Evidence map›Paper›PMID 21971053›Full record

ArticleEuropean journal of human genetics : EJHG2012

Genome-wide association study of coronary artery disease in the Japanese.

Fumihiko Takeuchi, Mitsuhiro Yokota, Ken Yamamoto, Eitaro Nakashima, Tomohiro Katsuya, Hiroyuki Asano, Masato Isono, Toru Nabika, Takao Sugiyama, Akihiro Fujioka and 15 more

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In one paragraph

Article in European journal of human genetics : EJHG, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 12 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 12 pooled it
8.6field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 12 syntheses or guidelines pooled it, 161 citations in OpenAlex.

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  14. Assessing genetic risk factors for early-onset coronary artery disease in Iranians.Research and practice in thrombosis and haemostasis · 2026
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32 more citing papers are in PubMed but not listed here.

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

25 authors at 16 institutions in 1 country.

Fumihiko TakeuchiDepartment of Gene Diagnostics and Therapeutics, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Mitsuhiro Yokota
Ken Yamamoto
Eitaro Nakashima
Tomohiro Katsuya
Hiroyuki Asano
Masato Isono
Toru Nabika
Takao Sugiyama
Akihiro Fujioka
Nobuhisa Awata
Keizo Ohnaka
Masahiro Nakatochi
Hidetoshi Kitajima
Hiromi Rakugi
Jiro Nakamura
Takayoshi Ohkubo
Yutaka Imai
Kazuaki Shimamoto
Yukio Yamori
Shuhei Yamaguchi
Shotai Kobayashi
Ryoichi Takayanagi
Toshio Ogihara
Norihiro Kato
Kyushu University · JPNational Center for Global Health and Medicine · JPOsaka University · JPNagoya University · JPShimane University · JPAichi Gakuin University · JPChubu Rosai Hospital · JPHyogo Prefectural Amagasaki General Medical Center · JPInstitute for Adult Diseases Asahi Life Foundation · JPMukogawa Women's University · JPOsaka Medical Center for Cancer and Cardiovascular Diseases · JPSapporo Medical University · JPShiga University · JPShimane University Hospital · JPShinKokura Hospital · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A new understanding of the genetic basis of coronary artery disease (CAD) has recently emerged from genome-wide association (GWA) studies of common single-nucleotide polymorphisms (SNPs), thus far performed mostly in European-descent populations. To identify novel susceptibility gene variants for CAD and confirm those previously identified mostly in populations of European descent, a multistage GWA study was performed in the Japanese. In the discovery phase, we first genotyped 806 cases and 1337 controls with 451 382 SNP markers and subsequently assessed 34 selected SNPs with direct genotyping (541 additional cases) and in silico comparison (964 healthy controls). In the replication phase, involving 3052 cases and 6335 controls, 12 SNPs were tested; CAD association was replicated and/or verified for 4 (of 12) SNPs from 3 loci: near BRAP and ALDH2 on 12q24 (P=1.6 × 10(-34)), HLA-DQB1 on 6p21 (P=4.7 × 10(-7)), and CDKN2A/B on 9p21 (P=6.1 × 10(-16)). On 12q24, we identified the strongest association signal with the strength of association substantially pronounced for a subgroup of myocardial infarction cases (P=1.4 × 10(-40)). On 6p21, an HLA allele, DQB1(*)0604, could show one of the most prominent association signals in an ∼8-Mb interval that encompasses the LTA gene, where an association with myocardial infarction had been reported in another Japanese study. CAD association was also identified at CDKN2A/B, as previously reported in different populations of European descent and Asians. Thus, three loci confirmed in the Japanese GWA study highlight the likely presence of risk alleles with two types of genetic effects - population specific and common - on susceptibility to CAD.

Indexed as

Genome-Wide Association StudyAdultAgedAllelesAsian PeopleCase-Control StudiesCoronary Artery DiseaseFemaleGenetic LociGenetic Predisposition to DiseaseHaplotypesHumansJapanMaleMiddle AgedPolymorphism, Single Nucleotide

Identifiers

PMID21971053
PMCPMC3283177
OpenAlexW2076760973

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.