Abstract A16: Regulation of TRAIL and NF-kappaB pathways in ovarian cancer.

Abstract

Abstract Objective: The equilibrium between apoptotic and survival pathways determines the fate of cells. Dysregulation in any one mechanism often leads to cancer. The present study was designed to determine the crosstalk between TRAIL and NF-kappaB pathways through study of the much controversial role of DcR2 in the induction of NF-kappaB. Methodology: A total of 50 epithelial ovarian tissue samples were used for immunohistochemical staining of DcR2 and NF-kappaB (p65) proteins along with the other players of TRAIL pathway including DR4, DR5, DcR1, FLIP and TRAIL. Correlations were drawn and survival analysis was performed using Kaplan Meier's method. Results: A total of 72% ovarian carcinomas showed positive DR4 expression, 68% showed positive DR5 expression, 42% showed positive DcR1 expression, 48% showed positive DcR2 expression, 44% had positive FLIP expression, 46% had positive TRAIL expression in epithelium while 28% had positive TRAIL expression in stroma. NF-kappaB was positive in 46% of the tissue samples. A strong but non-significant correlation was seen between DcR2 and NF-kappaB expression. Interestingly a similar correlation was also found between DR4 and NF-kappaB expression. Survival analysis showed better survival for patients with positive NF-kappaB expression as compared to negative expression. Conclusion: Coexpression of DcR2 and NF-kappaB suggests a potential therapeutic approach of targeting NF-kappaB through TRAIL pathway by using anti-DcR2 antibodies. However, the study may be elaborated with increased sample size to get significant results. Note: This abstract was not presented at the conference. Citation Format: Mariam Anees, Umaima Batool, Sidra Bukhari, Sohail Yousaf. Regulation of TRAIL and NF-kappaB pathways in ovarian cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A16.