Evidence map›Paper›PMID 24516561›Full record

ArticlePloS one2014

A gene expression and pre-mRNA splicing signature that marks the adenoma-adenocarcinoma progression in colorectal cancer.

Marine Pesson, Alain Volant, Arnaud Uguen, Kilian Trillet, Pierre De La Grange, Marc Aubry, Mélanie Daoulas, Michel Robaszkiewicz, Gérald Le Gac, Alain Morel and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  11. Rare Variants in the DNA Repair Pathway and the Risk of Colorectal Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
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  17. Prognostic impact of cancer stem cell markersAmerican journal of translational research · 2020
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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

12 authors at 4 institutions in 1 country.

Marine PessonInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France.
Alain VolantInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France ; Centre Hospitalier Régional Universitaire de Brest, Brest, France.
Arnaud UguenInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France ; Centre Hospitalier Régional Universitaire de Brest, Brest, France.
Kilian TrilletInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France.
Pierre De La GrangeGenoSplice technology, Hôpital Saint-Louis, Institut Universitaire d'Hématologie, Centre Hayem, Paris, France.
Marc AubryPlateforme de Génomique Santé, Laboratoire de Génomique Médicale, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 6290, Institut de Génétique et Développement de Rennes, Unité Mixte de Services 3480 Biosit, Université de Rennes 1, Rennes, France.
Mélanie DaoulasCentre Hospitalier Régional Universitaire de Brest, Brest, France.
Michel RobaszkiewiczCentre Hospitalier Régional Universitaire de Brest, Brest, France.
Gérald Le GacInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France ; Centre Hospitalier Régional Universitaire de Brest, Brest, France.
Alain MorelInstitut de Recherche contre le Cancer Nantes Atlantique, Institut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 892, Centre Paul Papin, Angers, France.
Brigitte SimonInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France.
Laurent CorcosInstitut National de la Santé Et de la Recherche Médicale, Unité Mixte de Recherche 1078, Université de Bretagne Occidentale, Structure Fédérative de Recherche ScInBioS, Faculté de Médecine, Brest, France ; Centre Hospitalier Régional Universitaire de Brest, Brest, France.
Université de Bretagne Occidentale · FRCentre Hospitalier Régional Universitaire de Brest · FRHôpital Saint-Louis · FRUniversité de Rennes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is widely accepted that most colorectal cancers (CRCs) arise from colorectal adenomas (CRAs), but transcriptomic data characterizing the progression from colorectal normal mucosa to adenoma, and then to adenocarcinoma are scarce. These transition steps were investigated using microarrays, both at the level of gene expression and alternative pre-mRNA splicing. Many genes and exons were abnormally expressed in CRAs, even more than in CRCs, as compared to normal mucosae. Known biological pathways involved in CRC were altered in CRA, but several new enriched pathways were also recognized, such as the complement and coagulation cascades. We also identified four intersectional transcriptional signatures that could distinguish CRAs from normal mucosae or CRCs, including a signature of 40 genes differentially deregulated in both CRA and CRC samples. A majority of these genes had been described in different cancers, including FBLN1 or INHBA, but only a few in CRC. Several of these changes were also observed at the protein level. In addition, 20% of these genes (i.e. CFH, CRYAB, DPT, FBLN1, ITIH5, NR3C2, SLIT3 and TIMP1) showed altered pre-mRNA splicing in CRAs. As a global variation occurring since the CRA stage, and maintained in CRC, the expression and splicing changes of this 40-gene set may mark the risk of cancer occurrence from analysis of CRA biopsies.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticAdenocarcinomaAdenomaBiopsyCluster AnalysisColorectal NeoplasmsDown-RegulationExonsGene Expression ProfilingHumansIntestinal MucosaRNA PrecursorsRNA SplicingUp-RegulationRNA Precursors

Identifiers

PMID24516561
PMCPMC3916340
OpenAlexW2060658193

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.