Evidence map›Paper›PMID 18637884›Full record

ArticleAnnals of human genetics2008

Cholesteryl ester transfer protein (CETP) genetic variation and early onset of non-fatal myocardial infarction.

V Meiner, Y Friedlander, H Milo, N Sharon, L Ben-Avi, S Shpitzen, E Leitersdorf, D S Siscovick, S M Schwartz

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In one paragraph

Article in Annals of human genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 7 pooled it
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 7 syntheses or guidelines pooled it, 24 citations in OpenAlex.

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  16. Evidence for an inherited predisposition contributing to the risk for rotator cuff disease.The Journal of bone and joint surgery. American volume · 2009
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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 2 institutions in 2 countries.

V MeinerDepartment of Human Genetics, Hadassah-Hebrew University Hospital, Jerusalem, Israel.
Y Friedlander
H Milo
N Sharon
L Ben-Avi
S Shpitzen
E Leitersdorf
D S Siscovick
S M Schwartz
Hebrew University of Jerusalem · ILUniversity of Washington · US

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI ALI SHOJAIE · 1995 to 2026
$42.5M
COMMON VARIANTS IN CANDIDATE GENES AND PREMATURE MI RISKR01HL056931 · NHLBI · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, STEPHEN MARC · 1998 to 2001
$1.5M
NHLBI NIH HHS R01 HL056931NHLBI NIH HHS R01HL056931NIEHS NIH HHS P30 ES007033NIEHS NIH HHS P30ES07033
6 · The paper itself

Abstract

Although Cholesteryl Ester Transfer Protein (CETP) mediates the transfer of cholesteryl esters and triglycerides between lipoprotein particles and thus plays a crucial role in reverse cholesterol transport, the association of variations in the CETP gene with acute myocardial infarction (MI) remains unclear. In this study we examined whether common genetic variation in the CETP gene is related to early-onset non-fatal MI risk in a population-based case-control study from western Washington State. Genotyping for the CETP -2708 G/A, -971 A/G, -629 A/C, Intron-I TaqI G/A and exon-14 A/G (I405V) SNPs was performed in 578 cases with first acute non-fatal MI and in 666 demographically similar controls, free of clinical cardiovascular disease, identified randomly from the community. In-person interviews and non-fasting blood specimens provided data on coronary heart disease risk factors. In men, there was little evidence for an association between single SNPs and MI risk, but in women the age- and race-adjusted OR was found to be significant in 4 out of the 5 CETP single variants. Haplotype analysis revealed two haplotypes associated with MI risk among men. As compared to men homozygous for the most common haplotype D (-2708 G, -971 G, -629 C, TaqI G and exon-14 A), the fully-adjusted multiplicative model identified haplotype G (-2708 G, -971 A, -629 A, TaqI G and exon-14 G) was associated with a 4.0-6.0-fold increased risk of MI for each additional copy; [95%CI 2.4-14.8] and haplotype B (-2708 G, -971 G, -629 A, TaqI A and exon-14 A) showed a significant decreased risk for early onset MI [OR = 0.18; 95%CI 0.04 - 0.75]. An evolutionary-based haplotype analysis indicated that the two haplotypes associated with the MI risk are most evolutionarily divergent from the other haplotypes. Variation at the CETP gene locus is associated with the risk of early-onset non-fatal MI. This association was found to be independent of HDL-C levels. These data and the sex-specific findings require confirmation in other populations.

Indexed as

Genetic Predisposition to DiseaseAdolescentAdultCase-Control StudiesCholesterol Ester Transfer ProteinsFemaleHaplotypesHumansMaleMiddle AgedMyocardial InfarctionPolymorphism, Single NucleotideRisk FactorsSex FactorsWashingtonCETP protein, humanCholesterol Ester Transfer Proteins

Identifiers

PMID18637884
PMCPMC2766633
OpenAlexW2032416836

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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.