Evidence map›Paper›PMID 31414579›Full record

ArticleCellular microbiology2019

Infection with genotoxin-producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells.

Océane C B Martin, Anna Bergonzini, Federica D'Amico, Puran Chen, Jerry W Shay, Jacques Dupuy, Mattias Svensson, Maria G Masucci, Teresa Frisan

Open access · hybridAbstract read
In one paragraph

Article in Cellular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  4. RETRACTED: The Impact ofInternational journal of molecular sciences · 2025
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  13. Article
  14. Genotoxin-producingFrontiers in immunology · 2023
    Article
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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

9 authors at 4 institutions in 4 countries.

Océane C B MartinDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Anna BergonziniDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Federica D'AmicoDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Puran ChenDepartment of Medicine, Karolinska Institutet, Stockholm, Sweden.
Jerry W ShayDepartment of Cell Biology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Jacques DupuyINRA, ToxAlim (Research Centre in Food Toxicology), INRA, ENVT, INP-Purpan, UPS, Université de Toulouse, Toulouse, France.
Mattias SvenssonDepartment of Medicine, Karolinska Institutet, Stockholm, Sweden.
Maria G MasucciDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Teresa FrisanDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-1209-0942
Karolinska Institutet · SEInserm · FRÉcole Nationale Vétérinaire de Toulouse · FRThe University of Texas Southwestern Medical Center · US

Funding

CancerfondenCancer Research Foundation in Northern SwedenKempestiftelsernaLillian Sagens och Curt Ericssons forskningsstiftelseSwedish Cancer SocietySwedish Research CouncilUmeå University
6 · The paper itself

Abstract

Several commensal and pathogenic Gram-negative bacteria produce DNA-damaging toxins that are considered bona fide carcinogenic agents. The microbiota of colorectal cancer (CRC) patients is enriched in genotoxin-producing bacteria, but their role in the pathogenesis of CRC is poorly understood. The adenomatous polyposis coli (APC) gene is mutated in familial adenomatous polyposis and in the majority of sporadic CRCs. We investigated whether the loss of APC alters the response of colonic epithelial cells to infection by Salmonella enterica, the only genotoxin-producing bacterium associated with cancer in humans. Using 2D and organotypic 3D cultures, we found that APC deficiency was associated with sustained activation of the DNA damage response, reduced capacity to repair different types of damage, including DNA breaks and oxidative damage, and failure to induce cell cycle arrest. The reduced DNA repair capacity and inability to activate adequate checkpoint responses was associated with increased genomic instability in APC-deficient cells exposed to the genotoxic bacterium. Inhibition of the checkpoint response was dependent on activation of the phosphatidylinositol 3-kinase pathway. These findings highlight the synergistic effect of the loss of APC and infection with genotoxin-producing bacteria in promoting a microenvironment conducive to malignant transformation.

Indexed as

Adenomatous Polyposis ColiAnimalsCarcinogenesisCell Cycle CheckpointsCell LineColonColorectal NeoplasmsDNA DamageEpithelial CellsGenes, Tumor SuppressorGenomic InstabilityHumansMiceMutagensPhosphatidylinositol 3-KinasesSalmonella entericaMutagensPhosphatidylinositol 3-KinasesAPCbacteria and cancerbacterial genotoxinDNA damage responseDNA repairorganotypic modeltumour-suppressor gene

Identifiers

PMID31414579
PMCPMC6899655
OpenAlexW2968516791

What OpenQuestion 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 OpenQuestion graph.