancer.

Material and Methods: A total of 260 patients who had undergone resection of a primary gastric cancer at our institute were enrolled. Sox2 expression was analyzed by immunohistochemistry. Sox2 expression was evaluated by intensity of staining and percentage of stained tumor cells: intensity was given scores 0-3 (0=no,1=weak, 2=moderate 3= intense) and population was given scores 0-5 (0=0%, 1=1-25%, 2=26-35%, 3=36-45%, 4=46-65%, 5=66-100%) The two scores were then added to obtain the final result of 0-8. Expression of Sox2 was considered high expression when scores were ≥5 and low expression when scores were ≤4.

Results: Sox2 expression was positive in 153 (58.8%) of 260 gastric cancers. There was a statistically significant correlation between Sox2 expression and depth of tumor invasion (p=0.002) and lymphatic invasion (p=0.002). The prognosis of patients with Sox2 expression positive tumors was significantly (p=0.046) worse, while a multivariate analysis revealed that Sox2 expression was not an independent prognostic factor.

Conclusion: Sox2 expression might be associated with invasion of gastric cancer. Sox2 expression might be a useful prognosis marker for patients with gastric cancer.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3366.