Evidence map›Paper›PMID 27245242›Full record

ArticleEpigenetics2016

Aberrant DNA methylation of WNT pathway genes in the development and progression of CIMP-negative colorectal cancer.

Orsolya Galamb, Alexandra Kalmár, Bálint Péterfia, István Csabai, András Bodor, Dezső Ribli, Tibor Krenács, Árpád V Patai, Barnabás Wichmann, Barbara Kinga Barták and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

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  7. Frizzled receptors: gatekeepers of Wnt signaling in development and disease.Frontiers in cell and developmental biology · 2025
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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

15 authors at 4 institutions in 2 countries.

Orsolya Galamba Molecular Medicine Research Group , Hungarian Academy of Sciences , Budapest , Hungary.
Alexandra Kalmárb 2nd Department of Internal Medicine , Semmelweis University , Budapest , Hungary.
Bálint Péterfiab 2nd Department of Internal Medicine , Semmelweis University , Budapest , Hungary.
István Csabaic Department of Physics of Complex Systems , Eötvös Loránd University , Budapest , Hungary.
András Bodorc Department of Physics of Complex Systems , Eötvös Loránd University , Budapest , Hungary.
Dezső Riblic Department of Physics of Complex Systems , Eötvös Loránd University , Budapest , Hungary.
Tibor Krenácsd 1st Department of Pathology and Experimental Cancer Research , Semmelweis University , Budapest , Hungary.
Árpád V Pataib 2nd Department of Internal Medicine , Semmelweis University , Budapest , Hungary.
Barnabás Wichmanna Molecular Medicine Research Group , Hungarian Academy of Sciences , Budapest , Hungary.
Barbara Kinga Bartákb 2nd Department of Internal Medicine , Semmelweis University , Budapest , Hungary.
Kinga Tóthb 2nd Department of Internal Medicine , Semmelweis University , Budapest , Hungary.
Gábor Valcza Molecular Medicine Research Group , Hungarian Academy of Sciences , Budapest , Hungary.
Sándor Spisákf Department of Medical Oncology , Dana-Farber Cancer Institute , Boston , MA , USA.
Zsolt Tulassaya Molecular Medicine Research Group , Hungarian Academy of Sciences , Budapest , Hungary.
Béla Molnára Molecular Medicine Research Group , Hungarian Academy of Sciences , Budapest , Hungary.
Semmelweis University · HUHungarian Academy of Sciences · HUEötvös Loránd University · HUDana-Farber Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The WNT signaling pathway has an essential role in colorectal carcinogenesis and progression, which involves a cascade of genetic and epigenetic changes. We aimed to analyze DNA methylation affecting the WNT pathway genes in colorectal carcinogenesis in promoter and gene body regions using whole methylome analysis in 9 colorectal cancer, 15 adenoma, and 6 normal tumor adjacent tissue (NAT) samples by methyl capture sequencing. Functional methylation was confirmed on 5-aza-2'-deoxycytidine-treated colorectal cancer cell line datasets. In parallel with the DNA methylation analysis, mutations of WNT pathway genes (APC, β-catenin/CTNNB1) were analyzed by 454 sequencing on GS Junior platform. Most differentially methylated CpG sites were localized in gene body regions (95% of WNT pathway genes). In the promoter regions, 33 of the 160 analyzed WNT pathway genes were differentially methylated in colorectal cancer vs. normal, including hypermethylated AXIN2, CHP1, PRICKLE1, SFRP1, SFRP2, SOX17, and hypomethylated CACYBP, CTNNB1, MYC; 44 genes in adenoma vs. NAT; and 41 genes in colorectal cancer vs. adenoma comparisons. Hypermethylation of AXIN2, DKK1, VANGL1, and WNT5A gene promoters was higher, while those of SOX17, PRICKLE1, DAAM2, and MYC was lower in colon carcinoma compared to adenoma. Inverse correlation between expression and methylation was confirmed in 23 genes, including APC, CHP1, PRICKLE1, PSEN1, and SFRP1. Differential methylation affected both canonical and noncanonical WNT pathway genes in colorectal normal-adenoma-carcinoma sequence. Aberrant DNA methylation appears already in adenomas as an early event of colorectal carcinogenesis.

Indexed as

DNA MethylationWnt Signaling PathwayAdenomaAgedBiomarkers, TumorColorectal NeoplasmsFemaleGenetic LociGenome, HumanHumansMaleMiddle AgedPromoter Regions, GeneticBiomarkers, TumorAdenomaAPCcolorectal cancergene expressionpromoter and gene body methylationwhole methylome analysisWNT signaling pathwayβ-catenin mutation

Identifiers

PMID27245242
PMCPMC4990228
OpenAlexW2414471948

What OpenQuestion holds

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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.