Copy Number Variants: Distribution in Patients with Coronary Atherosclerosis

Gancheva, K; Postadjian, A.; Brazma, Diana; Grace, Colin; Chanalaris, Anastasios; Nacheva, Elisabeth P.; Apostolova, Margarita D.

doi:10.1080/13102818.2009.10817620

Cited by 3 publications

(2 citation statements)

References 31 publications

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“…Работы, описывающие вклад CNV в риск развития атеросклероза и его осложнений, немногочисленны и противоречивы [37][38][39][40][41]. В данных исследованиях проводилось тестирование только одной ткани -лейкоцитов периферической крови.…”

Section: российскийunclassified

Structural Variablity of Leucocyte Genome and Arterial Cells in Human Atherosclerosis

Слепцов¹,

Nazarenko²,

Puzyrev³

2017

Russ J Cardiol

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Section: российскийunclassified

Structural Variablity of Leucocyte Genome and Arterial Cells in Human Atherosclerosis

Слепцов¹,

Nazarenko²,

Puzyrev³

2017

Russ J Cardiol

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“…The studies of CNVs in coronary artery disease have typically used DNA isolated from peripheral blood, and inconclusive results were obtained891011. The most pronounced genomic imbalance in patients with coronary artery disease and metabolic comorbidity are possibly detected in the target disease organs, such as coronary arteries.…”

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confidence: 99%

Genomic structural variations for cardiovascular and metabolic comorbidity

Nazarenko

Слепцов

Lebedev

et al. 2017

Sci Rep

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The objective of this study was to identify genes targeted by both copy number and copy-neutral changes in the right coronary arteries in the area of advanced atherosclerotic plaques and intact internal mammary arteries derived from the same individuals with comorbid coronary artery disease and metabolic syndrome. The artery samples from 10 patients were screened for genomic imbalances using array comparative genomic hybridization. Ninety high-confidence, identical copy number variations (CNVs) were detected. We also identified eight copy-neutral changes (cn-LOHs) > 1.5 Mb in paired arterial samples in 4 of 10 individuals. The frequencies of the two gains located in the 10q24.31 (ERLIN1) and 12q24.11 (UNG, ACACB) genomic regions were evaluated in 33 paired arteries and blood samples. Two patients contained the gain in 10q24.31 (ERLIN1) and one patient contained the gain in 12q24.11 (UNG, ACACB) that affected only the blood DNA. An additional two patients harboured these CNVs in both the arteries and blood. In conclusion, we discovered and confirmed a gain of the 10q24.31 (ERLIN1) and 12q24.11 (UNG, ACACB) genomic regions in patients with coronary artery disease and metabolic comorbidity. Analysis of DNA extracted from blood indicated a possible somatic origin for these CNVs.

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