Evidence map›Paper›PMID 41220415›Full record

ReviewOncoscience2025

From obesity to cancer: Gut microbiome mechanisms, biomarkers, and U.S. public health strategies.

Hashim Muhammad Moseeb, Mohsin Muhammad Aizaz, Khan Aiza, Thakur Hammed Hafsa, Muzaffar Sania, Zahoor Kamran, Zahra Tu Shamama, Ashraf Muhammad Usama, Qureshi Pir Maroof, Fatima Feroze and 3 more

Abstract readReview
In one paragraph

Review in Oncoscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Hashim Muhammad MoseebUniversity of Missouri-Columbia, Columbia, MO 65201, USA.
Mohsin Muhammad AizazSchool of Medicine, University of Buckingham, Buckingham, UK.
Khan AizaSchool of Medicine, University of Buckingham, Buckingham, UK.
Thakur Hammed HafsaResearch Associate, Alpha Clinical Developments Ltd., UK.
Muzaffar SaniaDepartment of Pathology, Dow University of Health Sciences, Karachi, Sindh 74200, Pakistan.
Zahoor KamranUniversity of Missouri-Columbia, Columbia, MO 65201, USA.
Zahra Tu ShamamaLahore General Hospital, Lahore 54000, Pakistan.
Ashraf Muhammad UsamaExcellent Medical Associates, Chicago, IL 60462, USA.
Qureshi Pir MaroofDepartment of Pathology, Liaquat University hospital, Hyderabad 71000, Pakistan.
Fatima FerozeDepartment of Pathology, Primary Health Care Corporation, Qatar.
Rahu AhmedDepartment of Pathology, University of Toledo Medical Center, OH 43606, USA.
Naeem AmmaraDepartment of Medicine, Pakistan Kidney Patient's Association, Islamabad, Pakistan.
Gandhi MahimaDepartment of Pathology, Dr Ziauddin Hospital Karachi, Karachi 74700, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity, metabolic syndrome, and colorectal cancer (CRC) remain major public health challenges in the United States, collectively driving substantial morbidity, mortality, and economic burden. Beyond diet and genetics, the gut microbiome has emerged as a pivotal determinant of host metabolism, immunity, and carcinogenesis, influenced by both environmental and behavioral factors.

objectiveThis review synthesizes current evidence linking gut microbial dysbiosis to obesity, metabolic syndrome, and CRC, emphasizing mechanistic pathways, environmental modifiers, and translational opportunities relevant to U.S. public health and precision medicine.

methodsComprehensive searches of PubMed and Scopus (2000-2025) identified large epidemiologic studies, mechanistic experiments, and clinical trials, prioritizing research from U.S. populations and nationally representative databases including NHANES, SEER, and the Nurses' Health Study.

resultsMicrobial alterations such as enrichment of Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and colibactin-producing Escherichia coli contribute to CRC initiation and progression. In obesity and metabolic syndrome, shifts in Firmicutes-to-Bacteroidetes ratios, altered short-chain fatty acid metabolism, and endotoxin-mediated inflammation disrupt metabolic homeostasis. Environmental and lifestyle exposures, including air pollutants, smoking, and Westernized diets, modulate microbial ecology across the aerodigestive tract, affecting disease susceptibility. The emerging discipline of Molecular Pathological Epidemiology (MPE) integrates lifestyle, microbiome, and biomarker data to elucidate exposure-outcome relationships, enabling personalized prevention and therapeutic strategies.

conclusionsThe gut microbiome functions as both a biomarker and therapeutic target across metabolic and neoplastic diseases. Integrating microbiome science with environmental epidemiology and MPE frameworks offers transformative potential for precision prevention and equitable public health strategies in the U.S.

Indexed as

colorectal cancerdysbiosisgut microbiomemetabolic syndromeobesity

Identifiers

PMID41220415
PMCPMC12598635

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.