Evidence map›Paper›PMID 15650110›Full record

ArticleGenes & development2005

Foxl1 is a mesenchymal Modifier of Min in carcinogenesis of stomach and colon.

Nathalie Perreault, Sara D Sackett, Jonathan P Katz, Emma E Furth, Klaus H Kaestner

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed, 79 citations in OpenAlex.

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  7. Aging · 2021
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  17. Low level of FOXL1 indicates a worse prognosis for gastric cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  18. Article
  19. Foxl1-expressing mesenchymal cells constitute the intestinal stem cell niche.Cellular and molecular gastroenterology and hepatology · 2016
    Article
  20. Article
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

5 authors at 1 institution in 1 country.

Nathalie PerreaultDepartment of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104-6145, USA.
Sara D Sackett
Jonathan P Katz
Emma E Furth
Klaus H Kaestner
University of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive activation of the Wnt/APC/beta-catenin pathway is a frequent initiating event in gastrointestinal carcinogenesis. Mutations in the Adenomatous Polyposis Coli (APC) gene up-regulate Wnt signaling by stabilizing beta-catenin and causing activation of targets important in proliferation control. Here we show that loss of the mesenchymal transcription factor Foxl1 leads to a marked increase in tumor multiplicity in the colon of Apc(Min) mice. Apc(Min/+);Foxl1-/- mice also develop gastric tumors not observed in Apc(Min) mice. These effects are caused by earlier tumor initiation due to accelerated loss of heterozygosity (LOH) at the Apc locus. Foxl1 is the first mesenchymal Modifier of Min and plays a key role in gastrointestinal tumorigenesis.

Indexed as

AnimalsColonic NeoplasmsDNA-Binding ProteinsForkhead Transcription FactorsGenes, APCLoss of HeterozygosityMiceStomach NeoplasmsTranscription FactorsDNA-Binding ProteinsForkhead Transcription FactorsFoxl1 protein, mouseTranscription Factors

Identifiers

PMID15650110
PMCPMC546508
OpenAlexW2120921989

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.