Evidence map›Paper›PMID 23951239›Full record

ArticlePloS one2013

Distinct gene expression signatures in lynch syndrome and familial colorectal cancer type x.

Mev Dominguez-Valentin, Christina Therkildsen, Srinivas Veerla, Mats Jönsson, Inge Bernstein, Ake Borg, Mef Nilbert

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Centromere protein U enhances the progression of bladder cancer by promoting mitochondrial ribosomal protein s28 expression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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  6. Review
  7. Article
  8. Familial Colorectal Cancer Type X.Current genomics · 2017
    Review
  9. Article
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  11. MLF1IP promotes cells proliferation and apoptosis by regulating CyclinD1 in breast cancer.International journal of clinical and experimental pathology · 2017
    Article
  12. Article
  13. Review
  14. Article
  15. Familial colorectal cancer type X: genetic profiles and phenotypic features.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015
    Review
  16. Article
  17. 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

7 authors at 2 institutions in 2 countries.

Mev Dominguez-ValentinDepartment of Oncology, Institute of Clinical Sciences, Lund University, Lund, Sweden. mev_dv@yahoo.com
Christina Therkildsen
Srinivas Veerla
Mats Jönsson
Inge Bernstein
Ake Borg
Mef Nilbert
Lund University · SECopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHeredity is estimated to cause at least 20% of colorectal cancer. The hereditary nonpolyposis colorectal cancer subset is divided into Lynch syndrome and familial colorectal cancer type X (FCCTX) based on presence of mismatch repair (MMR) gene defects. PURPOSE: We addressed the gene expression signatures in colorectal cancer linked to Lynch syndrome and FCCTX with the aim to identify candidate genes and to map signaling pathways relevant in hereditary colorectal carcinogenesis. EXPERIMENTAL

designThe 18 k whole-genome c-DNA-mediated annealing, selection, extension, and ligation (WG-DASL) assay was applied to 123 colorectal cancers, including 39 Lynch syndrome tumors and 37 FCCTX tumors. Target genes were technically validated using real-time quantitative RT-PCR (qRT-PCR) and the expression signature was validated in independent datasets.

resultsColorectal cancers linked to Lynch syndrome and FCCTX showed distinct gene expression profiles, which by significance analysis of microarrays (SAM) differed by 2188 genes. Functional pathways involved were related to G-protein coupled receptor signaling, oxidative phosphorylation, and cell cycle function and mitosis. qRT-PCR verified altered expression of the selected genes NDUFA9, AXIN2, MYC, DNA2 and H2AFZ. Application of the 2188-gene signature to independent datasets showed strong correlation to MMR status.

conclusionDistinct genetic profiles and deregulation of different canonical pathways apply to Lynch syndrome and FCCTX and key targets herein may be relevant to pursue for refined diagnostic and therapeutic strategies in hereditary colorectal cancer.

Indexed as

Gene Expression ProfilingTranscriptomeAdenomatous Polyposis ColiCluster AnalysisColorectal Neoplasms, Hereditary NonpolyposisGene Expression Regulation, NeoplasticHumansReproducibility of ResultsSignal Transduction

Identifiers

PMID23951239
PMCPMC3741139
OpenAlexW2085785287

What OpenQuestion holds

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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.