Evidence map›Paper›PMID 27927180›Full record

ArticleBMC cancer2016

Oral perfluorooctane sulfonate (PFOS) lessens tumor development in the APC

Jeffrey Wimsatt, Meghan Villers, Laurel Thomas, Stacey Kamarec, Caitlin Montgomery, Leo W Y Yeung, Yanqing Hu, Kim Innes

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 27% of its field
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Per- and poly-fluoroalkyl substances exposure and risk of gastrointestinal cancers: a systematic review and meta-analysis.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2025
    Pooled it
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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

8 authors at 2 institutions in 2 countries.

Jeffrey WimsattDepartment of Medicine, School of Medicine, West Virginia University, Morgantown, WV, 26506, USA. jefwimsatt@gmail.com.ORCID 0000-0002-7818-2479
Meghan VillersDepartment of Medicine, School of Medicine, West Virginia University, Morgantown, WV, 26506, USA.
Laurel ThomasDepartment of Medicine, School of Medicine, West Virginia University, Morgantown, WV, 26506, USA.
Stacey KamarecDepartment of Medicine, School of Medicine, West Virginia University, Morgantown, WV, 26506, USA.
Caitlin MontgomeryDepartment of Medicine, School of Medicine, West Virginia University, Morgantown, WV, 26506, USA.
Leo W Y YeungMan-Technology-Environment (MTM) Research Centre, School of Science and Technology, Örebro University, Fakultetsgatan 1, Örebro, SE-70182, Sweden.
Yanqing HuDepartment of Statistics, West Virginia University, Morgantown, WV, 26506, USA.
Kim InnesDepartment of Epidemiology, School of Public Health, West Virginia University, Morgantown, WV, 26506, USA.
West Virginia University · USÖrebro University · SE

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Laura F. Gibson · 2012 to 2026
$81.0M
NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

backgroundColorectal cancer is the second most common cause of cancer deaths for both men and women, and the third most common cause of cancer in the U.S. Toxicity of current chemotherapeutic agents for colorectal cancer, and emergence of drug resistance underscore the need to develop new, potentially less toxic alternatives. Our recent cross-sectional study in a large Appalachian population, showed a strong, inverse, dose-response association of serum perfluorooctane sulfonate (PFOS) levels to prevalent colorectal cancer, suggesting PFOS may have therapeutic potential in the prevention and/or treatment of colorectal cancer. In these preliminary studies using a mouse model of familial colorectal cancer, the APC

methodsAt 5-6 weeks of age, APC

resultsPFOS exposure was associated with a significant, dose-response reduction in total tumor number in both male and female mice. This inverse dose-response effect of PFOS exposure was particularly pronounced for larger tumors (r

conclusionsThe current study in a mouse model of familial adenomatous polyposis offers the first experimental evidence that chronic exposure to PFOS in drinking water can reduce formation of gastrointestinal tumors, and that these reductions are both significant and dose-dependent. If confirmed in further studies, these promising findings could lead to new therapeutic strategies for familial colorectal cancer, and suggest that PFOS testing in both preventive and therapeutic models for human colorectal cancer is warranted.

Indexed as

Disease Models, AnimalAdenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinAdministration, OralAlkanesulfonic AcidsAnimalsDose-Response Relationship, DrugFemaleFluorocarbonsMaleMiceMice, Inbred C57BLAdenomatous Polyposis Coli Proteinadenomatous polyposis coli protein, mouseAlkanesulfonic AcidsFluorocarbonsperfluorooctane sulfonic acidAPCmin mouseColorectal cancerDose–responseGenderPerfluorooctane sulfonatePFOS

Identifiers

PMID27927180
PMCPMC5143440
OpenAlexW2560030021

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.