Year: 2025
Type: article
Abstract: Immunotherapy has revolutionized cancer treatment; yet, a subset of patients with microsatellite instability‐high (MSI‐H) tumors fails to respond to treatment despite their elevated tumor mutational burden and immunogenic potential. In a recent study, Xu et al . uncover a key mechanism of immune evasion in MSI‐H tumors mediated by the exonuclease TREX1, which degrades cytosolic DNA and suppresses activation of the cyclic GMP‐AMP synthase—stimulator of interferon genes (cGAS‐STING)—type I interferon pathway. Loss of TREX1 restores cytosolic DNA sensing, promotes CD8 + T and NK cell infiltration, and enhances antitumor immunity. These findings highlight TREX1 as a potential therapeutic target to overcome resistance to immune checkpoint blockade.
Source: Molecular Oncology
Institutions: UCLouvain, Cliniques Universitaires Saint-Luc
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $4,300
OpenAlex ID: W4416673045