epigenetic reprogramming to preserve T-cell stemness and functionality
First-pass extracted concept
epigenetic reprogramming
Candidate: concept label3 source documents3 linked claims
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Evidence Snippets
approaches aimed at overcoming T-cell dysfunction through ... epigenetic reprogramming
Emerging evidence highlights hypoxia-centered signaling cascades, epigenetic reprogramming, and metabolic plasticity as pivotal regulators of trophoblast adaptation.
Supporting Sources
Linked Claims
Strategies explored to improve CAR-T function in solid tumors include optimizing receptor clustering to boost immune synapse formation, increasing ITAM number or strength, adding novel or multiple co-stimulatory domains, cytokine secretion, epigenetic reprogramming, and synthetic biology tools for tunable or logic-gated activation.
Quoted textsource-backed
To improve CAR-T-cell function in solid tumors, numerous studies have explored multiple strategies: engineering CARs to boost immune synapse formation via optimized receptor clustering, increasing the ITAM number/strength to amplify downstream signaling, and incorporating novel/multiple co-stimulatory domains to sustain T-cell activation and persistence. Additionally, approaches include the use of CAR-T cells that secrete pro-inflammatory cytokines, epigenetic reprogramming to preserve T-cell stemness and functionality, and the use of synthetic biology tools for tunable/logic-gated CAR activation.
Hypoxia-centered signaling cascades, epigenetic reprogramming, and metabolic plasticity are pivotal regulators of trophoblast adaptation.
Quoted textsource-backed
Emerging evidence highlights hypoxia-centered signaling cascades, epigenetic reprogramming, and metabolic plasticity as pivotal regulators of trophoblast adaptation.
Intrinsic checkpoint rewiring, cytokine armoring, and epigenetic reprogramming are approaches aimed at overcoming T-cell dysfunction to sustain antitumor activity in hostile microenvironments.