Evidence map›Paper›PMID 24089088›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2013

Aberrant DNA methylation at genes associated with a stem cell-like phenotype in cholangiocarcinoma tumors.

Ruethairat Sriraksa, Constanze Zeller, Wei Dai, Afshan Siddiq, Andrew J Walley, Temduang Limpaiboon, Robert Brown

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  7. Significant association ofOncology letters · 2019
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  11. Promoter hypermethylation ofClinical epigenetics · 2016
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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

7 authors at 2 institutions in 2 countries.

Ruethairat Sriraksa *Centre for Research and Development of Medical Diagnostic Laboratories, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen, 40002, Thailand.
Constanze Zeller *Epigenetics Unit, Department of Surgery and Cancer, Imperial College London, IRDB Building, Hammersmith Hospital Campus, London, W12 0NN, UK.
Wei DaiEpigenetics Unit, Department of Surgery and Cancer, Imperial College London, IRDB Building, Hammersmith Hospital Campus, London, W12 0NN, UK.
Afshan SiddiqDepartment of Genomics of Common Disease, School of Public Health, Burlington-Danes Building, Hammersmith Hospital Campus, London W12 0NN, UK.
Andrew J WalleyDepartment of Genomics of Common Disease, School of Public Health, Burlington-Danes Building, Hammersmith Hospital Campus, London W12 0NN, UK.
Temduang LimpaiboonCentre for Research and Development of Medical Diagnostic Laboratories, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen, 40002, Thailand.
Robert BrownEpigenetics Unit, Department of Surgery and Cancer, Imperial College London, IRDB Building, Hammersmith Hospital Campus, London, W12 0NN, UK.
Khon Kaen University · THImperial College London · GB

Funding

Cancer Research UK 13086Cancer Research UK A13086Cancer Research UK C536/A13086
6 · The paper itself

Abstract

Genetic abnormalities of cholangiocarcinoma have been widely studied; however, epigenomic changes related to cholangiocarcinogenesis have been less well characterized. We have profiled the DNA methylomes of 28 primary cholangiocarcinoma and six matched adjacent normal tissues using Infinium's HumanMethylation27 BeadChips with the aim of identifying gene sets aberrantly and epigenetically regulated in this tumor type. Using a linear model for microarray data, we identified 1610 differentially methylated autosomal CpG sites, with 809 hypermethylated (representing 603 genes) and 801 hypomethylated (representing 712 genes) in cholangiocarcinoma versus adjacent normal tissues (false-discovery rate ≤ 0.05). Gene ontology and gene set enrichment analyses identified gene sets significantly associated with hypermethylation at linked CpG sites in cholangiocarcinoma including homeobox genes and target genes of PRC2, EED, SUZ12, and histone H3 trimethylation at lysine 27. We confirmed frequent hypermethylation at the homeobox genes HOXA9 and HOXD9 by bisulfite pyrosequencing in a larger cohort of cholangiocarcinoma (n = 102). Our findings indicate a key role for hypermethylation of multiple CpG sites at genes associated with a stem cell-like phenotype as a common molecular aberration in cholangiocarcinoma. These data have implications for cholangiocarcinogenesis, as well as possible novel treatment options using histone methyltransferase inhibitors.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticBile Duct NeoplasmsBile DuctsBile Ducts, IntrahepaticBiomarkers, TumorCholangiocarcinomaCpG IslandsHumansNeoplastic Stem CellsPhenotypePromoter Regions, GeneticSulfitesBiomarkers, Tumorhydrogen sulfiteSulfites

Identifiers

PMID24089088
PMCPMC3855864
OpenAlexW2122080154

What OpenQuestion holds

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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.