ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
In Situ Engineering of Tumor Cells as Self-Sustaining cDC1 Programming Factories for Effective Cancer Immunotherapy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- In Situ Engineering of Tumor Cells as Self-Sustaining cDC1 Programming Factories for Effective Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
Conventional type 1 dendritic cells (cDC1s) play a crucial role in initiating and regulating antitumor immunity. However, the insufficient infiltration and dysfunctional state of these cells within the tumor microenvironment hinder antitumor immune response. A tumor-derived extracellular vesicle (EV), termed AS16-EL@MPLA/p-FX, is designed to engineer tumor cells into cDC1 programming factories. The EV lumen carries a plasmid encoding XCL1 and FLT3L. Leveraging the prolonged circulation time and homotypic targeting properties of tumor-derived EV, AS16-EL@MPLA/p-FX demonstrates enhanced tumor-selective accumulation and efficient cellular internalization. Following uptake, tumor cells are reprogrammed into in situ cytokine factories that continuously secrete XCL1 and FLT3L, which effectively recruit and differentiate cDC1s within the tumor microenvironment. Simultaneously, MPLA embedded in the EV membrane is released locally and activates the newly accumulated cDC1s through the TLR4 pathway. Furthermore, an AS16 peptide is tethered to the EV surface via a matrix metalloproteinase-2-cleavable linker. The enzymatic release of AS16 disrupts the VEGF-NRP1 interaction, preventing cDC1 exhaustion. The engineered EV, AS16-EL@MPLA/p-FX, exhibited remarkable tumor-targeting capabilities, promoting the recruitment, differentiation, and activation of cDC1s. This innovative approach not only significantly inhibited tumor growth but also triggered a robust immune memory response, safeguarding against tumor metastasis and recurrence.
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Registered trials
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.