Evidence map›Paper›PMID 26240067›Full record

ArticleThe EMBO journal2015

E-cadherin can limit the transforming properties of activating β-catenin mutations.

David J Huels, Rachel A Ridgway, Sorina Radulescu, Marc Leushacke, Andrew D Campbell, Sujata Biswas, Simon Leedham, Stefano Serra, Runjan Chetty, Guenievre Moreaux and 16 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Review
  9. Novel read through agent: ZKN-0013 demonstrates efficacy in APCJournal of molecular medicine (Berlin, Germany) · 2023
    Article
  10. Review
  11. Hepatic glutamine synthetase controls NNature chemical biology · 2023
    Article
  12. Polyacetylene Isomers Isolated fromMolecules (Basel, Switzerland) · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 11 institutions in 7 countries.

David J HuelsCancer Research UK Beatson Institute, Glasgow, UK.
Rachel A RidgwayCancer Research UK Beatson Institute, Glasgow, UK.
Sorina RadulescuCancer Research UK Beatson Institute, Glasgow, UK.
Marc LeushackeA∗STAR Institute of Medical Biology, Singapore City, Singapore.
Andrew D CampbellCancer Research UK Beatson Institute, Glasgow, UK.
Sujata BiswasGastrointestinal Stem Cell Biology Laboratory, Wellcome Trust Centre for Human Genetics University of Oxford, Oxford, UK Translational Gastroenterology Unit, Experimental Medicine Division, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, Headington, UK.
Simon LeedhamGastrointestinal Stem Cell Biology Laboratory, Wellcome Trust Centre for Human Genetics University of Oxford, Oxford, UK Translational Gastroenterology Unit, Experimental Medicine Division, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, Headington, UK.
Stefano SerraDepartment of Pathology, University Health Network/Toronto Medical Laboratories, Toronto, Canada.
Runjan ChettyDepartment of Pathology, University Health Network/Toronto Medical Laboratories, Toronto, Canada.
Guenievre MoreauxCancer Research UK Beatson Institute, Glasgow, UK.
Lee ParryEuropean Cancer Stem Cell Research Institute, Cardiff University, Cardiff, UK.
James MatthewsEuropean Cancer Stem Cell Research Institute, Cardiff University, Cardiff, UK.
Fei SongInstitute of Physiology, Justus-Liebig University Giessen, Giessen, Germany.
Ann HedleyCancer Research UK Beatson Institute, Glasgow, UK.
Gabriela KalnaCancer Research UK Beatson Institute, Glasgow, UK.
Fatih CeteciCancer Research UK Beatson Institute, Glasgow, UK.
Karen R ReedEuropean Cancer Stem Cell Research Institute, Cardiff University, Cardiff, UK.
Valerie S MenielEuropean Cancer Stem Cell Research Institute, Cardiff University, Cardiff, UK.
Aoife MaguireDepartment of Histopathology, Trinity College Dublin St James's Hospital, Dublin, Ireland.
Brendan DoyleCancer Research UK Beatson Institute, Glasgow, UK Department of Histopathology, Trinity College Dublin St James's Hospital, Dublin, Ireland.
Ola SöderbergDepartment of Immunology, Genetics and Pathology Science for Life Laboratory, BMC Uppsala University, Uppsala, Sweden.
Nick BarkerA∗STAR Institute of Medical Biology, Singapore City, Singapore.
Alastair WatsonNorwich Medical School, University of East Anglia, Norwich, UK.
Lionel LarueInstitut Curie, CNRS UMR3347 INSERM, U1021 Equipe labellisée - Ligue Nationale contre le Cancer, Orsay, France.
Alan R ClarkeEuropean Cancer Stem Cell Research Institute, Cardiff University, Cardiff, UK.
Owen J SansomCancer Research UK Beatson Institute, Glasgow, UK o.sansom@beatson.gla.ac.uk.
Cancer Research UK Scotland Institute · GBCardiff University · GBInstitute of Medical Biology · SGJohn Radcliffe Hospital · GBUniversity Health Network · CAInserm · FRScience for Life Laboratory · SESt. James's Hospital · IETrinity College Dublin · IEUniversity of East Anglia · GBUniversity of Giessen · DE

Funding

Cancer Research UK 16581Cancer Research UK 21139Cancer Research UK C596/A17196Medical Research Council MR/K000063/1Medical Research Council MR/L016508/1
6 · The paper itself

Abstract

Wnt pathway deregulation is a common characteristic of many cancers. Only colorectal cancer predominantly harbours mutations in APC, whereas other cancer types (hepatocellular carcinoma, solid pseudopapillary tumours of the pancreas) have activating mutations in β-catenin (CTNNB1). We have compared the dynamics and the potency of β-catenin mutations in vivo. Within the murine small intestine (SI), an activating mutation of β-catenin took much longer to achieve Wnt deregulation and acquire a crypt-progenitor cell (CPC) phenotype than Apc or Gsk3 loss. Within the colon, a single activating mutation of β-catenin was unable to drive Wnt deregulation or induce the CPC phenotype. This ability of β-catenin mutation to differentially transform the SI versus the colon correlated with higher expression of E-cadherin and a higher number of E-cadherin:β-catenin complexes at the membrane. Reduction in E-cadherin synergised with an activating mutation of β-catenin resulting in a rapid CPC phenotype within the SI and colon. Thus, there is a threshold of β-catenin that is required to drive transformation, and E-cadherin can act as a buffer to sequester mutated β-catenin.

Indexed as

beta CateninCell Transformation, NeoplasticColonic NeoplasmsMutationNeoplasm ProteinsWnt Signaling PathwayAnimalsCadherinsMiceMice, Transgenicbeta CateninCadherinsCTNNB1 protein, mouseNeoplasm ProteinsAPCcolorectal cancerE‐cadherinβ‐catenin

Identifiers

PMID26240067
PMCPMC4570519
OpenAlexW1955712601

What OpenQuestion holds

Textmetadata
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.