Abstract [Background] Survivin is a member of the inhibitor of apoptosis protein family, which is a bifunctional protein that suppresses apoptosis and regulates cell division. Survivin is expressed in various malignant tumors. The overexpression of survivin has been reported to be a poorer prognostic factor in various malignancies. However, the prognostic value of survivin expression in patients with oral cancer is still controversial. Moreover, there are few comparative studies of survivin expression between the cytoplasm and nucleus of individual cells. [Purpose] The aims of present study were to evaluate the expression of survivin protein in oral squamous cell carcinoma (OSCC) and to elucidate the relationships among the survivin expression, clinical stages, histological differentiation and YK classification. [Materials and Methods] Four human OSCC cell lines, B88, CAL27, HNt, and HSC3 cells were used in this study. Normal gingival epithelial cells served as control. Survivin expression of cultured cells was detected by western blot. Tissue specimens were obtains from 57 patients with OSCC after surgery or biopsy. Survivin expression was detected by an immunohistochemical method. [Results] The expression of survivin was detected in cancer cells, but not in normal cells. Immunohistochemical analysis of 57 cases of OSCC showed that 50 (88%) cases expressed survivin. Moreover, analysis of 50 positive cases revealed 28 cases with survivin-positive staining both in the cytoplasm and the nucleus, and 22 cases with survivin expression in cytoplasm only. There was no relationship between survivin expression and clinical stages, or histological differentiation. There were significant differences between survivin expression of nucleus and YK classification, implicated invasion mode of cancer. [Conclusions] These findings suggested that the expression of survivin in OSCC could be related to invasion mode. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 201. doi:10.1158/1538-7445.AM2011-201