Evidence map›Paper›PMID 23318432›Full record

ArticleOncogene2014

Stem cell CD44v isoforms promote intestinal cancer formation in Apc(min) mice downstream of Wnt signaling.

J Zeilstra, S P J Joosten, H van Andel, C Tolg, A Berns, M Snoek, M van de Wetering, M Spaargaren, H Clevers, S T Pals

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
4.9field-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

86 citing papers in PubMed, 135 citations in OpenAlex.

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  15. RNA-binding proteins regulating the CD44 alternative splicing.Frontiers in molecular biosciences · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

J ZeilstraDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
S P J JoostenDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
H van AndelDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
C TolgDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
A BernsDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
M SnoekDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
M van de WeteringHubrecht Institute and University Medical Center Utrecht, Utrecht, The Netherlands.
M SpaargarenDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
H CleversHubrecht Institute and University Medical Center Utrecht, Utrecht, The Netherlands.
S T PalsDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
University of Amsterdam · NLHubrecht Institute for Developmental Biology and Stem Cell Research · NLThe Netherlands Cancer Institute · NLAcademic Medical Center · NLOncode Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A gene signature specific for intestinal stem cells (ISCs) has recently been shown to predict relapse in colorectal cancer (CRC) but the tumorigenic role of individual signature genes remains poorly defined. A prominent ISC-signature gene is the cancer stem cell marker CD44, which encodes various splice variants comprising a diverse repertoire of adhesion and signaling molecules. Using Lgr5 as ISC marker, we have fluorescence-activated cell sorting-purified ISCs to define their CD44 repertoire. ISCs display a specific set of CD44 variant isoforms (CD44v), but remarkably lack the CD44 standard (CD44s) isoform. These CD44v also stand-out in transformed human ISCs isolated from microadenomas of familial adenomatous polyposis patients. By employing knock-in mice expressing either CD44v4-10 or CD44s, we demonstrate that the CD44v isoform, but not CD44s, promotes adenoma initiation in Apc(Min/+)mice. Our data identify CD44v as component of the ISCs program critical for tumor initiation, and as potential treatment target in CRC.

Indexed as

Adenomatous Polyposis ColiAnimalsCell Transformation, NeoplasticFlow CytometryGene Expression ProfilingGene Knock-In TechniquesHyaluronan ReceptorsIntestinal NeoplasmsMiceMice, TransgenicNeoplastic Stem CellsProtein IsoformsReceptors, G-Protein-CoupledTumor Cells, CulturedWnt Signaling PathwayCD44v10 antigenHyaluronan ReceptorsLgr5 protein, mouseProtein IsoformsReceptors, G-Protein-Coupled

Identifiers

PMID23318432
OpenAlexW2007126419

What OpenQuestion holds

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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.