ArticleCell reports. Medicine2026
An antibody-PROTAC conjugate targets BRD4/c-Myc/PD-L1 to enhance immunotherapy efficacy in triple-negative breast cancer.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Bridging BET bromodomain and immune checkpoint inhibitors through generative bioorganic frameworks for next-generation cancer immunotherapy.RSC medicinal chemistry · 2026Review
- Targeted protein degradation dismantles undruggable targets to reverse immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) remains an aggressive malignancy lacking effective and safe treatments. Proteolysis-targeting chimeras (PROTACs) represent a promising modality for intractable diseases, but their application in TNBC is hindered by inefficient delivery. Here, we develop ASA, a TNBC-targeting antibody-PROTAC conjugate that links a TROP2-specific antibody to a BRD4-degrading PROTAC, with specificity conferred by TROP2-dependent endocytosis and hypoxia-triggered linker cleavage. ASA exhibits superior TNBC targeting and antitumor efficacy compared with its unconjugated PROTAC moiety. ASA monotherapy elicits stronger long-term immunological memory than the antibody-drug conjugate (ADC) sacituzumab govitecan, an effect that is further amplified by anti-PD-L1 combination. Mechanistically, ASA induces sustained BRD4 degradation, suppressing c-Myc and PD-L1 to inhibit tumor progression and drive long-lasting immunity. By disrupting DNA repair pathways, ASA synergizes with anti-PD-L1 to enhance tumor control and increase CD8
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.