ArticleCell reports. Medicine2025
Selective apoptosis of tumor-associated platelets boosts the anti-metastatic potency of PD-1 blockade therapy.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Platelets as localized conduits of TGF-β1 in the tumor microenvironment: implications for cancer progression and therapy.Human cell · 2026Review
- Bidirectional regulatory mechanisms and therapeutic prospects of tumor hypercoagulable state and immunosuppressive tumor microenvironment.Oncology reviews · 2026Review
- Beyond monoclonal antibodies: constraints and the case for alternative PD-1/PD-L1-targeting formats.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the transformative impact of programmed cell death protein-1 (PD-1) blockade therapy on metastatic/advanced solid tumor treatment, its efficacy is hindered by a limited response rate. Platelets play a pivotal role in tumor metastasis by shielding circulating tumor cells and secreting immunosuppressive factors. We here demonstrate that selectively inducing apoptosis in tumor-associated platelets (TAPs) using ABT-737-loaded nanoparticles (cyclic arginine-glycine-aspartate containing peptide-modified ABT-737-loaded nanoparticles [cRGD-NP@A]) enhances the anti-metastatic efficacy of the anti-PD-1 antibody (aPD-1). cRGD-NP@A specifically binds to TAPs, disrupting platelet-tumor cell interactions and exposing tumor cells to immune surveillance in vivo. Combined with aPD-1, cRGD-NP@A substantially augments immune activation and reduces TAP-derived immunosuppressive factors, notably transforming growth factor β1 (TGF-β1), consequently improving anti-metastatic outcomes across multiple metastasis-bearing animal models without observable adverse effects. Our study underscores the importance of depleting TAPs to enhance PD-1 blockade therapy, presenting a promising strategy to improve response rates and clinical outcomes for patients with metastatic cancer.
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