ArticleNature communications2026
Chemical anchoring of immunotherapeutic drugs within senescent tumor cells overcomes senescence-driven immunotherapy resistance.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
Abstract
Multidrug resistance (MDR) compromises cancer treatment efficacy and leads to therapeutic failure. Therapy-induced senescence further complicates MDR through senescence-enhanced drug efflux and senescence-associated secretory phenotypes (SASPs), remaining a huge challenge. Here, we develop a self-generative senescence-associated β-galactosidase (SA-β-gal)-initiated chemical anchoring of lysosomal protein approach to counteract drug efflux and reprogram SASPs. A senescence-tumor-targeted immunotherapeutic drug (DN-Ghcy) is fabricated by a SA-β-gal-activatable bio-orthogonal receptor (Ghcy) and an engineered immunostimulatory prodrug (DN, an indoleamine 2,3-dioxygenase (IDO) inhibitor conjugated to a PD-L1 binding peptide). DN-Ghcy is selectively immobilized in senescent tumor cells via SA-β-gal-catalyzed bio-orthogonal nano-receptor, enabling drug retention and bypassing transporter-mediated efflux. Under near-infrared irradiation, DN-Ghcy concurrently mediates degradation of PD-L1, release of IDO inhibitor, and disruption of lysosomal integrity. This strategy reverses immunotherapy resistance in female mice with senescent tumors, establishing a promising modality to overcome senescence-driven immunotherapy resistance.
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