Abstract
Meeting abstracts Antigen escape tumor cell variants prevail in tumors recurring after treatment with chimeric antigen receptor (CAR) T cells with a single specificity. Recurrent tumors preserve alternative non-targeted tumor associated antigens. A bispecific CAR will mitigate antigen escape
Highlights
A bispecific chimeric antigen receptor molecule enhances T cell activation through dual immunological synapse formation and offsets antigen escape in glioblastoma
Antigen escape tumor cell variants prevail in tumors recurring after treatment with chimeric antigen receptor (CAR) T cells with a single specificity
HER2 and IL13Ra2 are currently targeted in Phase I glioblastoma (GBM) trials using CAR T cells
Summary
A bispecific chimeric antigen receptor molecule enhances T cell activation through dual immunological synapse formation and offsets antigen escape in glioblastoma. Meenakshi Hegde1*, Zakaria Grada, Antonella Pignata, Amanda Wakefield, Kristen Fousek, Kevin Bielamowicz, Kevin Chow, Vita Brawley, Tiara Byrd, Stephen Gottschalk, Malini Mukherjee, Winfried S Wels, Matthew Baker, Giapietro Dotti, Jordan Orange, Nabil Ahmed. From 30th Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2015) National Harbor, MD, USA. From 30th Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2015) National Harbor, MD, USA. 4-8 November 2015
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