Abstract 2811: Allogeneic cell cased vaccine development by shared antigen screening

Abstract

Abstract The fundamental premise of allogeneic vaccines for cancer relies upon the presence of common antigens that are shared between established cell lines and a large proportion of patients with histologically related tumors. Recent results from The Cancer Genome Atlas have clearly demonstrated that somatic mutations in exon region DNA, while potentially immunogenic, do not result in the translation of antigenic proteins that are similar from patient to patient. Instead, these data reinforce the concept that dysregulation of common pathways contributes to the general property of de-differentiation in tumor cells and the acquisition of immature phenotypes as compared to untransformed precursor cells. This phenomenon leads to expression of mucinous and embryonal antigens, collectively known as cancer testis antigens, that are otherwise rare in mature tissues and to which central tolerance remains incomplete. We have developed allogeneic vaccines based on parallel screening of non-small cell lung, bladder, triple-negative breast, ovarian and melanoma tumor cell lines and patient tumor samples. The baseline expression of certain antigens, including SSX2, SSX4, CT10, MAGE-A1, MAGE-A10, LAGE-1 and NY-ESO-1 was found to vary widely both between tumor samples and non-transformed tissue controls. Among all antigens screened, MAGE-A3 was most commonly upregulated across transformed tissue samples, however other antigens including BAGE-1, XAGE-1b and MAGE-A10 were found to be most dramatically upregulated. This analysis provides a screening tool with which to appropriately profile and prioritize individual cell lines for vaccine development in histologically diverse tumor types. Citation Format: Vadim V. Deyev, Neal Schilling, Taylor H. Schreiber. Allogeneic cell cased vaccine development by shared antigen screening. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2811. doi:10.1158/1538-7445.AM2014-2811