ReviewGut microbes2026
Microbiota as a modulator of drug response: targeting microbial-drug crosstalk in cancer therapy.
Review in Gut microbes, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, accumulating evidence has established mechanistic connections between the microbiota and the efficacy of anticancer treatments, encompassing microbial communities residing in the gut, within tumors, and across other tissue sites. Across diverse malignancies, distinct compositional and functional profiles of these microbial ecosystems have been associated with differential responses to chemotherapy, immunotherapy, and targeted agents, as observed in both clinical settings and experimental systems. It is now understood that microbial communities exert influence on drug activity through multiple pathways: they may compromise therapeutic efficacy by metabolic inactivation or structural modification of anticancer compounds, or, conversely, potentiate responses by enhancing tumor cell susceptibility. Furthermore, these communities modulate the tumor immune microenvironment, fostering antitumor immunity through augmented antigen presentation and effector cell function, or constraining immune responses via regulatory networks and immunosuppressive myeloid polarization. The crosstalk between microbial cues and signaling networks in malignant and surrounding stromal tissues is widely thought to influence therapeutic outcomes. Key challenges ahead involve proving causation, elucidating context-dependent mechanisms, and translating patient heterogeneity into robust biomarkers and targeted therapies. Anticancer interventions can reportedly alter microbial community structure and function, with therapy-associated dysbiosis potentially contributing to primary or acquired resistance. Microbiota-directed strategies, including transplantation, defined microbial consortia, targeted delivery systems, and lifestyle interventions, are under investigation, yet challenges remain in establishing causality, ensuring safety, and enabling patient stratification. Collectively, these insights establish a translational framework for rationally designed microbiota‒drug combination strategies aimed at enhancing anticancer therapeutic outcomes.
Indexed as
Identifiers
What Socratic 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 Socratic graph.