Evidence map›Paper›PMID 41722712›Full record

ArticleBrain, behavior, and immunity2026

Gut microbiota and metabolite disruption during breast cancer chemotherapy is associated with peripheral neuropathy sensory symptoms and pain.

Jeremy T Beales, Varshasnata Mohanty, Melina M Seng, Zoe M Tapp, Sagar D Sardesai, Nicole O Williams, Margaret E Gatti-Mays, Daniel G Stover, Preeti K Sudheendra, Robert Wesolowski and 4 more

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Jeremy T BealesInstitute of Brain, Behavior and Immunology, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Neuroscience Graduate Program, The Ohio State University, Columbus, OH, USA; Medical Scientist Training Program, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Varshasnata MohantyDepartment of Chemistry, University of Illinois Chicago, Chicago, IL, USA.
Melina M SengInstitute of Brain, Behavior and Immunology, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Zoe M TappInstitute of Brain, Behavior and Immunology, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Sagar D SardesaiDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Nicole O WilliamsDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Margaret E Gatti-MaysDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Daniel G StoverDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Preeti K SudheendraDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Robert WesolowskiDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Michael T BaileyInstitute of Brain, Behavior and Immunology, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Center for Microbial Pathogenesis, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA; Department of Pediatrics, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Ai NiDivision of Biostatistics, College of Public Health, The Ohio State University, Columbus, OH, USA.
Stephanie M ColognaDepartment of Chemistry, University of Illinois Chicago, Chicago, IL, USA.
Leah M PyterInstitute of Brain, Behavior and Immunology, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Psychiatry and Behavioral Health, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Electronic address: leah.pyter@osumc.edu.

Funding

(PQ #10) Gut-brain interactions underlying chemotherapy-induced behavioral comorbiditiesR01CA216290 · NCI · OHIO STATE UNIVERSITY · PI PYTER, LEAH M · 2017 to 2021
$2.1M
NCI NIH HHS R01 CA216290
6 · The paper itself

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a common and serious adverse effect of chemotherapeutic agents such as taxanes, platinum compounds, and vinca alkaloids. Efforts to prevent and treat CIPN are impeded by an incomplete understanding of its pathogenesis. Recently, the gut microbiota has been causally linked to CIPN in rodent models. However, human studies exploring this connection are limited. Here, in a cohort of 70 patients with early-stage breast cancer, relationships between disruptions in the gut microbiota during chemotherapy and both participant CIPN symptoms and general pain symptoms were investigated. Study participants provided fecal samples (for 16S rRNA sequencing and targeted metabolomics), blood samples, and sensory symptom information during the three days prior to their first and their final chemotherapy (including a taxane drug) infusions. Sensory neuropathy symptoms increased during treatment, as did circulating levels of neurofilament light chain (NFL), a putative biomarker of CIPN. Decreases in microbiota alpha diversity during chemotherapy were associated with worse neuropathy symptoms during treatment, along with worsening of general pain, after controlling for pre-treatment baseline symptoms. Larger shifts in beta diversity from baseline to last infusion also coincided with more severe neuropathy symptoms. Bacterial producers of short-chain fatty acids were decreased in participants with neuropathy symptoms at the final chemotherapy infusion. Furthermore, decreases in fecal levels of short-chain fatty acids during treatment were related to worse neuropathy symptoms, suggesting a potential mechanism by which gut microbiota alterations could influence CIPN. Collectively, these findings corroborate preclinical work linking the gut microbiota to CIPN and provide evidence of potential microbiota involvement in general pain symptoms as well. Larger confirmatory studies in the future could support microbiota-targeted interventions for CIPN, such as fecal microbiota transplants or dietary interventions.

Indexed as

Antineoplastic AgentsBreast NeoplasmsGastrointestinal MicrobiomePainPeripheral Nervous System DiseasesAdultFecesFemaleHumansMiddle AgedRNA, Ribosomal, 16STaxoidsAntineoplastic AgentsRNA, Ribosomal, 16STaxoidsBile acidsDifferential relative abundance analysisMicrobial diversityNeurofilament light chainShort-chain fatty acidsTargeted metabolomics

Identifiers

PMID41722712
PMCPMC13227551

What OpenQuestion holds

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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.