Evidence map›Paper›PMID 33579932›Full record

ArticleNature communications2021

Genomic aberrations after short-term exposure to colibactin-producing E. coli transform primary colon epithelial cells.

Amina Iftekhar, Hilmar Berger, Nassim Bouznad, Julian Heuberger, Francesco Boccellato, Ulrich Dobrindt, Heiko Hermeking, Michael Sigal, Thomas F Meyer

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 165 citations in OpenAlex.

  1. Trial
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  5. Gut microbiota in health and disease.Molecular biomedicine · 2026
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  11. Article
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  14. Decoding the power of the microbiome in human health.Frontiers in cellular and infection microbiology · 2026
    Review
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  18. Article
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50 more citing papers are in PubMed but not listed here.

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 7 institutions in 2 countries.

Amina IftekharDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID 0000-0002-0001-5590
Hilmar BergerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID 0000-0002-6304-4946
Nassim BouznadExperimental and Molecular Pathology, Institute of Pathology, Ludwig Maximilians University, München, Germany.
Julian HeubergerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Francesco BoccellatoDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID 0000-0001-6013-7154
Ulrich DobrindtInstitute of Hygiene, University of Münster, Münster, Germany.
Heiko HermekingExperimental and Molecular Pathology, Institute of Pathology, Ludwig Maximilians University, München, Germany.
Michael SigalDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany. michael.sigal@charite.de.ORCID 0000-0003-4772-0761
Thomas F MeyerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany. tfm@mpiib-berlin.mpg.de.ORCID 0000-0002-6120-8679
Christian-Albrechts-Universität zu Kiel · DEMax Planck Institute for Infection Biology · DEGerman Cancer Research Center · DELudwig-Maximilians-Universität München · DEMax Delbrück Center · DEUniversity of Münster · DEUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genotoxic colibactin-producing pks+ Escherichia coli induce DNA double-strand breaks, mutations, and promote tumor development in mouse models of colorectal cancer (CRC). Colibactin's distinct mutational signature is reflected in human CRC, suggesting a causal link. Here, we investigate its transformation potential using organoids from primary murine colon epithelial cells. Organoids recovered from short-term infection with pks+ E. coli show characteristics of CRC cells, e.g., enhanced proliferation, Wnt-independence, and impaired differentiation. Sequence analysis of Wnt-independent organoids reveals an enhanced mutational burden, including chromosomal aberrations typical of genomic instability. Although we do not find classic Wnt-signaling mutations, we identify several mutations in genes related to p53-signaling, including miR-34a. Knockout of Trp53 or miR-34 in organoids results in Wnt-independence, corroborating a functional interplay between the p53 and Wnt pathways. We propose larger chromosomal alterations and aneuploidy as the basis of transformation in these organoids, consistent with the early appearance of chromosomal instability in CRC.

Indexed as

GenomicsAnimalsChromosome AberrationsColonColonic NeoplasmsColorectal NeoplasmsDNA DamageEpithelial CellsEscherichia coliMaleMiceMice, KnockoutMutationOrganoidsPeptidesPolyketidescolibactinPeptidesPolyketides

Identifiers

PMID33579932
PMCPMC7881031
OpenAlexW3127796531

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.