TY  - JOUR
AU  - Đorđević, Ana
AU  - Živković, Maja
AU  - Bošković, Maja
AU  - Dekleva, Milica
AU  - Stanković, Goran
AU  - Stanković, Aleksandra
AU  - Đurić, Tamara
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10617
AB  - Galectin-3 is encoded by LGALS-3, located in a unique haplotype block in Caucasians. According to the Tagger server, rs4040064, rs11628437, and rs7159490 cover 82% (r2 > 0.8) of the genetic variance of this HapBlock. Our aims were to examine the association of their haplotypes with first myocardial infarction (MI), changes in left ventricular echocardiographic parameters over time, and impact on plasma galectin-3 and LGALS-3 mRNA in peripheral blood mononuclear cells, both 6 months post-MI. The study group consisted of 546 MI patients and 323 controls. Gene expression was assessed in 92 patients and plasma galectin-3 in 189 patients. Rs4040064, rs11628437, rs7159490, and LGALS-3 mRNA expression were detected using TaqMan® technology. Plasma galectin-3 concentrations were determined by the ELISA method. We found that the TGC haplotype could have a protective effect against MI (adjusted OR 0.19 [0.05–0.72], p = 0.015) and that the GAC haplotype had significantly higher galectin-3 concentrations (48.3 [37.3–59.4] ng/mL vs. 18.9 [14.5–23.4] ng/mL, p < 0.0001), both in males and compared to the referent haplotype GGC. Higher plasma Gal-3 was also associated with higher NYHA class and systolic dysfunction. Our results suggest that variants tagging LGALS-3 HapBlock could reflect plasma Gal-3 levels 6 months post-MI and may have a potential protective effect against MI in men. Further replication, validation, and functional studies are needed.
T2  - Genes
T1  - Variants Tagging LGALS-3 Haplotype Block in Association with First Myocardial Infarction and Plasma Galectin-3 Six Months after the Acute Event
VL  - 14
IS  - 1
SP  - 109
DO  - 10.3390/genes14010109
ER  - 

@article{
author = "Đorđević, Ana and Živković, Maja and Bošković, Maja and Dekleva, Milica and Stanković, Goran and Stanković, Aleksandra and Đurić, Tamara",
year = "2023",
abstract = "Galectin-3 is encoded by LGALS-3, located in a unique haplotype block in Caucasians. According to the Tagger server, rs4040064, rs11628437, and rs7159490 cover 82% (r2 > 0.8) of the genetic variance of this HapBlock. Our aims were to examine the association of their haplotypes with first myocardial infarction (MI), changes in left ventricular echocardiographic parameters over time, and impact on plasma galectin-3 and LGALS-3 mRNA in peripheral blood mononuclear cells, both 6 months post-MI. The study group consisted of 546 MI patients and 323 controls. Gene expression was assessed in 92 patients and plasma galectin-3 in 189 patients. Rs4040064, rs11628437, rs7159490, and LGALS-3 mRNA expression were detected using TaqMan® technology. Plasma galectin-3 concentrations were determined by the ELISA method. We found that the TGC haplotype could have a protective effect against MI (adjusted OR 0.19 [0.05–0.72], p = 0.015) and that the GAC haplotype had significantly higher galectin-3 concentrations (48.3 [37.3–59.4] ng/mL vs. 18.9 [14.5–23.4] ng/mL, p < 0.0001), both in males and compared to the referent haplotype GGC. Higher plasma Gal-3 was also associated with higher NYHA class and systolic dysfunction. Our results suggest that variants tagging LGALS-3 HapBlock could reflect plasma Gal-3 levels 6 months post-MI and may have a potential protective effect against MI in men. Further replication, validation, and functional studies are needed.",
journal = "Genes",
title = "Variants Tagging LGALS-3 Haplotype Block in Association with First Myocardial Infarction and Plasma Galectin-3 Six Months after the Acute Event",
volume = "14",
number = "1",
pages = "109",
doi = "10.3390/genes14010109"
}

Đorđević, A., Živković, M., Bošković, M., Dekleva, M., Stanković, G., Stanković, A.,& Đurić, T.. (2023). Variants Tagging LGALS-3 Haplotype Block in Association with First Myocardial Infarction and Plasma Galectin-3 Six Months after the Acute Event. in Genes, 14(1), 109.
https://doi.org/10.3390/genes14010109

Đorđević A, Živković M, Bošković M, Dekleva M, Stanković G, Stanković A, Đurić T. Variants Tagging LGALS-3 Haplotype Block in Association with First Myocardial Infarction and Plasma Galectin-3 Six Months after the Acute Event. in Genes. 2023;14(1):109.
doi:10.3390/genes14010109 .

Đorđević, Ana, Živković, Maja, Bošković, Maja, Dekleva, Milica, Stanković, Goran, Stanković, Aleksandra, Đurić, Tamara, "Variants Tagging LGALS-3 Haplotype Block in Association with First Myocardial Infarction and Plasma Galectin-3 Six Months after the Acute Event" in Genes, 14, no. 1 (2023):109,
https://doi.org/10.3390/genes14010109 . .

TY  - JOUR
AU  - Đurić, Tamara
AU  - Kuveljić, Jovana
AU  - Đorđević, Ana
AU  - Dekleva, Milica
AU  - Stanković, Goran
AU  - Stanković, Aleksandra
AU  - Živković, Maja
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10382
AB  - Background Myocardial infarction (MI) leads to ischemia and afterward to left ventricular (LV) remodeling. Matrix metalloproteinase−1 (MMP1) and −3 (MMP3) belong to the family of endopeptidases and together they can dissolve most of the components of the extracellular matrix. MMP1 and MMP3 variants have been investigated solely in association with ischemic heart disease and LV dysfunction, but not in haplotype. The aims of this study were to investigate the association of haplotypes inferred from MMP1 rs1799750 (−1607 1G/2G; NC_000011.9:g.102670497del) and MMP3 rs35068180 (−1612 5A/6A; NC_000011.9:g.102715952dup) with MI and their effect on the change in echocardiographic parameters of LV structure and function in patients within 6 months after MI. Methods The study included 325 patients with the first MI and 283 healthy controls. Gene variants were detected by PCR-RFLP method. Parameters of LV structure and function were assessed by conventional 2D echocardiography, 3–5 days and 6 months after the first MI, on a subgroup of 160 patients. Haplotype analysis was performed with Thesias software. Results Haplotypes 2G-5A and 1G-6A were significantly and independently associated with MI compared with the reference haplotype 2G-6A (adjusted, p = 0.009 and p = 0.026, respectively). After Bonferroni correction for multiple testing, MMP1 and MMP3 haplotypes lost their association with the change in LV long diameter and stroke volume within 6 months after MI. Conclusion MMP1 and MMP3 haplotypes are strongly associated with MI. Further studies are needed to validate this result and to examine their association with echocardiographic parameters of LV structure and function after MI.
T2  - Molecular Genetics & Genomic Medicine
T1  - Association of MMP1 and MMP3 haplotypes with myocardial infarction and echocardiographic parameters of the left ventricle
VL  - 10
IS  - 9
SP  - e2022
DO  - 10.1002/mgg3.2022
ER  - 

@article{
author = "Đurić, Tamara and Kuveljić, Jovana and Đorđević, Ana and Dekleva, Milica and Stanković, Goran and Stanković, Aleksandra and Živković, Maja",
year = "2022",
abstract = "Background Myocardial infarction (MI) leads to ischemia and afterward to left ventricular (LV) remodeling. Matrix metalloproteinase−1 (MMP1) and −3 (MMP3) belong to the family of endopeptidases and together they can dissolve most of the components of the extracellular matrix. MMP1 and MMP3 variants have been investigated solely in association with ischemic heart disease and LV dysfunction, but not in haplotype. The aims of this study were to investigate the association of haplotypes inferred from MMP1 rs1799750 (−1607 1G/2G; NC_000011.9:g.102670497del) and MMP3 rs35068180 (−1612 5A/6A; NC_000011.9:g.102715952dup) with MI and their effect on the change in echocardiographic parameters of LV structure and function in patients within 6 months after MI. Methods The study included 325 patients with the first MI and 283 healthy controls. Gene variants were detected by PCR-RFLP method. Parameters of LV structure and function were assessed by conventional 2D echocardiography, 3–5 days and 6 months after the first MI, on a subgroup of 160 patients. Haplotype analysis was performed with Thesias software. Results Haplotypes 2G-5A and 1G-6A were significantly and independently associated with MI compared with the reference haplotype 2G-6A (adjusted, p = 0.009 and p = 0.026, respectively). After Bonferroni correction for multiple testing, MMP1 and MMP3 haplotypes lost their association with the change in LV long diameter and stroke volume within 6 months after MI. Conclusion MMP1 and MMP3 haplotypes are strongly associated with MI. Further studies are needed to validate this result and to examine their association with echocardiographic parameters of LV structure and function after MI.",
journal = "Molecular Genetics & Genomic Medicine",
title = "Association of MMP1 and MMP3 haplotypes with myocardial infarction and echocardiographic parameters of the left ventricle",
volume = "10",
number = "9",
pages = "e2022",
doi = "10.1002/mgg3.2022"
}

Đurić, T., Kuveljić, J., Đorđević, A., Dekleva, M., Stanković, G., Stanković, A.,& Živković, M.. (2022). Association of MMP1 and MMP3 haplotypes with myocardial infarction and echocardiographic parameters of the left ventricle. in Molecular Genetics & Genomic Medicine, 10(9), e2022.
https://doi.org/10.1002/mgg3.2022

Đurić T, Kuveljić J, Đorđević A, Dekleva M, Stanković G, Stanković A, Živković M. Association of MMP1 and MMP3 haplotypes with myocardial infarction and echocardiographic parameters of the left ventricle. in Molecular Genetics & Genomic Medicine. 2022;10(9):e2022.
doi:10.1002/mgg3.2022 .

Đurić, Tamara, Kuveljić, Jovana, Đorđević, Ana, Dekleva, Milica, Stanković, Goran, Stanković, Aleksandra, Živković, Maja, "Association of MMP1 and MMP3 haplotypes with myocardial infarction and echocardiographic parameters of the left ventricle" in Molecular Genetics & Genomic Medicine, 10, no. 9 (2022):e2022,
https://doi.org/10.1002/mgg3.2022 . .

TY  - JOUR
AU  - Živković, Maja
AU  - Bubić, Maja
AU  - Kolaković, Ana
AU  - Dekleva, Milica
AU  - Stanković, Goran
AU  - Stanković, Aleksandra
AU  - Đurić, Tamara
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9842
AB  - Glutathione S-transferases (GSTs) are the family of enzymes involved in the second line of defense against oxidative stress (OS). The lack of GSTT1/GSTM1 enzyme quantity or activity, due to the presence of homozygous deletion compromises antioxidative defense resulting in OS. OS is the critical mechanism in the pathophysiology of atherosclerosis, coronary artery disease, and myocardial infarction (MI). The increase in reactive oxygen species together with the process of apoptosis plays a role in left ventricular remodeling (LVR) after MI. The associations of GSTT1 and GSTM1 gene polymorphisms with the risk of MI are inconsistent. The aim was to analyze the association of GSTT1/GSTM1 null genotypes with first MI and LVR 8 months after the MI. The study involved 330 controls and 438 consecutive patients with symptoms and signs of first MI. The subgroup of 150 MI patients was prospectively followed up for 6 months. Evidence of maladaptive LVR was obtained by 2D Doppler echocardiography 3-5 days and 6 months after the MI. A multiplex polymerase chain reaction was used to detect the deletion in GSTT1 and GSTM1 genes. GSTM1 null genotype was significantly and independently associated with first MI (adjusted OR = 1.45 95% CI 1.03-2.03, p = 0.03). Association of double null genotypes with maladaptive LVR in patients 6 months after the first MI was no longer significant after adjustment for factors that differed significantly between patients with and without maladaptive LVR. This study demonstrated the association of GSTM1 null genotypes with the risk of MI in the Serbian population.
T2  - Free Radical Research
T1  - The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction
VL  - 55
IS  - 3
SP  - 267
EP  - 274
DO  - 10.1080/10715762.2021.1931166
ER  - 

@article{
author = "Živković, Maja and Bubić, Maja and Kolaković, Ana and Dekleva, Milica and Stanković, Goran and Stanković, Aleksandra and Đurić, Tamara",
year = "2021",
abstract = "Glutathione S-transferases (GSTs) are the family of enzymes involved in the second line of defense against oxidative stress (OS). The lack of GSTT1/GSTM1 enzyme quantity or activity, due to the presence of homozygous deletion compromises antioxidative defense resulting in OS. OS is the critical mechanism in the pathophysiology of atherosclerosis, coronary artery disease, and myocardial infarction (MI). The increase in reactive oxygen species together with the process of apoptosis plays a role in left ventricular remodeling (LVR) after MI. The associations of GSTT1 and GSTM1 gene polymorphisms with the risk of MI are inconsistent. The aim was to analyze the association of GSTT1/GSTM1 null genotypes with first MI and LVR 8 months after the MI. The study involved 330 controls and 438 consecutive patients with symptoms and signs of first MI. The subgroup of 150 MI patients was prospectively followed up for 6 months. Evidence of maladaptive LVR was obtained by 2D Doppler echocardiography 3-5 days and 6 months after the MI. A multiplex polymerase chain reaction was used to detect the deletion in GSTT1 and GSTM1 genes. GSTM1 null genotype was significantly and independently associated with first MI (adjusted OR = 1.45 95% CI 1.03-2.03, p = 0.03). Association of double null genotypes with maladaptive LVR in patients 6 months after the first MI was no longer significant after adjustment for factors that differed significantly between patients with and without maladaptive LVR. This study demonstrated the association of GSTM1 null genotypes with the risk of MI in the Serbian population.",
journal = "Free Radical Research",
title = "The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction",
volume = "55",
number = "3",
pages = "267-274",
doi = "10.1080/10715762.2021.1931166"
}

Živković, M., Bubić, M., Kolaković, A., Dekleva, M., Stanković, G., Stanković, A.,& Đurić, T.. (2021). The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction. in Free Radical Research, 55(3), 267-274.
https://doi.org/10.1080/10715762.2021.1931166

Živković M, Bubić M, Kolaković A, Dekleva M, Stanković G, Stanković A, Đurić T. The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction. in Free Radical Research. 2021;55(3):267-274.
doi:10.1080/10715762.2021.1931166 .

Živković, Maja, Bubić, Maja, Kolaković, Ana, Dekleva, Milica, Stanković, Goran, Stanković, Aleksandra, Đurić, Tamara, "The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction" in Free Radical Research, 55, no. 3 (2021):267-274,
https://doi.org/10.1080/10715762.2021.1931166 . .

TY  - JOUR
AU  - Kuveljić, Jovana
AU  - Đurić, Tamara
AU  - Stanković, Goran
AU  - Dekleva, Milica
AU  - Stanković, Aleksandra
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9541
AB  - Background: Myocardial infarction (MI) and underlining atherosclerosis are the main causes of death worldwide. Phosphatase and actin regulator 1 (PHACTR1) variants have been associated with early onset MI, coronary artery disease and carotid dissection. PHACTR1 mRNA expression has been detected in tissues and cells related to atherosclerosis. Nonetheless, the true effect of PHACTR1 on vascular diseases is still unknown. Our aim was to examine the association of PHACTR1 intronic variants, rs9349379, rs2026458 and rs2876300, with MI and multi-vessel disease (MVD) and to assess their effect on PHACTR1 and EDN1 mRNA expression in PBMCs of patients six months after MI. Methods: The study enrolled 537 patients with the first MI and 310 controls. Gene expression was assessed in 74 patients six months after MI and 37 healthy controls. Rs9349379, rs2026458, rs2876300 and relative mRNA expressions were detected by TaqMan® technology. Results: The significant association between PHACTR1 variants and MI was not found, either individually or in haplotype. A higher frequency of rs2876300G-allele in MVD was rendered not significant after Bonferroni correction. PHACTR1 mRNA was significantly increased in PBMCs of patients six months after MI compared to controls (p = 0.02). Patients that carry ACG haplotype have increased PHACTR1 mRNA expression in PBMCs (p = 0.04). There was no effect of PHACTR1 variants on EDN1 mRNA expression. Conclusion: Our findings suggest that PHACTR1 intronic variants may have a role in severity and progression of coronary atherosclerosis. Future research is needed to clarify the mechanism underlying the role of PHACTR1 in coronary atherosclerosis and MI. © 2021 Elsevier B.V.
T2  - Gene
T1  - Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs
VL  - 775
SP  - 145428
DO  - 10.1016/j.gene.2021.145428
ER  - 

@article{
author = "Kuveljić, Jovana and Đurić, Tamara and Stanković, Goran and Dekleva, Milica and Stanković, Aleksandra and Alavantić, Dragan and Živković, Maja",
year = "2021",
abstract = "Background: Myocardial infarction (MI) and underlining atherosclerosis are the main causes of death worldwide. Phosphatase and actin regulator 1 (PHACTR1) variants have been associated with early onset MI, coronary artery disease and carotid dissection. PHACTR1 mRNA expression has been detected in tissues and cells related to atherosclerosis. Nonetheless, the true effect of PHACTR1 on vascular diseases is still unknown. Our aim was to examine the association of PHACTR1 intronic variants, rs9349379, rs2026458 and rs2876300, with MI and multi-vessel disease (MVD) and to assess their effect on PHACTR1 and EDN1 mRNA expression in PBMCs of patients six months after MI. Methods: The study enrolled 537 patients with the first MI and 310 controls. Gene expression was assessed in 74 patients six months after MI and 37 healthy controls. Rs9349379, rs2026458, rs2876300 and relative mRNA expressions were detected by TaqMan® technology. Results: The significant association between PHACTR1 variants and MI was not found, either individually or in haplotype. A higher frequency of rs2876300G-allele in MVD was rendered not significant after Bonferroni correction. PHACTR1 mRNA was significantly increased in PBMCs of patients six months after MI compared to controls (p = 0.02). Patients that carry ACG haplotype have increased PHACTR1 mRNA expression in PBMCs (p = 0.04). There was no effect of PHACTR1 variants on EDN1 mRNA expression. Conclusion: Our findings suggest that PHACTR1 intronic variants may have a role in severity and progression of coronary atherosclerosis. Future research is needed to clarify the mechanism underlying the role of PHACTR1 in coronary atherosclerosis and MI. © 2021 Elsevier B.V.",
journal = "Gene",
title = "Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs",
volume = "775",
pages = "145428",
doi = "10.1016/j.gene.2021.145428"
}

Kuveljić, J., Đurić, T., Stanković, G., Dekleva, M., Stanković, A., Alavantić, D.,& Živković, M.. (2021). Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs. in Gene, 775, 145428.
https://doi.org/10.1016/j.gene.2021.145428

Kuveljić J, Đurić T, Stanković G, Dekleva M, Stanković A, Alavantić D, Živković M. Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs. in Gene. 2021;775:145428.
doi:10.1016/j.gene.2021.145428 .

Kuveljić, Jovana, Đurić, Tamara, Stanković, Goran, Dekleva, Milica, Stanković, Aleksandra, Alavantić, Dragan, Živković, Maja, "Association of PHACTR1 intronic variants with the first myocardial infarction and their effect on PHACTR1 mRNA expression in PBMCs" in Gene, 775 (2021):145428,
https://doi.org/10.1016/j.gene.2021.145428 . .

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Milašinović, Dejan
AU  - Stanković, Goran
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nataša
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8432
AB  - Background: Chromosomal region 9p21.3 is most robustly associated with coronary artery disease (CAD) in western European populations. However, heterogeneity in CAD phenotypes leads to uncertainty whether 9p21.3 is associated with stable and/or acute clinical presentations of CAD. 9p21.3 is rich in regulatory elements, but the underlying mechanisms of its actions in CAD remain unclear. We investigate the association of 9p21.3 two haplotype blocks lead variants (rs10757278 and rs518394) with first-ever non-fatal myocardial infarction (MI) in CAD patients and their association with CDKN2B mRNA expression in peripheral blood mononuclear cells 6 months after the event. Methods: We included CAD patients with sustained first MI (n = 523) and controls (n = 583). Gene expression was assessed in 72 patients 6 months after MI and 43 healthy controls. TaqMan® technology was used for the gene expression and genotyping analysis. Results: CDKN2B mRNA was significantly lower in MI patients compared with the controls (p = 0.002) and in patients carrying the rs10757278 G risk allele versus AA homozygotes (p = 0.012) 6 months after the event. While we confirmed the association of rs10757278 with CDKN2B expression in MI patients, we failed to find an association between the investigated variants and MI or disease burden. Conclusions: We suggest a dysregulation of gene expression in the 9p21.3 region six months after acute MI, which is affected by a genetic variant in patients. The rs10757278 rare allele is one factor that might lead to prolonged risk for proatherogenic complications. © 2019 The Canadian Society of Clinical Chemists
T2  - Clinical Biochemistry
T1  - CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI
VL  - 73
SP  - 70
EP  - 76
DO  - 10.1016/j.clinbiochem.2019.08.003
ER  - 

@article{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Milašinović, Dejan and Stanković, Goran and Dekleva, Milica and Marković-Nikolić, Nataša and Alavantić, Dragan and Živković, Maja",
year = "2019",
abstract = "Background: Chromosomal region 9p21.3 is most robustly associated with coronary artery disease (CAD) in western European populations. However, heterogeneity in CAD phenotypes leads to uncertainty whether 9p21.3 is associated with stable and/or acute clinical presentations of CAD. 9p21.3 is rich in regulatory elements, but the underlying mechanisms of its actions in CAD remain unclear. We investigate the association of 9p21.3 two haplotype blocks lead variants (rs10757278 and rs518394) with first-ever non-fatal myocardial infarction (MI) in CAD patients and their association with CDKN2B mRNA expression in peripheral blood mononuclear cells 6 months after the event. Methods: We included CAD patients with sustained first MI (n = 523) and controls (n = 583). Gene expression was assessed in 72 patients 6 months after MI and 43 healthy controls. TaqMan® technology was used for the gene expression and genotyping analysis. Results: CDKN2B mRNA was significantly lower in MI patients compared with the controls (p = 0.002) and in patients carrying the rs10757278 G risk allele versus AA homozygotes (p = 0.012) 6 months after the event. While we confirmed the association of rs10757278 with CDKN2B expression in MI patients, we failed to find an association between the investigated variants and MI or disease burden. Conclusions: We suggest a dysregulation of gene expression in the 9p21.3 region six months after acute MI, which is affected by a genetic variant in patients. The rs10757278 rare allele is one factor that might lead to prolonged risk for proatherogenic complications. © 2019 The Canadian Society of Clinical Chemists",
journal = "Clinical Biochemistry",
title = "CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI",
volume = "73",
pages = "70-76",
doi = "10.1016/j.clinbiochem.2019.08.003"
}

Životić, I., Đurić, T., Stanković, A., Milašinović, D., Stanković, G., Dekleva, M., Marković-Nikolić, N., Alavantić, D.,& Živković, M.. (2019). CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI. in Clinical Biochemistry, 73, 70-76.
https://doi.org/10.1016/j.clinbiochem.2019.08.003

Životić I, Đurić T, Stanković A, Milašinović D, Stanković G, Dekleva M, Marković-Nikolić N, Alavantić D, Živković M. CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI. in Clinical Biochemistry. 2019;73:70-76.
doi:10.1016/j.clinbiochem.2019.08.003 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Milašinović, Dejan, Stanković, Goran, Dekleva, Milica, Marković-Nikolić, Nataša, Alavantić, Dragan, Živković, Maja, "CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI" in Clinical Biochemistry, 73 (2019):70-76,
https://doi.org/10.1016/j.clinbiochem.2019.08.003 . .

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Ivancevic, Ilija
AU  - Končar, Igor
AU  - Milašinović, Dejan
AU  - Stanković, Goran
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1843
AB  - The 9p21.3 region is rich in regulatory elements and the variants in this region had been robustly associated with carotid plaque (CP) and coronary artery disease (CAD). Recently, the HACD4 was detected as one of the six 9p21.3 differentially expressed genes associated with accelerated atherosclerosis and greater mean lesion area in the Athsq1 congenic mice. We aimed to investigate association of two potentially regulatory HACD4 variants (rs36212560 I/D, rs2275888 T/C) and their haplotypes with CP occurrence and the level of HACD4 and FOCAD mRNA in human CP tissue. Association study was replicated in CAD patients who suffered the first myocardial infarction. Study included 477 CP patients, 303 healthy controls and replication sample of 224 CAD males from the population of Serbia. Genotypes were determined by polymerase chain reaction (PCR) and real-time PCR using TaqMan (R) technology. The gene expression was detected with TaqMan (R) technology. We have found significant and independent association of DT haplotype with CP presence in men (adjusted OR = 1.64 CI = 1.12-2.42, p = 0.011). The result was replicated in CAD males (adjusted OR = 1.84 CI = 1.21-2.80, p = 0.004). We have found significant effect of the HACD4 rs2275888 on FOCAD mRNA level in human CP tissue. Correction for multiple testing was performed. Independent association of HACD4 haplotypes with atherosclerotic phenotypes connotes a further validation and replication in larger cohorts as well as functional studies to enlighten the potential mechanism of its action in pathophysiology of atherosclerosis.
T2  - Gene
T1  - The HACD4 haplotype as a risk factor for atherosclerosis in males
VL  - 641
SP  - 35
EP  - 40
DO  - 10.1016/j.gene.2017.10.030
ER  - 

@article{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Ivancevic, Ilija and Končar, Igor and Milašinović, Dejan and Stanković, Goran and Alavantić, Dragan and Živković, Maja",
year = "2018",
abstract = "The 9p21.3 region is rich in regulatory elements and the variants in this region had been robustly associated with carotid plaque (CP) and coronary artery disease (CAD). Recently, the HACD4 was detected as one of the six 9p21.3 differentially expressed genes associated with accelerated atherosclerosis and greater mean lesion area in the Athsq1 congenic mice. We aimed to investigate association of two potentially regulatory HACD4 variants (rs36212560 I/D, rs2275888 T/C) and their haplotypes with CP occurrence and the level of HACD4 and FOCAD mRNA in human CP tissue. Association study was replicated in CAD patients who suffered the first myocardial infarction. Study included 477 CP patients, 303 healthy controls and replication sample of 224 CAD males from the population of Serbia. Genotypes were determined by polymerase chain reaction (PCR) and real-time PCR using TaqMan (R) technology. The gene expression was detected with TaqMan (R) technology. We have found significant and independent association of DT haplotype with CP presence in men (adjusted OR = 1.64 CI = 1.12-2.42, p = 0.011). The result was replicated in CAD males (adjusted OR = 1.84 CI = 1.21-2.80, p = 0.004). We have found significant effect of the HACD4 rs2275888 on FOCAD mRNA level in human CP tissue. Correction for multiple testing was performed. Independent association of HACD4 haplotypes with atherosclerotic phenotypes connotes a further validation and replication in larger cohorts as well as functional studies to enlighten the potential mechanism of its action in pathophysiology of atherosclerosis.",
journal = "Gene",
title = "The HACD4 haplotype as a risk factor for atherosclerosis in males",
volume = "641",
pages = "35-40",
doi = "10.1016/j.gene.2017.10.030"
}

Životić, I., Đurić, T., Stanković, A., Ivancevic, I., Končar, I., Milašinović, D., Stanković, G., Alavantić, D.,& Živković, M.. (2018). The HACD4 haplotype as a risk factor for atherosclerosis in males. in Gene, 641, 35-40.
https://doi.org/10.1016/j.gene.2017.10.030

Životić I, Đurić T, Stanković A, Ivancevic I, Končar I, Milašinović D, Stanković G, Alavantić D, Živković M. The HACD4 haplotype as a risk factor for atherosclerosis in males. in Gene. 2018;641:35-40.
doi:10.1016/j.gene.2017.10.030 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Ivancevic, Ilija, Končar, Igor, Milašinović, Dejan, Stanković, Goran, Alavantić, Dragan, Živković, Maja, "The HACD4 haplotype as a risk factor for atherosclerosis in males" in Gene, 641 (2018):35-40,
https://doi.org/10.1016/j.gene.2017.10.030 . .

TY  - CONF
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Stanković, Goran
AU  - Milašinović, Dejan
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nataša
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018309699
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7953
AB  - Aim: Myocardial infarction (MI) incidence is still a major burden in the
terms of premature death and disability world-wide. Genetic studies up to
date explained a limited portion of disease inheritance. Recently, the DT
haplotype of variants rs36212560 I/D (insertion/deletion) and 2275888 T/C
in HACD gene (9p21.3) have been significantly associated with the risk of
carotid plaque occurrence among males.
Methods: We aimed to validate these results by investigating 518 MI patients (366 males) and 303 (167 males) healthy controls from Serbia. Also, he HACD4 gene expression analysis has been conducted in the peripheral
blood mononuclear cells of 72 MI patients, 6 months after the MI. Results
were obtained using ABI-Prism 7500 RT-PCR for rs2275888 allelic
discrimination and HACD4 mRNA relative quantitation. PCR and acrylamide gel electrophoresis were used to distinguish 5 base pairs
rs36212560 insertion deletion polymorphisms.
Results: Haplotype analysis (using Thesias software) showed that DT
haplotype carriers had significantly higher risk for MI (OR ¼ 1.42, CI 1.08-
1.85, p¼0.01) compared with most frequent IT haplotype. In gender
separated groups association remained significant only among males (OR
¼ 1.76, 1.266-2.46, p¼0.0008). Results were adjusted for MI traditional risk
factors (Age, BMI, HDLC, LDLC, Tg, hypertension and smoking). Investigated
genetic variants were not associated with HACD4 expression. Significant
correlation was found between HACD4 mRNA level and age (r¼0.36,
p¼0.001).
Conclusions: We have shown that rs36212560 and rs2275888 DT haplotype from HACD4 gene is significantly and independently associated with
the MI occurrence in males. Additional studies are needed to confirm these
results.
C3  - Atherosclerosis
T1  - HACD4 haplotype confers risk of myocardial infarction among males in the population of Serbia
VL  - 275
SP  - e210
EP  - e211
DO  - 10.1016/j.atherosclerosis.2018.06.657
ER  - 

@conference{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Stanković, Goran and Milašinović, Dejan and Dekleva, Milica and Marković-Nikolić, Nataša and Alavantić, Dragan and Živković, Maja",
year = "2018",
abstract = "Aim: Myocardial infarction (MI) incidence is still a major burden in the
terms of premature death and disability world-wide. Genetic studies up to
date explained a limited portion of disease inheritance. Recently, the DT
haplotype of variants rs36212560 I/D (insertion/deletion) and 2275888 T/C
in HACD gene (9p21.3) have been significantly associated with the risk of
carotid plaque occurrence among males.
Methods: We aimed to validate these results by investigating 518 MI patients (366 males) and 303 (167 males) healthy controls from Serbia. Also, he HACD4 gene expression analysis has been conducted in the peripheral
blood mononuclear cells of 72 MI patients, 6 months after the MI. Results
were obtained using ABI-Prism 7500 RT-PCR for rs2275888 allelic
discrimination and HACD4 mRNA relative quantitation. PCR and acrylamide gel electrophoresis were used to distinguish 5 base pairs
rs36212560 insertion deletion polymorphisms.
Results: Haplotype analysis (using Thesias software) showed that DT
haplotype carriers had significantly higher risk for MI (OR ¼ 1.42, CI 1.08-
1.85, p¼0.01) compared with most frequent IT haplotype. In gender
separated groups association remained significant only among males (OR
¼ 1.76, 1.266-2.46, p¼0.0008). Results were adjusted for MI traditional risk
factors (Age, BMI, HDLC, LDLC, Tg, hypertension and smoking). Investigated
genetic variants were not associated with HACD4 expression. Significant
correlation was found between HACD4 mRNA level and age (r¼0.36,
p¼0.001).
Conclusions: We have shown that rs36212560 and rs2275888 DT haplotype from HACD4 gene is significantly and independently associated with
the MI occurrence in males. Additional studies are needed to confirm these
results.",
journal = "Atherosclerosis",
title = "HACD4 haplotype confers risk of myocardial infarction among males in the population of Serbia",
volume = "275",
pages = "e210-e211",
doi = "10.1016/j.atherosclerosis.2018.06.657"
}

Životić, I., Đurić, T., Stanković, A., Stanković, G., Milašinović, D., Dekleva, M., Marković-Nikolić, N., Alavantić, D.,& Živković, M.. (2018). HACD4 haplotype confers risk of myocardial infarction among males in the population of Serbia. in Atherosclerosis, 275, e210-e211.
https://doi.org/10.1016/j.atherosclerosis.2018.06.657

Životić I, Đurić T, Stanković A, Stanković G, Milašinović D, Dekleva M, Marković-Nikolić N, Alavantić D, Živković M. HACD4 haplotype confers risk of myocardial infarction among males in the population of Serbia. in Atherosclerosis. 2018;275:e210-e211.
doi:10.1016/j.atherosclerosis.2018.06.657 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Stanković, Goran, Milašinović, Dejan, Dekleva, Milica, Marković-Nikolić, Nataša, Alavantić, Dragan, Živković, Maja, "HACD4 haplotype confers risk of myocardial infarction among males in the population of Serbia" in Atherosclerosis, 275 (2018):e210-e211,
https://doi.org/10.1016/j.atherosclerosis.2018.06.657 . .