ArticleJournal of nanobiotechnology2026
Dual-loaded homotypic exosomes with endogenous IR808 and pH-responsive DOX drive sequenced chemo-PDT and convert "cold" OSCC tumors "hot".
Article in Journal of nanobiotechnology, 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
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
backgroundChemotherapy remains central to oral squamous cell carcinoma (OSCC) management but is constrained by poor specificity, systemic toxicity, multidrug resistance, and limited durability. Tumor-derived exosomes (TEX) offer a clinically relevant carrier owing to their biocompatibility, low immunogenicity, and homotypic targeting; however, prevailing high-efficiency loading methods (electroporation/sonication/extrusion, etc.) may disrupt membrane proteins, promote cargo leakage and aggregation, and increase costs-hindering clinical translation.
resultsHere we report IR808/Doxorubicin@Tumor-derived Exosomes (ID-TEX) that combine endogenous IR808 loading (preserving membrane integrity and homotypic ligands) at cell level with covalent, pH-responsive anchoring of doxorubicin via a hydrazone linker on the exosome surface (HYD-DOX). Upon cellular uptake, acidification in endosomes/lysosomes rapidly cleaves the linker, releasing DOX to induce nuclear DNA damage, followed by IR808-mediated photodynamic therapy (PDT) to amplify oxidative stress-establishing a sequenced chemo-PDT cascade. Leveraging the native integrin repertoire and CD47 signaling of TEX, ID-TEX achieves active homing, prolonged circulation, uniform intratumoral distribution, and deep penetration. Mechanistically, the intensified oxidative and multi-pathway cytotoxic stress elicits immunogenic cell death (ICD), promotes dendritic cell maturation, and recruits CD8⁺ and CD4⁺ T cells, converting "cold" OSCC into "hot" tumors and transforming localized photochemotherapy into systemic antitumor immunity.
conclusionsCentering this chemo-photodynamic-immunotherapeutic cascade on enhanced ROS, ID-TEX concurrently improves efficacy, reduces toxicity, and strengthens immune modulation, underscoring strong translational potential for precision OSCC therapy.
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.