Evidence map›Paper›PMID 26291085›Full record

ArticlePloS one2015

Comprehensive DNA Methylation Analysis Reveals a Common Ten-Gene Methylation Signature in Colorectal Adenomas and Carcinomas.

Árpád V Patai, Gábor Valcz, Péter Hollósi, Alexandra Kalmár, Bálint Péterfia, Árpád Patai, Barnabás Wichmann, Sándor Spisák, Barbara Kinga Barták, Katalin Leiszter and 7 more

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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  5. Detection of rare mutations, copy number alterations, and methylation in the same template DNA molecules.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

17 authors.

Árpád V Patai2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Gábor ValczMolecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Péter Hollósi1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary; Tumor Progression Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Alexandra Kalmár2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Bálint PéterfiaMolecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Árpád PataiDepartment of Gastroenterology and Medicine, Markusovszky University Teaching Hospital, Szombathely, Hungary.
Barnabás WichmannMolecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Sándor SpisákMolecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary; Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, United States of America.
Barbara Kinga Barták2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Katalin Leiszter2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Kinga Tóth2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Ferenc Sipos2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Ilona Kovalszky1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Zoltán Péter2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Pál Miheller2nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Zsolt Tulassay2nd Department of Medicine, Semmelweis University, Budapest, Hungary; Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Béla Molnár2nd Department of Medicine, Semmelweis University, Budapest, Hungary; Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest, Hungary.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microarray analysis of promoter hypermethylation provides insight into the role and extent of DNA methylation in the development of colorectal cancer (CRC) and may be co-monitored with the appearance of driver mutations. Colonic biopsy samples were obtained endoscopically from 10 normal, 23 adenoma (17 low-grade (LGD) and 6 high-grade dysplasia (HGD)), and 8 ulcerative colitis (UC) patients (4 active and 4 inactive). CRC samples were obtained from 24 patients (17 primary, 7 metastatic (MCRC)), 7 of them with synchronous LGD. Field effects were analyzed in tissues 1 cm (n = 5) and 10 cm (n = 5) from the margin of CRC. Tissue materials were studied for DNA methylation status using a 96 gene panel and for KRAS and BRAF mutations. Expression levels were assayed using whole genomic mRNA arrays. SFRP1 was further examined by immunohistochemistry. HT29 cells were treated with 5-aza-2' deoxycytidine to analyze the reversal possibility of DNA methylation. More than 85% of tumor samples showed hypermethylation in 10 genes (SFRP1, SST, BNC1, MAL, SLIT2, SFRP2, SLIT3, ALDH1A3, TMEFF2, WIF1), whereas the frequency of examined mutations were below 25%. These genes distinguished precancerous and cancerous lesions from inflamed and healthy tissue. The mRNA alterations that might be caused by systematic methylation could be partly reversed by demethylation treatment. Systematic changes in methylation patterns were observed early in CRC carcinogenesis, occuring in precursor lesions and CRC. Thus we conclude that DNA hypermethylation is an early and systematic event in colorectal carcinogenesis, and it could be potentially reversed by systematic demethylation therapy, but it would need more in vitro and in vivo experiments to support this theory.

Indexed as

AdenomaAdolescentCarcinomaCell Line, TumorColitis, UlcerativeColorectal NeoplasmsDNA MethylationGene Expression Regulation, NeoplasticHT29 CellsHumansMutationPromoter Regions, GeneticRNA, MessengerTranscriptomeRNA, Messenger

Identifiers

PMID26291085
PMCPMC4546193

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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.