Evidence map›Paper›PMID 30374835›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2019

Synergistic triad epistasis of epigenetic H3K27me modifier genes, EZH2, KDM6A, and KDM6B, in gastric cancer susceptibility.

Seon Woo Lee, Do Youn Park, Mi-Young Kim, Changwon Kang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Seon Woo LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Do Youn ParkDepartment of Pathology, Pusan National University Hospital, Busan, 49241, Republic of Korea.
Mi-Young KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Changwon KangDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea. ckang@kaist.ac.kr.ORCID 0000-0002-0867-6385
Korea Advanced Institute of Science and Technology · KRPusan National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFor an epigenetic regulation of human genome, three enzymes write or erase methylation of lysine-27 residue on histone H3 (H3K27me). This methylation is catalyzed by EZH2 (KMT6A) methyltransferase and reversed by KDM6A (UTX) or KDM6B (JMJD3) demethylase. Genetic cancer risk association has been reported on EZH2, but not on KDM6A or KDM6B yet.

methodsA total of 23 tag single-nucleotide polymorphisms (SNPs) of the three genes were genotyped in 2349 Korean participants, and their gastric cancer risk associations and epistases were statistically examined by comparing the SNP genotypes of 1100 gastric cancer patients and 1249 healthy controls.

resultsAll three genes are individually associated with gastric cancer susceptibility, as evident with the genotypes of KDM6A SNP rs5952279 (P = 0.00010) and rs144974719 (P = 0.00024), KDM6B rs78633955 (P = 0.0019) and rs11657063 (P = 0.0036), and EZH2 rs67648693 (P = 0.0028) and rs1061037 (P = 0.023). Furthermore, when odds ratio of interaction (OR

conclusionsAll three H3K27me modifier genes are individually associated with gastric cancer susceptibility with synergistic triad interaction. Not only two enzymes with the same function (KDM6A and KDM6B), but also those with opposite functions (EZH2 versus KDM6A or KDM6B) synergistically affect H3K27me consequences such as gastric cancer susceptibility.

Indexed as

Epistasis, GeneticGenetic Predisposition to DiseaseAdultAgedAged, 80 and overBiomarkers, TumorCase-Control StudiesEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticGenes, ModifierHistone DemethylasesHistonesHumansBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistone DemethylasesHistonesJumonji Domain-Containing Histone DemethylasesKDM6A protein, humanKDM6B protein, humanNuclear ProteinsCancer susceptibility associationEpigenetic codeGene–gene interactionHistone methylationSingle-nucleotide polymorphism

Identifiers

PMID30374835
OpenAlexW2899044097

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.