Evidence map›Paper›PMID 22278361›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2012

Colorectal adenoma to carcinoma progression is accompanied by changes in gene expression associated with ageing, chromosomal instability, and fatty acid metabolism.

Beatriz Carvalho, Anke H Sillars-Hardebol, Cindy Postma, Sandra Mongera, Jochim Terhaar Sive Droste, Askar Obulkasim, Mark van de Wiel, Wim van Criekinge, Bauke Ylstra, Remond J A Fijneman and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 5% 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, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Beatriz CarvalhoDepartment of Pathology, VU University Medical Center, Amsterdam, the Netherlands. b.carvalho@vumc.nl
Anke H Sillars-Hardebol
Cindy Postma
Sandra Mongera
Jochim Terhaar Sive Droste
Askar Obulkasim
Mark van de Wiel
Wim van Criekinge
Bauke Ylstra
Remond J A Fijneman
Gerrit A Meijer
Amsterdam UMC Location VUmc · NLGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer develops in a multi-step manner from normal epithelium, through a pre-malignant lesion (so-called adenoma), into a malignant lesion (carcinoma), which invades surrounding tissues and eventually can spread systemically (metastasis). It is estimated that only about 5% of adenomas do progress to a carcinoma.

aimThe present study aimed to unravel the biology of adenoma to carcinoma progression by mRNA expression profiling, and to identify candidate biomarkers for adenomas that are truly at high risk of progression.

methodsGenome-wide mRNA expression profiles were obtained from a series of 37 colorectal adenomas and 31 colorectal carcinomas using oligonucleotide microarrays. Differentially expressed genes were validated in an independent colorectal gene expression data set. Gene Set Enrichment Analysis (GSEA) was used to identify altered expression of sets of genes associated with specific biological processes, in order to better understand the biology of colorectal adenoma to carcinoma progression.

resultsmRNA expression of 248 genes was significantly different, of which 96 were upregulated and 152 downregulated in carcinomas compared to adenomas. Classification of adenomas and carcinomas using the expression of these genes showed to be very accurate, also when tested in an independent expression data set. Gene-sets associated with ageing (which is related to senescence) and chromosomal instability were upregulated, and a gene-set associated with fatty acid metabolism was downregulated in carcinomas compared to adenomas. Moreover, gene-sets associated with chromosomal location revealed chromosome 4q22 loss and chromosome 20q gain of gene-set expression as being relevant in this progression. CONCLUDING REMARK: These data are consistent with the notion that adenomas and carcinomas are distinct biological entities. Disruption of specific biological processes like senescence (ageing), maintenance of chromosomal instability and altered metabolism, are key factors in the progression from adenoma to carcinoma.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticAdenomaAgedAged, 80 and overAgingChromosomal InstabilityColorectal NeoplasmsDatabases, GeneticDown-RegulationFatty AcidsFemaleGenes, NeoplasmHumansMaleMiddle AgedFatty Acids

Identifiers

PMID22278361
PMCPMC3308003
OpenAlexW2092426144

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LicenceCC BY-NC
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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.