ReviewCancer cell international2026
Exosomes in cancer drug resistance: dual roles in therapy failure and emerging precision therapeutics.
Review in Cancer cell international, 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
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exosomes play a key role in cancer, functioning both as drivers of drug resistance and as tools for therapy. Tumor-derived exosomes facilitate intercellular communication through selective transfer of bioactive cargo, including proteins (e.g., P-gp, PD-L1), nucleic acids (e.g., miR-21, lncRNA H19), lipids, and metabolites. These cargos remodel the tumor microenvironment, activate oncogenic pathways such as PI3K/AKT and MAPK, and promote drug resistance, immune evasion, and metabolic reprogramming. This work presents a conceptually integrated translational perspective, introducing the 'exosome paradox' to unify the dual roles of exosomes in therapy resistance and therapeutic application. The review incorporates cancer-specific insights, highlighting how resistance mechanisms vary across pancreatic, breast, lung, colorectal, and ovarian cancers, underscoring the need for context-dependent strategies. Mechanistically, we integrate emerging advances in exosome heterogeneity, selective cargo loading (including SUMOylation-dependent pathways), and the metabolic-epigenetic interface, particularly the lactate-lactylation axis. We also explore the growing role of artificial intelligence in biomarker discovery, cargo profiling, and rational design of engineered exosomes. Therapeutically, two complementary strategies are emphasized: inhibition of pathogenic exosome biogenesis, secretion, and uptake, and development of engineered exosomes as delivery vehicles for chemotherapeutics, RNA-based therapies, and CRISPR/Cas9 systems. Despite promising preclinical advances, clinical translation remains limited by challenges in targeting specificity, pharmacokinetics, scalable manufacturing, and regulatory standardization. This review provides a unified framework combining suppression of pathogenic exosome signaling with strategic engineering of therapeutic exosomes, offering new directions for overcoming drug resistance and advancing precision oncology.
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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.