TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
PY  - 2017
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/2207
AB  - Chronic obstructive pulmonary disease (COPD) is a complex disorder influenced by multiple genetic and environmental factors, as well as their interactions. Since elevated oxidative stress and protease activity characterize the pathogenesis of COPD, variants of genes that can affect these processes have been commonly studied in COPD. However, interactions among genes that can influence oxidative stress and protease activity remain poorly investigated in COPD. The aim of this study was to look into the role of functional variants in matrix metalloproteinases (MMPs) 1, 9, and 12 in the occurrence and/or modulation of COPD, and to analyze their interactions with glutathione S-transferases (GSTs) M1, T1, and P1 in the pathogenesis of COPD in Serbians. The MMP1 rs1799750 G > GG, MMP9 rs3918242 C > T, and MMP12 rs2276109 A > G variants were analyzed by direct detection methods. Gene-gene interactions between variants in MMPs and GSTs were assessed using a case-control model. Our results showed association of the MMP1 GG/GG genotype with COPD (p = 0.036, OR = 2.50). Gene-gene interactions between the GSTM1 null and MMP1 GG (p = 0.028, OR = 2.99) and the GSTM1 null and MMP12 AA variants (p = 0.015, OR = 3.82) were found to significantly increase the risk of COPD occurrence. Furthermore, the MMP12 G variant was found to modify the age of COPD onset (p = 0.025, OR = 3.30), while interaction between the GSTM1 null and MMP9 T variants was found to modify the severity of disease (p = 0.019, OR = 4.83). To our best knowledge, this is the first study revealing several gene-gene interactions affecting oxidative stress and protease activity in the pathogenesis of COPD.
PB  - Taylor & Francis Inc, Philadelphia
T2  - COPD - Journal of Chronic Obstructive Pulmonary Disease
T1  - Gene-Gene Interactions Between Glutathione S-Transferase M1 and Matrix Metalloproteinases 1, 9, and 12 in Chronic Obstructive Pulmonary Disease in Serbians
VL  - 14
IS  - 6
SP  - 581
EP  - 589
DO  - 10.1080/15412555.2017.1369022
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Nagorni-Obradović, Ljudmila and Petrović-Stanojević, Nataša and Radojković, Dragica",
year = "2017",
abstract = "Chronic obstructive pulmonary disease (COPD) is a complex disorder influenced by multiple genetic and environmental factors, as well as their interactions. Since elevated oxidative stress and protease activity characterize the pathogenesis of COPD, variants of genes that can affect these processes have been commonly studied in COPD. However, interactions among genes that can influence oxidative stress and protease activity remain poorly investigated in COPD. The aim of this study was to look into the role of functional variants in matrix metalloproteinases (MMPs) 1, 9, and 12 in the occurrence and/or modulation of COPD, and to analyze their interactions with glutathione S-transferases (GSTs) M1, T1, and P1 in the pathogenesis of COPD in Serbians. The MMP1 rs1799750 G > GG, MMP9 rs3918242 C > T, and MMP12 rs2276109 A > G variants were analyzed by direct detection methods. Gene-gene interactions between variants in MMPs and GSTs were assessed using a case-control model. Our results showed association of the MMP1 GG/GG genotype with COPD (p = 0.036, OR = 2.50). Gene-gene interactions between the GSTM1 null and MMP1 GG (p = 0.028, OR = 2.99) and the GSTM1 null and MMP12 AA variants (p = 0.015, OR = 3.82) were found to significantly increase the risk of COPD occurrence. Furthermore, the MMP12 G variant was found to modify the age of COPD onset (p = 0.025, OR = 3.30), while interaction between the GSTM1 null and MMP9 T variants was found to modify the severity of disease (p = 0.019, OR = 4.83). To our best knowledge, this is the first study revealing several gene-gene interactions affecting oxidative stress and protease activity in the pathogenesis of COPD.",
publisher = "Taylor & Francis Inc, Philadelphia",
journal = "COPD - Journal of Chronic Obstructive Pulmonary Disease",
title = "Gene-Gene Interactions Between Glutathione S-Transferase M1 and Matrix Metalloproteinases 1, 9, and 12 in Chronic Obstructive Pulmonary Disease in Serbians",
volume = "14",
number = "6",
pages = "581-589",
doi = "10.1080/15412555.2017.1369022"
}

Stanković, M., Nikolić, A., Nagorni-Obradović, L., Petrović-Stanojević, N.,& Radojković, D.. (2017). Gene-Gene Interactions Between Glutathione S-Transferase M1 and Matrix Metalloproteinases 1, 9, and 12 in Chronic Obstructive Pulmonary Disease in Serbians. in COPD - Journal of Chronic Obstructive Pulmonary Disease
Taylor & Francis Inc, Philadelphia., 14(6), 581-589.
https://doi.org/10.1080/15412555.2017.1369022

Stanković M, Nikolić A, Nagorni-Obradović L, Petrović-Stanojević N, Radojković D. Gene-Gene Interactions Between Glutathione S-Transferase M1 and Matrix Metalloproteinases 1, 9, and 12 in Chronic Obstructive Pulmonary Disease in Serbians. in COPD - Journal of Chronic Obstructive Pulmonary Disease. 2017;14(6):581-589.
doi:10.1080/15412555.2017.1369022 .

Stanković, Marija, Nikolić, Aleksandra, Nagorni-Obradović, Ljudmila, Petrović-Stanojević, Nataša, Radojković, Dragica, "Gene-Gene Interactions Between Glutathione S-Transferase M1 and Matrix Metalloproteinases 1, 9, and 12 in Chronic Obstructive Pulmonary Disease in Serbians" in COPD - Journal of Chronic Obstructive Pulmonary Disease, 14, no. 6 (2017):581-589,
https://doi.org/10.1080/15412555.2017.1369022 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Kojić, Snežana
AU  - Đorđević, Valentina
AU  - Tomović, Andrija
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Mitic-Milikić, Marija
AU  - Radojković, Dragica
PY  - 2016
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/2089
AB  - The aetiology of chronic obstructive pulmonary disease (COPD) is complex. While cigarette smoking is a well-established cause of COPD, a myriad of assessed genetic factors has given conflicting data. Since gene-environment interactions are thought to be implicated in aetiopathogenesis of COPD, we aimed to examine the matrix metalloproteinase (MMP) 9 C-1562T (rs3918242) functional variant and cigarette smoke in the pathogenesis of this disease. The distribution of the MMP9 C-1562T variant was analyzed in COPD patients and controls with normal pulmonary function from Serbia. Interaction between the C-1562T genetic variant and cigarette smoking was assessed using a case-control model. The response of the C-1562T promoter variant to cigarette smoke condensate (CSC) exposure was examined using a dual luciferase reporter assay. The frequency of T allele carriers was higher in the COPD group than in smoker controls (38.4% vs. 20%; OR=2.7, P=0.027). Interaction between the T allele and cigarette smoking was identified in COPD occurrence (OR=4.38, P=0.005) and severity (P=0.001). A functional analysis of the C-1562T variant demonstrated a dose-dependent and allele-specific response (P lt 0.01) to CSC. Significantly higher MMP9 promoter activity following CSC exposure was found for the promoter harboring the T allele compared to the promoter harboring the C allele (P lt 0.05). Our study is the first to reveal an interaction between the MMP9-1562T allele and cigarette smoke in COPD, emphasising gene-environment interactions as a possible cause of lung damage in the pathogenesis of COPD. Environ. Mol. Mutagen. 57:447-454, 2016.
PB  - Wiley, Hoboken
T2  - Environmental & Molecular Mutagenesis
T1  - Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease
VL  - 57
IS  - 6
SP  - 447
EP  - 454
DO  - 10.1002/em.22025
ER  - 

@article{
author = "Stanković, Marija and Kojić, Snežana and Đorđević, Valentina and Tomović, Andrija and Nagorni-Obradović, Ljudmila and Petrović-Stanojević, Nataša and Mitic-Milikić, Marija and Radojković, Dragica",
year = "2016",
abstract = "The aetiology of chronic obstructive pulmonary disease (COPD) is complex. While cigarette smoking is a well-established cause of COPD, a myriad of assessed genetic factors has given conflicting data. Since gene-environment interactions are thought to be implicated in aetiopathogenesis of COPD, we aimed to examine the matrix metalloproteinase (MMP) 9 C-1562T (rs3918242) functional variant and cigarette smoke in the pathogenesis of this disease. The distribution of the MMP9 C-1562T variant was analyzed in COPD patients and controls with normal pulmonary function from Serbia. Interaction between the C-1562T genetic variant and cigarette smoking was assessed using a case-control model. The response of the C-1562T promoter variant to cigarette smoke condensate (CSC) exposure was examined using a dual luciferase reporter assay. The frequency of T allele carriers was higher in the COPD group than in smoker controls (38.4% vs. 20%; OR=2.7, P=0.027). Interaction between the T allele and cigarette smoking was identified in COPD occurrence (OR=4.38, P=0.005) and severity (P=0.001). A functional analysis of the C-1562T variant demonstrated a dose-dependent and allele-specific response (P lt 0.01) to CSC. Significantly higher MMP9 promoter activity following CSC exposure was found for the promoter harboring the T allele compared to the promoter harboring the C allele (P lt 0.05). Our study is the first to reveal an interaction between the MMP9-1562T allele and cigarette smoke in COPD, emphasising gene-environment interactions as a possible cause of lung damage in the pathogenesis of COPD. Environ. Mol. Mutagen. 57:447-454, 2016.",
publisher = "Wiley, Hoboken",
journal = "Environmental & Molecular Mutagenesis",
title = "Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease",
volume = "57",
number = "6",
pages = "447-454",
doi = "10.1002/em.22025"
}

Stanković, M., Kojić, S., Đorđević, V., Tomović, A., Nagorni-Obradović, L., Petrović-Stanojević, N., Mitic-Milikić, M.,& Radojković, D.. (2016). Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease. in Environmental & Molecular Mutagenesis
Wiley, Hoboken., 57(6), 447-454.
https://doi.org/10.1002/em.22025

Stanković M, Kojić S, Đorđević V, Tomović A, Nagorni-Obradović L, Petrović-Stanojević N, Mitic-Milikić M, Radojković D. Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease. in Environmental & Molecular Mutagenesis. 2016;57(6):447-454.
doi:10.1002/em.22025 .

Stanković, Marija, Kojić, Snežana, Đorđević, Valentina, Tomović, Andrija, Nagorni-Obradović, Ljudmila, Petrović-Stanojević, Nataša, Mitic-Milikić, Marija, Radojković, Dragica, "Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease" in Environmental & Molecular Mutagenesis, 57, no. 6 (2016):447-454,
https://doi.org/10.1002/em.22025 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Tomović, Andrija
AU  - Mitic-Milikić, Marija
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
PY  - 2015
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1960
AB  - Background: Chronic obstructive pulmonary disease (COPD) is a complex disorder characterized by increased oxidative stress. Functional genetic variants of phase I and II genes are implicated in oxidants antioxidants imbalance and may be involved in COPD development. In this study, we aimed to investigate the role of cytochrome P450 (CYP), glutathione S-transferase (GST) and microsomal epoxide hydrolase (mEH) functional variants in the pathogenesis of COPD in a Serbian population. Methods: The genotypes of 122 COPD patients and 100 controls with normal lung function were determined for CYP1A1 *1A/*2A, CYP2E1 *1A/*5B, GSTM1 null, GSTT1 null GSTP1 11e105Val, mEH Tyr113His and mEH His139Arg gene variants. Results: Results obtained showed that GSTM1 null variant was significantly more represented in COPD patients than in controls (61.5% vs. 47.0%; OR=1.80; p=0.042). Also, a significant difference was observed for combinations of GSTM1 null and GSTP1 105Val/(Val) (38.5% vs. 24.0%; OR=1.98; p=0.029), as well as for CYP1A1 *1A/*2A, GSTM1 null and mEH 113His/(His) genotypes (7.4% vs. 1.0%; OR=7.88; p=0.025). Conclusions: These are the first data concerning the analysis of the variants of phase I and II genes in the pathogenesis of COPD in a Serbian population. Results obtained in this study open up the possibility for thorough analyses of the role of genetic factors in COPD on larger cohorts. Also, they implicate the importance of previously described genetic associations with COPD in our population, as well as reveal a new one, not reported so far.
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - Association of functional variants of phase i and ii genes with chronic obstructive pulmonary disease in a Serbian population
VL  - 34
IS  - 2
SP  - 207
EP  - 214
DO  - 10.2478/jomb-2014-0024
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Tomović, Andrija and Mitic-Milikić, Marija and Nagorni-Obradović, Ljudmila and Petrović-Stanojević, Nataša and Radojković, Dragica",
year = "2015",
abstract = "Background: Chronic obstructive pulmonary disease (COPD) is a complex disorder characterized by increased oxidative stress. Functional genetic variants of phase I and II genes are implicated in oxidants antioxidants imbalance and may be involved in COPD development. In this study, we aimed to investigate the role of cytochrome P450 (CYP), glutathione S-transferase (GST) and microsomal epoxide hydrolase (mEH) functional variants in the pathogenesis of COPD in a Serbian population. Methods: The genotypes of 122 COPD patients and 100 controls with normal lung function were determined for CYP1A1 *1A/*2A, CYP2E1 *1A/*5B, GSTM1 null, GSTT1 null GSTP1 11e105Val, mEH Tyr113His and mEH His139Arg gene variants. Results: Results obtained showed that GSTM1 null variant was significantly more represented in COPD patients than in controls (61.5% vs. 47.0%; OR=1.80; p=0.042). Also, a significant difference was observed for combinations of GSTM1 null and GSTP1 105Val/(Val) (38.5% vs. 24.0%; OR=1.98; p=0.029), as well as for CYP1A1 *1A/*2A, GSTM1 null and mEH 113His/(His) genotypes (7.4% vs. 1.0%; OR=7.88; p=0.025). Conclusions: These are the first data concerning the analysis of the variants of phase I and II genes in the pathogenesis of COPD in a Serbian population. Results obtained in this study open up the possibility for thorough analyses of the role of genetic factors in COPD on larger cohorts. Also, they implicate the importance of previously described genetic associations with COPD in our population, as well as reveal a new one, not reported so far.",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Association of functional variants of phase i and ii genes with chronic obstructive pulmonary disease in a Serbian population",
volume = "34",
number = "2",
pages = "207-214",
doi = "10.2478/jomb-2014-0024"
}

Stanković, M., Nikolić, A., Tomović, A., Mitic-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, N.,& Radojković, D.. (2015). Association of functional variants of phase i and ii genes with chronic obstructive pulmonary disease in a Serbian population. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 34(2), 207-214.
https://doi.org/10.2478/jomb-2014-0024

Stanković M, Nikolić A, Tomović A, Mitic-Milikić M, Nagorni-Obradović L, Petrović-Stanojević N, Radojković D. Association of functional variants of phase i and ii genes with chronic obstructive pulmonary disease in a Serbian population. in Journal of Medical Biochemistry. 2015;34(2):207-214.
doi:10.2478/jomb-2014-0024 .

Stanković, Marija, Nikolić, Aleksandra, Tomović, Andrija, Mitic-Milikić, Marija, Nagorni-Obradović, Ljudmila, Petrović-Stanojević, Nataša, Radojković, Dragica, "Association of functional variants of phase i and ii genes with chronic obstructive pulmonary disease in a Serbian population" in Journal of Medical Biochemistry, 34, no. 2 (2015):207-214,
https://doi.org/10.2478/jomb-2014-0024 . .

TY  - JOUR
AU  - Petrović-Stanojević, Nataša
AU  - Topić, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Stanković, Marija
AU  - Dopuđa-Pantić, Vesna
AU  - Milenković, Branislava
AU  - Radojković, Dragica
PY  - 2014
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1887
AB  - Background and Objectives Polymorphisms of beta2-adrenergic receptor gene (ADRB2) are clinically relevant for several reasons, including as a risk factor for asthma development/severity and predicting the effectiveness of treatment with beta2-agonists in reducing asthma symptoms. The aim of this study was to examine the association between ADRB2 gene polymorphisms and asthma in the Serbian population, and to evaluate the therapeutic response in relation to the ADRB2 genotype. Methods The study included 171 patients with asthma and 101 healthy subjects as the control group. Genotyping of Arg16Gly and Gln27Glu polymorphisms was performed by direct sequencing of polymerase chain reaction (PCR) products. Results In Serbian adults, carriers of the 27Gln allele and 27Gln/Gln genotype were at higher risk of asthma [odds ratio (OR) 2.5, 95 % confidence interval (CI) 1.6-3.8, and OR 3.00, 95 % CI 1.7-5.3, respectively], while the presence of the 27Glu allele and 27Gln/Glu genotype were found to be protective of asthma (OR 0.4, 95 % CI 0.3-0.6, and OR 0.3, 95 % CI 0.1-0.7, respectively). Furthermore, we found that the presence of the 27Gln allele in asthmatics younger than 50 years leads to a better response to therapy with long-acting beta2-agonists (LABA) in combination with prevailing low and moderate doses of inhaled corticosteroids (ICS), while carriers of the 27Glu allele over 50 years old are more likely to respond to LABA + ICS therapy. Conclusion We identified that in Serbian adults the 27Gln allele and 27Gln homozygosity are risk factors for asthma, which may be of clinical interest in disease prevention. The finding that younger carriers of the 27Gln allele respond better to LABA + ICS therapy may be utilized in personalized asthma treatment.
PB  - Adis Int Ltd, Northcote
T2  - Molecular Diagnosis & Therapy
T1  - Polymorphisms of Beta2-Adrenergic Receptor Gene in Serbian Asthmatic Adults: Effects on Response to Beta-Agonists
VL  - 18
IS  - 6
SP  - 639
EP  - 646
DO  - 10.1007/s40291-014-0116-1
ER  - 

@article{
author = "Petrović-Stanojević, Nataša and Topić, Aleksandra and Nikolić, Aleksandra and Stanković, Marija and Dopuđa-Pantić, Vesna and Milenković, Branislava and Radojković, Dragica",
year = "2014",
abstract = "Background and Objectives Polymorphisms of beta2-adrenergic receptor gene (ADRB2) are clinically relevant for several reasons, including as a risk factor for asthma development/severity and predicting the effectiveness of treatment with beta2-agonists in reducing asthma symptoms. The aim of this study was to examine the association between ADRB2 gene polymorphisms and asthma in the Serbian population, and to evaluate the therapeutic response in relation to the ADRB2 genotype. Methods The study included 171 patients with asthma and 101 healthy subjects as the control group. Genotyping of Arg16Gly and Gln27Glu polymorphisms was performed by direct sequencing of polymerase chain reaction (PCR) products. Results In Serbian adults, carriers of the 27Gln allele and 27Gln/Gln genotype were at higher risk of asthma [odds ratio (OR) 2.5, 95 % confidence interval (CI) 1.6-3.8, and OR 3.00, 95 % CI 1.7-5.3, respectively], while the presence of the 27Glu allele and 27Gln/Glu genotype were found to be protective of asthma (OR 0.4, 95 % CI 0.3-0.6, and OR 0.3, 95 % CI 0.1-0.7, respectively). Furthermore, we found that the presence of the 27Gln allele in asthmatics younger than 50 years leads to a better response to therapy with long-acting beta2-agonists (LABA) in combination with prevailing low and moderate doses of inhaled corticosteroids (ICS), while carriers of the 27Glu allele over 50 years old are more likely to respond to LABA + ICS therapy. Conclusion We identified that in Serbian adults the 27Gln allele and 27Gln homozygosity are risk factors for asthma, which may be of clinical interest in disease prevention. The finding that younger carriers of the 27Gln allele respond better to LABA + ICS therapy may be utilized in personalized asthma treatment.",
publisher = "Adis Int Ltd, Northcote",
journal = "Molecular Diagnosis & Therapy",
title = "Polymorphisms of Beta2-Adrenergic Receptor Gene in Serbian Asthmatic Adults: Effects on Response to Beta-Agonists",
volume = "18",
number = "6",
pages = "639-646",
doi = "10.1007/s40291-014-0116-1"
}

Petrović-Stanojević, N., Topić, A., Nikolić, A., Stanković, M., Dopuđa-Pantić, V., Milenković, B.,& Radojković, D.. (2014). Polymorphisms of Beta2-Adrenergic Receptor Gene in Serbian Asthmatic Adults: Effects on Response to Beta-Agonists. in Molecular Diagnosis & Therapy
Adis Int Ltd, Northcote., 18(6), 639-646.
https://doi.org/10.1007/s40291-014-0116-1

Petrović-Stanojević N, Topić A, Nikolić A, Stanković M, Dopuđa-Pantić V, Milenković B, Radojković D. Polymorphisms of Beta2-Adrenergic Receptor Gene in Serbian Asthmatic Adults: Effects on Response to Beta-Agonists. in Molecular Diagnosis & Therapy. 2014;18(6):639-646.
doi:10.1007/s40291-014-0116-1 .

Petrović-Stanojević, Nataša, Topić, Aleksandra, Nikolić, Aleksandra, Stanković, Marija, Dopuđa-Pantić, Vesna, Milenković, Branislava, Radojković, Dragica, "Polymorphisms of Beta2-Adrenergic Receptor Gene in Serbian Asthmatic Adults: Effects on Response to Beta-Agonists" in Molecular Diagnosis & Therapy, 18, no. 6 (2014):639-646,
https://doi.org/10.1007/s40291-014-0116-1 . .

TY  - JOUR
AU  - Miletić, Aleksandra
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
AU  - Nikolić, Aleksandra
PY  - 2014
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1878
AB  - Considering the importance of the TGF-beta signaling pathway for normal lung function and especially its roles in inflammation and tissue remodeling, key features of asthma pathology, it can be assumed that these molecules may harbor mutations in asthmatics. The aim of this study was to analyze the SMAD4 gene in patients with asthma. Analysis has encompassed exons 10, 11, 12 and 13 encoding the carboxy-terminal (MH2) domain of the SMAD4 protein, where mutations most frequently occur. The study included 50 patients (20 men and 30 women) with asthma aged between 17 and 73 years (average age 45.2 +/- 15.6 years). Polymerase chain reaction (PCR) was used to amplify exons 10, 11, 12 and 13 of the SMAD4 gene and the obtained PCR products were subjected to direct DNA sequencing. No nucleotide changes were found in any of the analyzed exons in either of the subjects. Based on the results of this study, it seems that mutations in the carboxy-terminal (MH2) domain of the SMAD4 are not present in asthmatic patients. Future research should be directed at the analysis of the complete gene, including regulatory elements, in order to resolve the exact role of SMAD4 in asthma.
PB  - Sciendo, Warsaw
T2  - Central European Journal of Medicine
T1  - Analysis of the SMAD4 gene in asthma
VL  - 9
IS  - 6
SP  - 811
EP  - 813
DO  - 10.2478/s11536-013-0316-9
ER  - 

@article{
author = "Miletić, Aleksandra and Petrović-Stanojević, Nataša and Radojković, Dragica and Nikolić, Aleksandra",
year = "2014",
abstract = "Considering the importance of the TGF-beta signaling pathway for normal lung function and especially its roles in inflammation and tissue remodeling, key features of asthma pathology, it can be assumed that these molecules may harbor mutations in asthmatics. The aim of this study was to analyze the SMAD4 gene in patients with asthma. Analysis has encompassed exons 10, 11, 12 and 13 encoding the carboxy-terminal (MH2) domain of the SMAD4 protein, where mutations most frequently occur. The study included 50 patients (20 men and 30 women) with asthma aged between 17 and 73 years (average age 45.2 +/- 15.6 years). Polymerase chain reaction (PCR) was used to amplify exons 10, 11, 12 and 13 of the SMAD4 gene and the obtained PCR products were subjected to direct DNA sequencing. No nucleotide changes were found in any of the analyzed exons in either of the subjects. Based on the results of this study, it seems that mutations in the carboxy-terminal (MH2) domain of the SMAD4 are not present in asthmatic patients. Future research should be directed at the analysis of the complete gene, including regulatory elements, in order to resolve the exact role of SMAD4 in asthma.",
publisher = "Sciendo, Warsaw",
journal = "Central European Journal of Medicine",
title = "Analysis of the SMAD4 gene in asthma",
volume = "9",
number = "6",
pages = "811-813",
doi = "10.2478/s11536-013-0316-9"
}

Miletić, A., Petrović-Stanojević, N., Radojković, D.,& Nikolić, A.. (2014). Analysis of the SMAD4 gene in asthma. in Central European Journal of Medicine
Sciendo, Warsaw., 9(6), 811-813.
https://doi.org/10.2478/s11536-013-0316-9

Miletić A, Petrović-Stanojević N, Radojković D, Nikolić A. Analysis of the SMAD4 gene in asthma. in Central European Journal of Medicine. 2014;9(6):811-813.
doi:10.2478/s11536-013-0316-9 .

Miletić, Aleksandra, Petrović-Stanojević, Nataša, Radojković, Dragica, Nikolić, Aleksandra, "Analysis of the SMAD4 gene in asthma" in Central European Journal of Medicine, 9, no. 6 (2014):811-813,
https://doi.org/10.2478/s11536-013-0316-9 . .

TY  - JOUR
AU  - Topić, Aleksandra
AU  - Stanković, Marija
AU  - Divac-Rankov, Aleksandra
AU  - Petrović-Stanojević, Nataša
AU  - Mitic-Milikić, Marija
AU  - Nagorni-Obradović, Ljudmila
AU  - Radojković, Dragica
PY  - 2012
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1758
AB  - Aim: Alpha-1-antitrypsin (A1AT) is the main inhibitor of neutrophil elastase, and severe alpha-1-antitrypsin deficiency (A1ATD) is a genetic risk factor for early-onset emphysema. Despite the relatively high prevalence of A1ATD, this condition is frequently underdiagnosed. Our aim was to determine the distribution of the A1ATD phenotypes/alleles in patients with lung diseases as well as in the Serbian population. Methods: The study included the adults with chronic obstructive pulmonary disease (COPD) (n = 348), asthma (n = 71), and bronchiectasis (n = 35); the control was 1435 healthy blood donors. The A1ATD variants were identified by isoelectric focusing or polymerase chain reaction-mediated site-directed mutagenesis. Results: PiMZ heterozygotes, PiZZ homozygotes, and Z allele carriers are associated with significantly higher risk of developing COPD than healthy individuals (odds ratios 3.43, 42.42, and 5.49 respectively). The calculated prevalence of PiZZ, PiMZ, and PiSZ was higher in patients with COPD (1:202, 1:8, and 1:1243) than in the Serbian population (1: 5519, 1: 38, and 1:5519). Conclusion: The high prevalence of A1ATD phenotypes/allele in our population has confirmed the necessity of screening for A1ATD in patients with COPD. On the other hand, on the basis of the estimated number of those with A1ATD among the COPD patients, it is possible to assess the diagnostic efficiency of A1ATD in the Serbian population.
PB  - Mary Ann Liebert, Inc, New Rochelle
T2  - Genetic Testing & Molecular Biomarkers
T1  - Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases
VL  - 16
IS  - 11
SP  - 1282
EP  - 1286
DO  - 10.1089/gtmb.2012.0152
ER  - 

@article{
author = "Topić, Aleksandra and Stanković, Marija and Divac-Rankov, Aleksandra and Petrović-Stanojević, Nataša and Mitic-Milikić, Marija and Nagorni-Obradović, Ljudmila and Radojković, Dragica",
year = "2012",
abstract = "Aim: Alpha-1-antitrypsin (A1AT) is the main inhibitor of neutrophil elastase, and severe alpha-1-antitrypsin deficiency (A1ATD) is a genetic risk factor for early-onset emphysema. Despite the relatively high prevalence of A1ATD, this condition is frequently underdiagnosed. Our aim was to determine the distribution of the A1ATD phenotypes/alleles in patients with lung diseases as well as in the Serbian population. Methods: The study included the adults with chronic obstructive pulmonary disease (COPD) (n = 348), asthma (n = 71), and bronchiectasis (n = 35); the control was 1435 healthy blood donors. The A1ATD variants were identified by isoelectric focusing or polymerase chain reaction-mediated site-directed mutagenesis. Results: PiMZ heterozygotes, PiZZ homozygotes, and Z allele carriers are associated with significantly higher risk of developing COPD than healthy individuals (odds ratios 3.43, 42.42, and 5.49 respectively). The calculated prevalence of PiZZ, PiMZ, and PiSZ was higher in patients with COPD (1:202, 1:8, and 1:1243) than in the Serbian population (1: 5519, 1: 38, and 1:5519). Conclusion: The high prevalence of A1ATD phenotypes/allele in our population has confirmed the necessity of screening for A1ATD in patients with COPD. On the other hand, on the basis of the estimated number of those with A1ATD among the COPD patients, it is possible to assess the diagnostic efficiency of A1ATD in the Serbian population.",
publisher = "Mary Ann Liebert, Inc, New Rochelle",
journal = "Genetic Testing & Molecular Biomarkers",
title = "Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases",
volume = "16",
number = "11",
pages = "1282-1286",
doi = "10.1089/gtmb.2012.0152"
}

Topić, A., Stanković, M., Divac-Rankov, A., Petrović-Stanojević, N., Mitic-Milikić, M., Nagorni-Obradović, L.,& Radojković, D.. (2012). Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases. in Genetic Testing & Molecular Biomarkers
Mary Ann Liebert, Inc, New Rochelle., 16(11), 1282-1286.
https://doi.org/10.1089/gtmb.2012.0152

Topić A, Stanković M, Divac-Rankov A, Petrović-Stanojević N, Mitic-Milikić M, Nagorni-Obradović L, Radojković D. Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases. in Genetic Testing & Molecular Biomarkers. 2012;16(11):1282-1286.
doi:10.1089/gtmb.2012.0152 .

Topić, Aleksandra, Stanković, Marija, Divac-Rankov, Aleksandra, Petrović-Stanojević, Nataša, Mitic-Milikić, Marija, Nagorni-Obradović, Ljudmila, Radojković, Dragica, "Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases" in Genetic Testing & Molecular Biomarkers, 16, no. 11 (2012):1282-1286,
https://doi.org/10.1089/gtmb.2012.0152 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Divac, Aleksandra
AU  - Tomović, Andrija
AU  - Petrović-Stanojević, Nataša
AU  - Anđelić-Jelić, Marina
AU  - Dopuđa-Pantić, Vesna
AU  - Surlan, Mirjana
AU  - Vujicić, Ivan
AU  - Ponomarev, Dimitrije
AU  - Mitic-Milikić, Marija
AU  - Kusić, Jelena
AU  - Radojković, Dragica
PY  - 2008
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1452
AB  - Chronic obstructive pulmonary disease (COPD) is a complex disease influenced by genetic and environmental factors. Cystic fibrosis transmembrane conductance regulator (CFTR) protein is an important component of the lung tissue homeostasis, involved in the regulation of the rate of mucociliary clearance. As it is known that certain CFTR variants have consequences on the function of CFTR protein, the aim of this study was to examine the possible role of F508del, M470V, Tn locus, and R75Q variants in COPD development and modulation. Total number of 86 COPD patients and 102 control subjects were included in the study. Possible association between COPD susceptibility, severity, and onset of the disease and allele or genotype of four analyzed CFTR variants was examined. No associations were detected between COPD development, onset of the disease and tested CFTR alleles and genotypes. However, VV470 genotype was associated with mild/moderate COPD stages in comparison to severe/very severe ones (OR = 0.29, 95% CI = 0.11-0.80, p = 0.016). Our study showed that patients with VV470 genotype had a 3.4-fold decreased risk for the appearance of severe/very severe COPD symptoms, and the obtained results indicate that this genotype may have a protective role. These results also suggest the importance of studying CFTR gene as a modifier of this disease.
PB  - Mary Ann Liebert, Inc, New Rochelle
T2  - Genetic Testing
T1  - The CFTR M470V gene variant as a potential modifier of COPD severity: Study of Serbian population
VL  - 12
IS  - 3
SP  - 357
EP  - 362
DO  - 10.1089/gte.2007.0069
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Divac, Aleksandra and Tomović, Andrija and Petrović-Stanojević, Nataša and Anđelić-Jelić, Marina and Dopuđa-Pantić, Vesna and Surlan, Mirjana and Vujicić, Ivan and Ponomarev, Dimitrije and Mitic-Milikić, Marija and Kusić, Jelena and Radojković, Dragica",
year = "2008",
abstract = "Chronic obstructive pulmonary disease (COPD) is a complex disease influenced by genetic and environmental factors. Cystic fibrosis transmembrane conductance regulator (CFTR) protein is an important component of the lung tissue homeostasis, involved in the regulation of the rate of mucociliary clearance. As it is known that certain CFTR variants have consequences on the function of CFTR protein, the aim of this study was to examine the possible role of F508del, M470V, Tn locus, and R75Q variants in COPD development and modulation. Total number of 86 COPD patients and 102 control subjects were included in the study. Possible association between COPD susceptibility, severity, and onset of the disease and allele or genotype of four analyzed CFTR variants was examined. No associations were detected between COPD development, onset of the disease and tested CFTR alleles and genotypes. However, VV470 genotype was associated with mild/moderate COPD stages in comparison to severe/very severe ones (OR = 0.29, 95% CI = 0.11-0.80, p = 0.016). Our study showed that patients with VV470 genotype had a 3.4-fold decreased risk for the appearance of severe/very severe COPD symptoms, and the obtained results indicate that this genotype may have a protective role. These results also suggest the importance of studying CFTR gene as a modifier of this disease.",
publisher = "Mary Ann Liebert, Inc, New Rochelle",
journal = "Genetic Testing",
title = "The CFTR M470V gene variant as a potential modifier of COPD severity: Study of Serbian population",
volume = "12",
number = "3",
pages = "357-362",
doi = "10.1089/gte.2007.0069"
}

Stanković, M., Nikolić, A., Divac, A., Tomović, A., Petrović-Stanojević, N., Anđelić-Jelić, M., Dopuđa-Pantić, V., Surlan, M., Vujicić, I., Ponomarev, D., Mitic-Milikić, M., Kusić, J.,& Radojković, D.. (2008). The CFTR M470V gene variant as a potential modifier of COPD severity: Study of Serbian population. in Genetic Testing
Mary Ann Liebert, Inc, New Rochelle., 12(3), 357-362.
https://doi.org/10.1089/gte.2007.0069

Stanković M, Nikolić A, Divac A, Tomović A, Petrović-Stanojević N, Anđelić-Jelić M, Dopuđa-Pantić V, Surlan M, Vujicić I, Ponomarev D, Mitic-Milikić M, Kusić J, Radojković D. The CFTR M470V gene variant as a potential modifier of COPD severity: Study of Serbian population. in Genetic Testing. 2008;12(3):357-362.
doi:10.1089/gte.2007.0069 .

Stanković, Marija, Nikolić, Aleksandra, Divac, Aleksandra, Tomović, Andrija, Petrović-Stanojević, Nataša, Anđelić-Jelić, Marina, Dopuđa-Pantić, Vesna, Surlan, Mirjana, Vujicić, Ivan, Ponomarev, Dimitrije, Mitic-Milikić, Marija, Kusić, Jelena, Radojković, Dragica, "The CFTR M470V gene variant as a potential modifier of COPD severity: Study of Serbian population" in Genetic Testing, 12, no. 3 (2008):357-362,
https://doi.org/10.1089/gte.2007.0069 . .

TY  - CONF
AU  - Nikolić, A.
AU  - Nisević, I
AU  - Dinić, J.
AU  - Lukić, S.
AU  - Anđelić-Jelić, Marina
AU  - Petrović-Stanojević, Nataša
AU  - Đorđević, V
AU  - Rakićević, Ljiljana
AU  - Ugljesić, M.
AU  - Radojković, Dragica
PY  - 2007
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1333
PB  - Oxford Univ Press, Oxford
C3  - Annals of Oncology
T1  - Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer
VL  - 18
SP  - VII64
EP  - VII65
UR  - https://hdl.handle.net/21.15107/rcub_smile_1333
ER  - 

@conference{
author = "Nikolić, A. and Nisević, I and Dinić, J. and Lukić, S. and Anđelić-Jelić, Marina and Petrović-Stanojević, Nataša and Đorđević, V and Rakićević, Ljiljana and Ugljesić, M. and Radojković, Dragica",
year = "2007",
publisher = "Oxford Univ Press, Oxford",
journal = "Annals of Oncology",
title = "Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer",
volume = "18",
pages = "VII64-VII65",
url = "https://hdl.handle.net/21.15107/rcub_smile_1333"
}

Nikolić, A., Nisević, I., Dinić, J., Lukić, S., Anđelić-Jelić, M., Petrović-Stanojević, N., Đorđević, V., Rakićević, L., Ugljesić, M.,& Radojković, D.. (2007). Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer. in Annals of Oncology
Oxford Univ Press, Oxford., 18, VII64-VII65.
https://hdl.handle.net/21.15107/rcub_smile_1333

Nikolić A, Nisević I, Dinić J, Lukić S, Anđelić-Jelić M, Petrović-Stanojević N, Đorđević V, Rakićević L, Ugljesić M, Radojković D. Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer. in Annals of Oncology. 2007;18:VII64-VII65.
https://hdl.handle.net/21.15107/rcub_smile_1333 .

Nikolić, A., Nisević, I, Dinić, J., Lukić, S., Anđelić-Jelić, Marina, Petrović-Stanojević, Nataša, Đorđević, V, Rakićević, Ljiljana, Ugljesić, M., Radojković, Dragica, "Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer" in Annals of Oncology, 18 (2007):VII64-VII65,
https://hdl.handle.net/21.15107/rcub_smile_1333 .