The data will be presented today in two poster sessions titled: 'Multi-armored allogeneic MUC-1 CAR T-cells efficiently control triple negative breast cancer tumor growth' (Poster Number: 217) and 'TALEN-edited smart CAR T-cells leverage solid tumor microenvironment for specific and effective immunotherapy' (Poster Number: 325).
The poster presentations highlight the following preclinical data
Multi-armored allogeneic MUC-1 CAR T-cells efficiently control triple negative breast cancer tumor growth
This poster highlights TALEN-edited smart CAR T-cells targeting MUC1- expressing solid tumors.
MUC1 is a tumor-associated antigen that is overexpressed in triple-negative breast cancer (TNBC) and other solid tumor malignancies.
MUC-1 CAR T-cells infiltrate tumors more efficiently and extend survival when enhanced with attributes catered towards the tumor microenvironment (TME) of TNBC tumors.
TGFBR2 knock-out (KO) circumvents the inhibitory effects of TGF1, and IL-12 release follows CAR T-cell activation pattern restricting it to the tumor site for increased safety.
Enhanced MUC-1 CAR T-cells could address some of the current challenges in development of CAR Ts for TNBC patients with unmet medical needs.
Overall, we can efficiently generate allogeneic CAR T-cells and engineer them to overcome several key challenges of immune suppressive solid tumors.
TALEN-edited smart CAR T-cells leverage solid tumor microenvironment for specific and effective immunotherapy
This poster highlights innovative T-cell engineering strategies designed to increase the activity of CAR T-cells for solid tumors while mitigating toxicity risk.
Therapeutic efficacy of CAR T-cell therapy has so far been restricted to only a few malignancies, with solid tumors proving to be especially recalcitrant to efficient therapy. Our TALEN-based gene editing platform allows innovative T cell engineering strategies that can combat some of the challenges posed by CAR T cell development for solid tumors.
Inducible expression of a tumor-antigen directed CAR by a constitutive CAR specific to TME cues greatly enhanced anti-tumor activity, while limiting 'on target, off-tumor' cytotoxicity. Additionally, CAR-induced gene expression could boost anti-tumor CART only within the TME.
This proof-of-concept study demonstrates the feasibility of developing CART cell engineering strategies that can improve solid tumor targeting while mitigating potential safety risks, paving the way for clinical development.
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