Evidence map›Paper›PMID 26291246›Full record

ArticleEpigenetics2015

Interplay between promoter methylation and chromosomal loss in gene silencing at 3p11-p14 in cervical cancer.

Malin Lando, Christina S Fjeldbo, Saskia M Wilting, Barbara C Snoek, Eva-Katrine Aarnes, Malin F Forsberg, Gunnar B Kristensen, Renske Dm Steenbergen, Heidi Lyng

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  3. Identification of a novel hypermethylation marker, ZSCAN18, and construction of a diagnostic model in cervical cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  17. Epigenetically Silenced Candidate Tumor Suppressor Genes in Prostate Cancer: Identified by Modeling Methylation Stratification and Applied to Progression Prediction.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
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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

9 authors at 4 institutions in 4 countries.

Malin Landoa Department of Radiation Biology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Christina S Fjeldboa Department of Radiation Biology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Saskia M Wiltingb Department of Pathology ; VU University Medical Center ; Amsterdam , the Netherlands.
Barbara C Snoekb Department of Pathology ; VU University Medical Center ; Amsterdam , the Netherlands.
Eva-Katrine Aarnesa Department of Radiation Biology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Malin F Forsberga Department of Radiation Biology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Gunnar B Kristensenc Department of Gynecologic Oncology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Renske Dm Steenbergenb Department of Pathology ; VU University Medical Center ; Amsterdam , the Netherlands.
Heidi Lynga Department of Radiation Biology ; Norwegian Radium Hospital; Oslo University Hospital ; Oslo , Norway.
Oslo University Hospital · NONorwegian Cancer Society · NOUniversity Medical Center · USAmsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of 3p11-p14 is a frequent event in epithelial cancer and a candidate prognostic biomarker in cervical cancer. In addition to loss, promoter methylation can participate in gene silencing and promote tumor aggressiveness. We have performed a complete mapping of promoter methylation at 3p11-p14 in two independent cohorts of cervical cancer patients (n = 149, n = 121), using Illumina 450K methylation arrays. The aim was to investigate whether hyperm-ethylation was frequent and could contribute to gene silencing and disease aggressiveness either alone or combined with loss. By comparing the methylation level of individual CpG sites with corresponding data of normal cervical tissue, 26 out of 41 genes were found to be hypermethylated in both cohorts. The frequency of patients with hypermethylation of these genes was found to be higher at tumor stages of 3 and 4 than in stage 1 tumors. Seventeen of the 26 genes were transcriptionally downregulated in cancer compared to normal tissue, whereof 6 genes showed a significant correlation between methylation and expression. Integrated analysis of methylation, gene dosage, and expression of the 26 hypermethylated genes identified 3 regulation patterns encompassing 8 hypermethylated genes; a methylation driven pattern (C3orf14, GPR27, ZNF717), a gene dosage driven pattern (THOC7, PSMD6), and a combined methylation and gene dosage driven pattern (FHIT, ADAMTS9, LRIG1). In survival analysis, patients with both hypermethylation and loss of LRIG1 had a worse outcome compared to those harboring only hypermethylation or none of the events. C3orf14 emerged as a novel methylation regulated suppressor gene, for which knockdown was found to promote invasive growth in human papilloma virus (HPV)-transformed keratinocytes. In conclusion, hypermethylation at 3p11-p14 is common in cervical cancer and may exert a selection pressure during carcinogenesis alone or combined with loss. Information on both events could lead to improved prognostic markers.

Indexed as

Epigenesis, GeneticAdultAgedCarcinogenesisChromosome DeletionChromosomes, Human, Pair 3CpG IslandsDisease-Free SurvivalDNA MethylationFemaleGene Expression Regulation, NeoplasticGene SilencingHumansKaplan-Meier EstimateMiddle AgedNeoplasm ProteinsNeoplasm Proteins3pcervical cancerchromosomal lossgene expressionintegrative genomic profilingpromoter methylationtumor suppressor genes

Identifiers

PMID26291246
PMCPMC4844207
OpenAlexW2193969951

What OpenQuestion holds

Textmetadata
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.