ArticleJournal of materials science. Materials in medicine2026
M1 macrophage membrane-engineered PLGA nanoparticles reprogram M2 tumor-associated macrophages to enhance anti-tumor immunity in breast cancer.
Article in Journal of materials science. Materials in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Nanoparticles (NPs) are used as a suitable delivery system in cancer immunotherapy. Coating NPs with cell membranes can improve their therapeutic efficacy. Tumor-associated macrophages (TAMs) with a dominant phenotype of M2 and anti-inflammatory properties are found within the tumor microenvironment and contribute to tumor progression. Reprogramming TAMs toward a pro-inflammatory M1 phenotype can be a suitable approach to alter the tumor microenvironment and improve treatment outcomes. In this study, we synthesized poly(lactic-co-glycolic acid) (PLGA) NPs loaded with a TLR7/8 agonist (R848) and coated with M1 macrophage cell membranes (CM1), along with a cyclic dinucleotide (CDN) agonist (PLGA-CM1-CDN-R848 NPs), and their ability to reprogram M2-like macrophages was investigated using an in vitro model. PLGA-CM1-CDN-R848 NPs were preferentially taken up by M2-like macrophages and efficiently stimulated the pro-inflammatory cytokines (IL-6, TNF-α, and iNOS) as well as the STING pathway (IFN-β). The reprogrammed macrophages induced apoptosis and cell cycle arrest (G0/G1 and G2/M phases) in 4T1 breast cancer cells. In conclusion, the PLGA-CM1-CDN-R848 NPs formulation represents a promising strategy for breast cancer immunotherapy by targeting M2 TAMs within the TME and reprogramming them toward the M1 phenotype.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.