Evidence map›Paper›PMID 30850842›Full record

ArticleCarcinogenesis2019

Genome-wide DNA methylation profile of early-onset endometrial cancer: its correlation with genetic aberrations and comparison with late-onset endometrial cancer.

Takeshi Makabe, Eri Arai, Takuro Hirano, Nanako Ito, Yukihiro Fukamachi, Yoriko Takahashi, Akira Hirasawa, Wataru Yamagami, Nobuyuki Susumu, Daisuke Aoki and 1 more

Abstract read
In one paragraph

Article in Carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
–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

38 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Takeshi MakabeDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Eri AraiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Takuro HiranoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Nanako ItoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yukihiro FukamachiBioscience Department, Mitsui Knowledge Industry Co, Ltd, Tokyo, Japan.
Yoriko TakahashiBioscience Department, Mitsui Knowledge Industry Co, Ltd, Tokyo, Japan.
Akira HirasawaDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Wataru YamagamiDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Nobuyuki SusumuDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Daisuke AokiDepartment of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan.
Yae KanaiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was performed to clarify the significance of DNA methylation alterations during endometrial carcinogenesis. Genome-wide DNA methylation analysis and targeted sequencing of tumor-related genes were performed using the Infinium MethylationEPIC BeadChip and the Ion AmpliSeq Cancer Hotspot Panel v2, respectively, for 31 samples of normal control endometrial tissue from patients without endometrial cancer and 81 samples of endometrial cancer tissue. Principal component analysis revealed that tumor samples had a DNA methylation profile distinct from that of control samples. Gene Ontology enrichment analysis revealed significant differences of DNA methylation at 1034 CpG sites between early-onset endometrioid endometrial cancer (EE) tissue (patients aged ≤40 years) and late-onset endometrioid endometrial cancer (LE) tissue, which were accumulated among 'transcriptional factors'. Mutations of the CTNNB1 gene or DNA methylation alterations of genes participating in Wnt signaling were frequent in EEs, whereas genetic and epigenetic alterations of fibroblast growth factor signaling genes were observed in LEs. Unsupervised hierarchical clustering grouped EE samples in Cluster EA (n = 22) and samples in Cluster EB (n = 12). Clinicopathologically less aggressive tumors tended to be accumulated in Cluster EB, and DNA methylation levels of 18 genes including HOXA9, HOXD10 and SOX11 were associated with differences in such aggressiveness between the two clusters. We identified 11 marker CpG sites that discriminated EB samples from EA samples with 100% sensitivity and specificity. These data indicate that genetically and epigenetically different pathways may participate in the development of EEs and LEs, and that DNA methylation profiling may help predict tumors that are less aggressive and amenable to fertility preservation treatment.

Indexed as

DNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticGenome-Wide Association StudyAdultAge of OnsetBiomarkers, TumorCarcinogenesisEndometrial NeoplasmsFemaleGenome, HumanHumansMiddle AgedPromoter Regions, GeneticBiomarkers, Tumor

Identifiers

PMID30850842
PMCPMC6610171

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Registered trials

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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.