Evidence map›Paper›PMID 21860640›Full record

ArticleKorean circulation journal2011

Deoxyribonucleic Acid copy number aberrations in vasospastic angina patients using an array comparative genomic hybridization.

Suk Min Seo, Yoon Seok Koh, Hae Ok Jung, Jin Soo Choi, Pum Joon Kim, Sang Hong Baek, Ho-Joong Youn, Kweon-Haeng Lee, Ki-Bae Seung

Open access · hybridAbstract read
In one paragraph

Article in Korean circulation journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 86% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Suk Min SeoCardiovascular Center and Cardiology Division, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Yoon Seok Koh
Hae Ok Jung
Jin Soo Choi
Pum Joon Kim
Sang Hong Baek
Ho-Joong Youn
Kweon-Haeng Lee
Ki-Bae Seung
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesVasospastic angina (VA) is a specific type of coronary artery disease and develops as a result of coronary artery spasm. Recently, a few studies have revealed that VA caused by coronary artery spasm is related to genetic traits. The objective of this study was to use the recently developed technique of array comparative genomic hybridization (CGH) to screen the genetic aberrations of VA. SUBJECTS AND

methodsTo identify candidate genes that might be causally involved in the pathogenesis of VA, genomic deoxyribonucleic acids were extracted from whole blood of 28 patients with VA who presented at Department of Cardiology at Seoul St. Mary's Hospital, Seoul, Korea. The copy number profiles of these patients was then analyzed using array CGH and reverse transcriptase (RT) quantitative polymerase chain reaction (PCR).

resultsArray CGH revealed gains in 31 different regions, with losses in the 4q35.2, 7q22.1, 10q26.3, 15q11.2, 16p13.11, 17p11.2 and 19q13.3 regions (more than 32% aberration in these regions). Several loci were found to be frequently including gains of 5p and 11q (50% of samples). The most common losses were found in 7q (54% of samples). Copy number aberrations in chromosomal regions were detected and corresponding genes were confirmed by RT quantitative PCR. The fold change levels were highest in the CTDP1 (18q23), HDAC10 (22q13.33), KCNQ1 (11p15.5-p15.4), NINJ2 (12p13.33), NOTCH2 (1p12-p11.2), PCSK6 (15q26.3), SDHA (5p15.33), and MUC17 (7q22.1) genes.

conclusionMany candidate chromosomal regions that might be related to the pathogenesis of VA were detected by array CGH and should be systematically investigated to establish the causative and specific genes for VA.

Indexed as

Array comparative genomic hybridizationVasospastic angina

Identifiers

PMID21860640
PMCPMC3152733
OpenAlexW2114064751

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