By targeting two gene regulators of inflammation, the engineered T cells expand and last longer inside the solid tumor, raising the possibility that they could have the same therapeutic effect they have in blood cancers. It is the concept on which a new approach against solid tumors is based, being studied in the preclinical phase, developed by researchers at the University of Pennsylvania.
17 MAR – Targeting two regulators that control inflammation-related gene functions leads to a tenfold expansion of T cells, with an increase in anti-tumor immune activity and their persistence at the tumor site. It is the concept on which a new approach against solid tumors is based, being studied in the preclinical phase, developed by researchers at the University of Pennsylvania. The methodology has been described in Proceedings of the National Academy of Sciences (PNAS).
Since the first CAR-T cell treatment was approved, personalized cell treatments have revolutionized blood cancer therapy, but remain ineffective against solid tumors. One of the obstacles in this application is the phenomenon known as T-cell ‘burnout’, in which persistent exposure to antigen causes immune cells to lose their ability to respond to the tumour.
Using the CRISPR-Cas9 technique, the research team went on to inhibit the inflammation regulatory genes Regnase-1 and Roquin-1, individually or together, in T cells from healthy donors, with two different immune receptors currently in phase I of clinical study: the mesothelin-targeting M5 CAR (mesoCAR) and the NY-ESO-1-targeting 8F TCR (NYESO TCR). After editing, the cells were expanded and infused into animal models of solid tumors, where the researchers observed that double inhibition increased the amount of engineered T cells by at least tenfold, and showed increased antitumor activity. and increased life span of engineered T cells.
Source: Proceedings of the National Academy of Sciences 2023
March 17, 2023
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