TY  - JOUR
AU  - Stanković, Marija
AU  - Đorđević, Valentina
AU  - Tomović, Valentina
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Kovač, Mirjana
AU  - Radojković, Dragica
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1654
AB  - Background: Chronic  obstructive  pulmonary  disease(COPD) is a complex disorder with unexplained heritability.Interactions  of  genetic  and  environmental  factors  arethought  to  be  crucial  in  COPD.  So,  we  aim  to  examineinteractions of the endothelial nitric oxide synthase (eNOS)and angiotensin converting enzyme (ACE) genes and ciga-rette smoking in COPD. Methods:The  eNOS  G894T  and  ACE  ID  variants  wereanalyzed  in  122  COPD  patients  and  200  controls  fromSerbia. The effect of the variants on COPD was assessed bylogistic  regression.  Interactions  between  eNOS,  ACE  andcigarette  smoking  in  COPD  were  evaluated  using  a  case-control model. Interaction between the genes was analyzedin silico. Results:No effect of the eNOS G894T and ACE ID variantson  COPD  was  found  in  our  study.  Gene-gene  interactionbetween  the  eNOS  TT  and  ACE  D  was  identified(p=0.033) in COPD. The interaction is realized within the complex network of biochemical pathways. Gene-environ-ment  interactions  between  the  eNOS  T  and  cigarettesmoking (p=0.013), and the ACE II and cigarette smoking(p=0.009) were detected in COPD in our study. Conclusions:This is the first research to reveal interactionsof  the  eNOS  and  ACE  genes  and  cigarette  smoking  inCOPD progressing our understanding of COPD heritabilityand contributing to the development of appropriate treat-ments.
AB  - Uvod: Hronična opstruktivna bolest pluća (HOBP) je složeno oboljenje sa nerazjašnjenom genetičkom osnovom.Smatra se da su interakcije genetskih i spoljašnjih faktora ključne u HOBP. Stoga je naš cilj bio da ispitamo interakcijegena za endotelijalnu azot-monoksid sintazu (eNOS) i angiotenzin konvertujući enzim (ACE) i duvanskog dima uHOBP. Metode :eNOS G894T i ACE ID varijante su analiziranekod 122 HOBP pacijenta i 200 kontrola iz Srbije. Uticajvarijanti na HOBP je ispitan logističkom regresijom. Interakcije izme|u eNOS, ACE i duvanskog dima u HOBP suispitane korišćenjem modela slučaj-kontrola. Interakciaja između gena je analizirana in silico. Rezultati: Prema ovoj studiji eNOS G894T i ACE ID varijante nemaju uticaj na HOBP. Gen-gen interakcija između eNOS TT i ACE D je identifikovana (p=0,033) u HOBP.Ova interakcija se ostvaruje u okviru složene mreže bio-hemijskih puteva. Gen-sredina interakcije izme|u eNOS Ti duvanskog dima (p=0,013), i ACE II i duvanskog dima(p=0,009) su detektovane u HOBP u ovoj studiji.Zaključak: Ovo je prvo istraživanje u kome su otkriveneinterakcije između eNOS i ACE gena i duvanskog dima uHOBP što doprinosi našem razumevanju genetičke osnove HOBP i razvoju adekvatnog tretmana.
PB  - Belgrade : Society of Medical Biochemists of Serbia
T2  - Journal of Medical Biochemistry
T1  - Interactions of the eNOS and ACE genes and cigarette smoking in chronic obstructive pulmonary disease
T1  - Interakcije eNOS i ACE gena i duvanskog dima u hroničnoj opstruktivnoj bolesti pluća
EP  - 104
IS  - 1
SP  - 94
VL  - 41
DO  - 10.5937/jomb0-34017
ER  - 

@article{
author = "Stanković, Marija and Đorđević, Valentina and Tomović, Valentina and Nagorni-Obradović, Ljudmila and Petrović-Stanojević, Nataša and Kovač, Mirjana and Radojković, Dragica",
year = "2023",
abstract = "Background: Chronic  obstructive  pulmonary  disease(COPD) is a complex disorder with unexplained heritability.Interactions  of  genetic  and  environmental  factors  arethought  to  be  crucial  in  COPD.  So,  we  aim  to  examineinteractions of the endothelial nitric oxide synthase (eNOS)and angiotensin converting enzyme (ACE) genes and ciga-rette smoking in COPD. Methods:The  eNOS  G894T  and  ACE  ID  variants  wereanalyzed  in  122  COPD  patients  and  200  controls  fromSerbia. The effect of the variants on COPD was assessed bylogistic  regression.  Interactions  between  eNOS,  ACE  andcigarette  smoking  in  COPD  were  evaluated  using  a  case-control model. Interaction between the genes was analyzedin silico. Results:No effect of the eNOS G894T and ACE ID variantson  COPD  was  found  in  our  study.  Gene-gene  interactionbetween  the  eNOS  TT  and  ACE  D  was  identified(p=0.033) in COPD. The interaction is realized within the complex network of biochemical pathways. Gene-environ-ment  interactions  between  the  eNOS  T  and  cigarettesmoking (p=0.013), and the ACE II and cigarette smoking(p=0.009) were detected in COPD in our study. Conclusions:This is the first research to reveal interactionsof  the  eNOS  and  ACE  genes  and  cigarette  smoking  inCOPD progressing our understanding of COPD heritabilityand contributing to the development of appropriate treat-ments., Uvod: Hronična opstruktivna bolest pluća (HOBP) je složeno oboljenje sa nerazjašnjenom genetičkom osnovom.Smatra se da su interakcije genetskih i spoljašnjih faktora ključne u HOBP. Stoga je naš cilj bio da ispitamo interakcijegena za endotelijalnu azot-monoksid sintazu (eNOS) i angiotenzin konvertujući enzim (ACE) i duvanskog dima uHOBP. Metode :eNOS G894T i ACE ID varijante su analiziranekod 122 HOBP pacijenta i 200 kontrola iz Srbije. Uticajvarijanti na HOBP je ispitan logističkom regresijom. Interakcije izme|u eNOS, ACE i duvanskog dima u HOBP suispitane korišćenjem modela slučaj-kontrola. Interakciaja između gena je analizirana in silico. Rezultati: Prema ovoj studiji eNOS G894T i ACE ID varijante nemaju uticaj na HOBP. Gen-gen interakcija između eNOS TT i ACE D je identifikovana (p=0,033) u HOBP.Ova interakcija se ostvaruje u okviru složene mreže bio-hemijskih puteva. Gen-sredina interakcije izme|u eNOS Ti duvanskog dima (p=0,013), i ACE II i duvanskog dima(p=0,009) su detektovane u HOBP u ovoj studiji.Zaključak: Ovo je prvo istraživanje u kome su otkriveneinterakcije između eNOS i ACE gena i duvanskog dima uHOBP što doprinosi našem razumevanju genetičke osnove HOBP i razvoju adekvatnog tretmana.",
publisher = "Belgrade : Society of Medical Biochemists of Serbia",
journal = "Journal of Medical Biochemistry",
title = "Interactions of the eNOS and ACE genes and cigarette smoking in chronic obstructive pulmonary disease, Interakcije eNOS i ACE gena i duvanskog dima u hroničnoj opstruktivnoj bolesti pluća",
pages = "104-94",
number = "1",
volume = "41",
doi = "10.5937/jomb0-34017"
}

Stanković, M., Đorđević, V., Tomović, V., Nagorni-Obradović, L., Petrović-Stanojević, N., Kovač, M.,& Radojković, D.. (2023). Interactions of the eNOS and ACE genes and cigarette smoking in chronic obstructive pulmonary disease. in Journal of Medical Biochemistry
Belgrade : Society of Medical Biochemists of Serbia., 41(1), 94-104.
https://doi.org/10.5937/jomb0-34017

Stanković M, Đorđević V, Tomović V, Nagorni-Obradović L, Petrović-Stanojević N, Kovač M, Radojković D. Interactions of the eNOS and ACE genes and cigarette smoking in chronic obstructive pulmonary disease. in Journal of Medical Biochemistry. 2023;41(1):94-104.
doi:10.5937/jomb0-34017 .

Stanković, Marija, Đorđević, Valentina, Tomović, Valentina, Nagorni-Obradović, Ljudmila, Petrović-Stanojević, Nataša, Kovač, Mirjana, Radojković, Dragica, "Interactions of the eNOS and ACE genes and cigarette smoking in chronic obstructive pulmonary disease" in Journal of Medical Biochemistry, 41, no. 1 (2023):94-104,
https://doi.org/10.5937/jomb0-34017 . .

TY  - CONF
AU  - Dragičević, Sandra
AU  - Milosević, K.
AU  - Nestorović, B.
AU  - Petrović-Stanojević, Nataša
AU  - Nikolić, Aleksandra
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1121
PB  - Wiley, Hoboken
C3  - Allergy
T1  - Analysis of the TGFB1 gene promoter variants as risk factors and modulators of response to asthma therapy
EP  - 257
SP  - 257
VL  - 73
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1121
ER  - 

@conference{
author = "Dragičević, Sandra and Milosević, K. and Nestorović, B. and Petrović-Stanojević, Nataša and Nikolić, Aleksandra",
year = "2018",
publisher = "Wiley, Hoboken",
journal = "Allergy",
title = "Analysis of the TGFB1 gene promoter variants as risk factors and modulators of response to asthma therapy",
pages = "257-257",
volume = "73",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1121"
}

Dragičević, S., Milosević, K., Nestorović, B., Petrović-Stanojević, N.,& Nikolić, A.. (2018). Analysis of the TGFB1 gene promoter variants as risk factors and modulators of response to asthma therapy. in Allergy
Wiley, Hoboken., 73, 257-257.
https://hdl.handle.net/21.15107/rcub_imagine_1121

Dragičević S, Milosević K, Nestorović B, Petrović-Stanojević N, Nikolić A. Analysis of the TGFB1 gene promoter variants as risk factors and modulators of response to asthma therapy. in Allergy. 2018;73:257-257.
https://hdl.handle.net/21.15107/rcub_imagine_1121 .

Dragičević, Sandra, Milosević, K., Nestorović, B., Petrović-Stanojević, Nataša, Nikolić, Aleksandra, "Analysis of the TGFB1 gene promoter variants as risk factors and modulators of response to asthma therapy" in Allergy, 73 (2018):257-257,
https://hdl.handle.net/21.15107/rcub_imagine_1121 .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1032
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  gt  GG, MMP9 rs3918242 C  gt  T, and MMP12 rs2276109 A  gt  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
EP  - 589
IS  - 6
SP  - 581
VL  - 14
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  gt  GG, MMP9 rs3918242 C  gt  T, and MMP12 rs2276109 A  gt  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",
pages = "589-581",
number = "6",
volume = "14",
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  - Mitić-Milikić, Marija
AU  - Radojković, Dragica
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/901
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 and Molecular Mutagenesis
T1  - Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease
EP  - 454
IS  - 6
SP  - 447
VL  - 57
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 Mitić-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 and Molecular Mutagenesis",
title = "Gene-environment interaction between the MMP9 C-1562T promoter variant and cigarette smoke in the pathogenesis of chronic obstructive pulmonary disease",
pages = "454-447",
number = "6",
volume = "57",
doi = "10.1002/em.22025"
}

Stanković, M., Kojić, S., Đorđević, V., Tomović, A., Nagorni-Obradović, L., Petrović-Stanojević, N., Mitić-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 and 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, Mitić-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 and 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, Mitić-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 and Molecular Mutagenesis, 57, no. 6 (2016):447-454,
https://doi.org/10.1002/em.22025 . .

TY  - JOUR
AU  - Dragičević, Sandra
AU  - Petrović-Stanojević, Nataša
AU  - Nikolić, Aleksandra
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/948
AB  - Background. Asthma is a chronic respiratory disease caused by a combination of genetic and environmental factors. Transforming growth factor beta 1 (TGFB1) is a multifunctional cytokine that plays an important role in airway remodeling in asthma. Objectives. The aim of this study was to analyze common TGFB1 gene promoter polymorphisms C-509T and G-800A in Serbian asthmatics and to investigate their association with exacerbations. Material and Methods. The study involved 102 asthmatics and 58 healthy individuals from Serbia, age and gender matched. An analysis of the TGFB1 promoter was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results. For polymorphism C-509T a significant difference in the allele frequency was observed between the patients and the controls (p = 0.011), while the genotype distribution was similar in the analyzed groups, with statistical significance near the borderline (p = 0.061). For the polymorphism G-800A no difference was observed between the groups. The frequency of the -509TT genotype was higher in patients with exacerbations compared to patients without exacerbations (36.4% vs. 17.0%), with statistical significance near the borderline (p = 0.080). Conclusions. The results suggest that polymorphism C-509T may be associated with asthma and disease exacerbations, while G-800A is not significant for the etiology and clinical course of the disease. These findings should be confirmed in a larger study group, and since the TGFB1 promoter is highly complex and very responsive to environmental factors, future studies should also take other genetic and non-genetic factors into consideration.
PB  - Wroclaw Medical Univ, Wroclaw
T2  - Advances in Clinical and Experimental Medicine
T1  - TGFB1 Gene Promoter Polymorphisms in Serbian Asthmatics
EP  - 278
IS  - 2
SP  - 273
VL  - 25
DO  - 10.17219/acem/32211
ER  - 

@article{
author = "Dragičević, Sandra and Petrović-Stanojević, Nataša and Nikolić, Aleksandra",
year = "2016",
abstract = "Background. Asthma is a chronic respiratory disease caused by a combination of genetic and environmental factors. Transforming growth factor beta 1 (TGFB1) is a multifunctional cytokine that plays an important role in airway remodeling in asthma. Objectives. The aim of this study was to analyze common TGFB1 gene promoter polymorphisms C-509T and G-800A in Serbian asthmatics and to investigate their association with exacerbations. Material and Methods. The study involved 102 asthmatics and 58 healthy individuals from Serbia, age and gender matched. An analysis of the TGFB1 promoter was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results. For polymorphism C-509T a significant difference in the allele frequency was observed between the patients and the controls (p = 0.011), while the genotype distribution was similar in the analyzed groups, with statistical significance near the borderline (p = 0.061). For the polymorphism G-800A no difference was observed between the groups. The frequency of the -509TT genotype was higher in patients with exacerbations compared to patients without exacerbations (36.4% vs. 17.0%), with statistical significance near the borderline (p = 0.080). Conclusions. The results suggest that polymorphism C-509T may be associated with asthma and disease exacerbations, while G-800A is not significant for the etiology and clinical course of the disease. These findings should be confirmed in a larger study group, and since the TGFB1 promoter is highly complex and very responsive to environmental factors, future studies should also take other genetic and non-genetic factors into consideration.",
publisher = "Wroclaw Medical Univ, Wroclaw",
journal = "Advances in Clinical and Experimental Medicine",
title = "TGFB1 Gene Promoter Polymorphisms in Serbian Asthmatics",
pages = "278-273",
number = "2",
volume = "25",
doi = "10.17219/acem/32211"
}

Dragičević, S., Petrović-Stanojević, N.,& Nikolić, A.. (2016). TGFB1 Gene Promoter Polymorphisms in Serbian Asthmatics. in Advances in Clinical and Experimental Medicine
Wroclaw Medical Univ, Wroclaw., 25(2), 273-278.
https://doi.org/10.17219/acem/32211

Dragičević S, Petrović-Stanojević N, Nikolić A. TGFB1 Gene Promoter Polymorphisms in Serbian Asthmatics. in Advances in Clinical and Experimental Medicine. 2016;25(2):273-278.
doi:10.17219/acem/32211 .

Dragičević, Sandra, Petrović-Stanojević, Nataša, Nikolić, Aleksandra, "TGFB1 Gene Promoter Polymorphisms in Serbian Asthmatics" in Advances in Clinical and Experimental Medicine, 25, no. 2 (2016):273-278,
https://doi.org/10.17219/acem/32211 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Tomović, Andrija
AU  - Mitić-Milikić, Marija
AU  - Nagorni-Obradović, Ljudmila
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/849
AB  - Uvod: Hronična opstruktivna bolest pluća (HOBP) jeste složeno oboljenje koje karakteriše povišen oksidativni stres. Funkcionalne varijante gena faze I i II ksenobiotičkog metabolizma mogu uticati na ravnotežu oksidanti-antioksidanti i mogu dovesti do razvoja HOBP. Cilj ove studije je bio ispitivanje uloge funkcionalnih genskih varijanti u genima za citohrom P450 (CYP), glutation S-transferazu (GST) i mikrozomalnu epoksidnu hidrolazu (mEH) u patogenezi HOBP u srpskoj populaciji. Metode: U ovoj studiji analizirane su genske varijante CYP1A1 *1A/*2A, CYP2E1 *1A/*5B, GSTM1 null, GSTT1 null, GSTP1 Ile105Val, mEH Tyr113His i mEH His139Arg u grupi obolelih od HOBP koja je obuhvatala 122 ispitanika i kontrolnoj grupi koja je obuhvatala 100 ispitanika sa normalnom funkcijom pluća. Rezultati: Dobijeni rezultati su pokazali da je GSTM1 null varijanta statistički značajno povišena u grupi obolelih od HOBP u poređenju sa kontrolnom grupom (61,5% i 47,0%; or = 1,80; p = 0,042). Takođe, uočena je značajna razlika u zastupljenosti kombinacije genotipova GSTM1 null i GSTP1 105Val/(Val) (38,5% i 24,0%; or = 1,98; p = 0,029), kao i kombinacije CYP1A1 *1A/*2A, GSTM1 null i mEH 113H is/(H is) (7,4% i 1,0% ; or = 7 ,88; p = 0,025). Zaključak: Ovo su prvi podaci o ulozi genskih varijanti gena faze I i II u patogenezi HOBP u srpskoj populaciji. Rezultati dobijeni u ovoj studiji otvaraju mogućnost za detaljniju analizu uloge genetičkih faktora u HOBP na većim grupama ispitanika. Pored toga, podaci dobijeni u našoj studiji potvrđuju važnost genetičkih determinanti povezanih sa HOBP u prethodnim studijama, ali takođe otkrivaju nove genetičke faktore, koji nisu objavljeni do sada.
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 l2 2 COPD patients and 100 controls with normal lung function were determined for CYP1A1 *1A /*2A , CYP2E1 *1 A /*5B , GSTM1 null, GSTT1 null GSTP1 Ile105Val, 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  - Udruženost funkcionalnih varijanti gena faze I I II sa hroničnom opstruktivnom bolešću pluća u srpskoj populaciji
T1  - Association of functional variants of phase I and II genes with chronic obstructive pulmonary disease in a Serbian population
EP  - 214
IS  - 2
SP  - 207
VL  - 34
DO  - 10.2478/jomb-2014-0024
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Tomović, Andrija and Mitić-Milikić, Marija and Nagorni-Obradović, Ljudmila and Petrović-Stanojević, Nataša and Radojković, Dragica",
year = "2015",
abstract = "Uvod: Hronična opstruktivna bolest pluća (HOBP) jeste složeno oboljenje koje karakteriše povišen oksidativni stres. Funkcionalne varijante gena faze I i II ksenobiotičkog metabolizma mogu uticati na ravnotežu oksidanti-antioksidanti i mogu dovesti do razvoja HOBP. Cilj ove studije je bio ispitivanje uloge funkcionalnih genskih varijanti u genima za citohrom P450 (CYP), glutation S-transferazu (GST) i mikrozomalnu epoksidnu hidrolazu (mEH) u patogenezi HOBP u srpskoj populaciji. Metode: U ovoj studiji analizirane su genske varijante CYP1A1 *1A/*2A, CYP2E1 *1A/*5B, GSTM1 null, GSTT1 null, GSTP1 Ile105Val, mEH Tyr113His i mEH His139Arg u grupi obolelih od HOBP koja je obuhvatala 122 ispitanika i kontrolnoj grupi koja je obuhvatala 100 ispitanika sa normalnom funkcijom pluća. Rezultati: Dobijeni rezultati su pokazali da je GSTM1 null varijanta statistički značajno povišena u grupi obolelih od HOBP u poređenju sa kontrolnom grupom (61,5% i 47,0%; or = 1,80; p = 0,042). Takođe, uočena je značajna razlika u zastupljenosti kombinacije genotipova GSTM1 null i GSTP1 105Val/(Val) (38,5% i 24,0%; or = 1,98; p = 0,029), kao i kombinacije CYP1A1 *1A/*2A, GSTM1 null i mEH 113H is/(H is) (7,4% i 1,0% ; or = 7 ,88; p = 0,025). Zaključak: Ovo su prvi podaci o ulozi genskih varijanti gena faze I i II u patogenezi HOBP u srpskoj populaciji. Rezultati dobijeni u ovoj studiji otvaraju mogućnost za detaljniju analizu uloge genetičkih faktora u HOBP na većim grupama ispitanika. Pored toga, podaci dobijeni u našoj studiji potvrđuju važnost genetičkih determinanti povezanih sa HOBP u prethodnim studijama, ali takođe otkrivaju nove genetičke faktore, koji nisu objavljeni do sada., 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 l2 2 COPD patients and 100 controls with normal lung function were determined for CYP1A1 *1A /*2A , CYP2E1 *1 A /*5B , GSTM1 null, GSTT1 null GSTP1 Ile105Val, 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 = "Udruženost funkcionalnih varijanti gena faze I I II sa hroničnom opstruktivnom bolešću pluća u srpskoj populaciji, Association of functional variants of phase I and II genes with chronic obstructive pulmonary disease in a Serbian population",
pages = "214-207",
number = "2",
volume = "34",
doi = "10.2478/jomb-2014-0024"
}

Stanković, M., Nikolić, A., Tomović, A., Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, N.,& Radojković, D.. (2015). Udruženost funkcionalnih varijanti gena faze I I II sa hroničnom opstruktivnom bolešću pluća u srpskoj populaciji. 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, Mitić-Milikić M, Nagorni-Obradović L, Petrović-Stanojević N, Radojković D. Udruženost funkcionalnih varijanti gena faze I I II sa hroničnom opstruktivnom bolešću pluća u srpskoj populaciji. in Journal of Medical Biochemistry. 2015;34(2):207-214.
doi:10.2478/jomb-2014-0024 .

Stanković, Marija, Nikolić, Aleksandra, Tomović, Andrija, Mitić-Milikić, Marija, Nagorni-Obradović, Ljudmila, Petrović-Stanojević, Nataša, Radojković, Dragica, "Udruženost funkcionalnih varijanti gena faze I I II sa hroničnom opstruktivnom bolešću pluća u srpskoj populaciji" 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  - Dopudja-Pantić, Vesna
AU  - Milenković, Branislava
AU  - Radojković, Dragica
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/737
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
EP  - 646
IS  - 6
SP  - 639
VL  - 18
DO  - 10.1007/s40291-014-0116-1
ER  - 

@article{
author = "Petrović-Stanojević, Nataša and Topić, Aleksandra and Nikolić, Aleksandra and Stanković, Marija and Dopudja-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",
pages = "646-639",
number = "6",
volume = "18",
doi = "10.1007/s40291-014-0116-1"
}

Petrović-Stanojević, N., Topić, A., Nikolić, A., Stanković, M., Dopudja-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, Dopudja-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, Dopudja-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://imagine.imgge.bg.ac.rs/handle/123456789/754
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
EP  - 813
IS  - 6
SP  - 811
VL  - 9
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",
pages = "813-811",
number = "6",
volume = "9",
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  - CONF
AU  - Petrović-Stanojević, Nataša
AU  - Topić, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Stanković, Marija
AU  - Dopudja-Pantić, Vesna
AU  - Milenković, Branislava
AU  - Radojković, Dragica
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/774
PB  - European Respiratory Soc Journals Ltd, Sheffield
C3  - European Respiratory Journal
T1  - Age-dependent influence of ADRB2 gene polymorphisms on asthma severity in Serbian population
VL  - 44
UR  - https://hdl.handle.net/21.15107/rcub_imagine_774
ER  - 

@conference{
author = "Petrović-Stanojević, Nataša and Topić, Aleksandra and Nikolić, Aleksandra and Stanković, Marija and Dopudja-Pantić, Vesna and Milenković, Branislava and Radojković, Dragica",
year = "2014",
publisher = "European Respiratory Soc Journals Ltd, Sheffield",
journal = "European Respiratory Journal",
title = "Age-dependent influence of ADRB2 gene polymorphisms on asthma severity in Serbian population",
volume = "44",
url = "https://hdl.handle.net/21.15107/rcub_imagine_774"
}

Petrović-Stanojević, N., Topić, A., Nikolić, A., Stanković, M., Dopudja-Pantić, V., Milenković, B.,& Radojković, D.. (2014). Age-dependent influence of ADRB2 gene polymorphisms on asthma severity in Serbian population. in European Respiratory Journal
European Respiratory Soc Journals Ltd, Sheffield., 44.
https://hdl.handle.net/21.15107/rcub_imagine_774

Petrović-Stanojević N, Topić A, Nikolić A, Stanković M, Dopudja-Pantić V, Milenković B, Radojković D. Age-dependent influence of ADRB2 gene polymorphisms on asthma severity in Serbian population. in European Respiratory Journal. 2014;44.
https://hdl.handle.net/21.15107/rcub_imagine_774 .

Petrović-Stanojević, Nataša, Topić, Aleksandra, Nikolić, Aleksandra, Stanković, Marija, Dopudja-Pantić, Vesna, Milenković, Branislava, Radojković, Dragica, "Age-dependent influence of ADRB2 gene polymorphisms on asthma severity in Serbian population" in European Respiratory Journal, 44 (2014),
https://hdl.handle.net/21.15107/rcub_imagine_774 .

TY  - JOUR
AU  - Topić, Aleksandra
AU  - Stanković, Marija
AU  - Divac Rankov, Aleksandra
AU  - Petrović-Stanojević, Nataša
AU  - Mitić-Milikić, Marija
AU  - Nagorni-Obradović, Ljudmila
AU  - Radojković, Dragica
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/595
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 and Molecular Biomarkers
T1  - Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases
EP  - 1286
IS  - 11
SP  - 1282
VL  - 16
DO  - 10.1089/gtmb.2012.0152
ER  - 

@article{
author = "Topić, Aleksandra and Stanković, Marija and Divac Rankov, Aleksandra and Petrović-Stanojević, Nataša and Mitić-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 and Molecular Biomarkers",
title = "Alpha-1-Antitrypsin Deficiency in Serbian Adults with Lung Diseases",
pages = "1286-1282",
number = "11",
volume = "16",
doi = "10.1089/gtmb.2012.0152"
}

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

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

TY  - JOUR
AU  - Topić, Aleksandra
AU  - Ljujić, Mila
AU  - Nikolić, Aleksandra
AU  - Petrović-Stanojević, Nataša
AU  - Dopudja-Pantić, Vesna
AU  - Mitić-Milikić, Marija
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/508
AB  - Imbalance between neutrophil elastase and alpha-1-antitrypsin (AAT) leads to emphysema in smokers as well as in patients with inherited alpha-1-antitrypsin deficiency. AAT as a proven inhibitor of apoptosis may play role in lung cancer (LC) progression. The aim was to analyse AAT protein variants and polymorphism in promoter region of the neutrophil elastase gene (ELA2) in patients with primary lung cancer. AAT phenotypisation by isoelectric focusing method and ELA2 gene promoter characterization by DNA sequencing were performed in 66 patients with primary lung cancer. Results showed that the frequency of M1 allele and PiM1 homozygotes in LC patients was significantly higher when compared to the healthy subjects (f = 0.6360 and 0.7424 respectively). The most frequent ELA2 promoter region genotypes in LC patients were -903TT and -741GG. There were significantly more patients with intermediate and high ELA2 genotype activity, compared to those with low activity (91% vs. 9%, respectively). In conclusion, we found that PiM1 homozygosity could be associated with the lung cancer, probably due to increased synthesis of this antiapoptotic protein. Non-MM variants of AAT and ELA2 genotypes with predicted intermediate or high activity could also represent a risk factor for aggressive form of lung cancer associated with extrathoracic metastases.
PB  - Frontiers Media Sa, Lausanne
T2  - Pathology & Oncology Research
T1  - Alpha-1-antitrypsin Phenotypes and Neutrophil Elastase Gene Promoter Polymorphisms in Lung Cancer
EP  - 80
IS  - 1
SP  - 75
VL  - 17
DO  - 10.1007/s12253-010-9283-5
ER  - 

@article{
author = "Topić, Aleksandra and Ljujić, Mila and Nikolić, Aleksandra and Petrović-Stanojević, Nataša and Dopudja-Pantić, Vesna and Mitić-Milikić, Marija and Radojković, Dragica",
year = "2011",
abstract = "Imbalance between neutrophil elastase and alpha-1-antitrypsin (AAT) leads to emphysema in smokers as well as in patients with inherited alpha-1-antitrypsin deficiency. AAT as a proven inhibitor of apoptosis may play role in lung cancer (LC) progression. The aim was to analyse AAT protein variants and polymorphism in promoter region of the neutrophil elastase gene (ELA2) in patients with primary lung cancer. AAT phenotypisation by isoelectric focusing method and ELA2 gene promoter characterization by DNA sequencing were performed in 66 patients with primary lung cancer. Results showed that the frequency of M1 allele and PiM1 homozygotes in LC patients was significantly higher when compared to the healthy subjects (f = 0.6360 and 0.7424 respectively). The most frequent ELA2 promoter region genotypes in LC patients were -903TT and -741GG. There were significantly more patients with intermediate and high ELA2 genotype activity, compared to those with low activity (91% vs. 9%, respectively). In conclusion, we found that PiM1 homozygosity could be associated with the lung cancer, probably due to increased synthesis of this antiapoptotic protein. Non-MM variants of AAT and ELA2 genotypes with predicted intermediate or high activity could also represent a risk factor for aggressive form of lung cancer associated with extrathoracic metastases.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Pathology & Oncology Research",
title = "Alpha-1-antitrypsin Phenotypes and Neutrophil Elastase Gene Promoter Polymorphisms in Lung Cancer",
pages = "80-75",
number = "1",
volume = "17",
doi = "10.1007/s12253-010-9283-5"
}

Topić, A., Ljujić, M., Nikolić, A., Petrović-Stanojević, N., Dopudja-Pantić, V., Mitić-Milikić, M.,& Radojković, D.. (2011). Alpha-1-antitrypsin Phenotypes and Neutrophil Elastase Gene Promoter Polymorphisms in Lung Cancer. in Pathology & Oncology Research
Frontiers Media Sa, Lausanne., 17(1), 75-80.
https://doi.org/10.1007/s12253-010-9283-5

Topić A, Ljujić M, Nikolić A, Petrović-Stanojević N, Dopudja-Pantić V, Mitić-Milikić M, Radojković D. Alpha-1-antitrypsin Phenotypes and Neutrophil Elastase Gene Promoter Polymorphisms in Lung Cancer. in Pathology & Oncology Research. 2011;17(1):75-80.
doi:10.1007/s12253-010-9283-5 .

Topić, Aleksandra, Ljujić, Mila, Nikolić, Aleksandra, Petrović-Stanojević, Nataša, Dopudja-Pantić, Vesna, Mitić-Milikić, Marija, Radojković, Dragica, "Alpha-1-antitrypsin Phenotypes and Neutrophil Elastase Gene Promoter Polymorphisms in Lung Cancer" in Pathology & Oncology Research, 17, no. 1 (2011):75-80,
https://doi.org/10.1007/s12253-010-9283-5 . .

TY  - JOUR
AU  - Topić, Aleksandra
AU  - Ljujić, Mila
AU  - Petrović-Stanojević, Nataša
AU  - Dopudja-Pantić, V.
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/520
AB  - Propose: Alpha-1-antitrypsin (AAT) as the major circulating inhibitor of proteases has important role in protease-antiprotease homeostasis. Recent studies have confirmed its antiapoptotic role. AAT is a highly polymorphic protein. Individuals with normal variants have normal serum levels and functional activity of ATT. However, individuals with hereditary AAT deficiency (AATD) have low circulating levels of AAT. Severe AATD was identified as genetic risk factor for early onset of pulmonary emphysema. Association between AAT phenotypes and lung cancer (LC) is not clear; and different studies show contradictory results. The aim of this case-control study was to investigate phenotypes and serum level of AAT in LC. Methods: The study group included 147 patients with LC, classified as small cell lung cancer (SCLC, n=42) and non-small cell lung cancer (NSCLC, n=105). The control group consisted of 273 healthy blood donors. AAT phenotyping was performed by isoelectric-focusing and AAT concentration was measured using nephelometry. Results: There were no differences in the frequencies of AAT phenotypes and alleles between the control group and LC patients, as well as between NSCLC and SCLC groups. An elevated level of AAT was obtained in LC patients. PiMZ and PiMS phenotypes in LC patients were not deficient in the classical sense. AAT levels were 90 and 134%, respectively, when compared to PiMM phenotype in the control group. Conclusion: Our findings revealed that moderate deficiency of AAT is not risk factor for LC development. Although polymorphism of AAT was not associated with risk of LC, further research of this antiprotease and antiapoptotic protein could clarify its role in carcinogenesis, given its high concentration in LC patients, even in AATD patients.
PB  - Balkan Union of Oncology (B.U.ON.)
T2  - Journal of Buon
T1  - Phenotypes and serum level of alpha-1-antitrypsin in lung cancer
EP  - 676
IS  - 4
SP  - 672
VL  - 16
UR  - https://hdl.handle.net/21.15107/rcub_imagine_520
ER  - 

@article{
author = "Topić, Aleksandra and Ljujić, Mila and Petrović-Stanojević, Nataša and Dopudja-Pantić, V. and Radojković, Dragica",
year = "2011",
abstract = "Propose: Alpha-1-antitrypsin (AAT) as the major circulating inhibitor of proteases has important role in protease-antiprotease homeostasis. Recent studies have confirmed its antiapoptotic role. AAT is a highly polymorphic protein. Individuals with normal variants have normal serum levels and functional activity of ATT. However, individuals with hereditary AAT deficiency (AATD) have low circulating levels of AAT. Severe AATD was identified as genetic risk factor for early onset of pulmonary emphysema. Association between AAT phenotypes and lung cancer (LC) is not clear; and different studies show contradictory results. The aim of this case-control study was to investigate phenotypes and serum level of AAT in LC. Methods: The study group included 147 patients with LC, classified as small cell lung cancer (SCLC, n=42) and non-small cell lung cancer (NSCLC, n=105). The control group consisted of 273 healthy blood donors. AAT phenotyping was performed by isoelectric-focusing and AAT concentration was measured using nephelometry. Results: There were no differences in the frequencies of AAT phenotypes and alleles between the control group and LC patients, as well as between NSCLC and SCLC groups. An elevated level of AAT was obtained in LC patients. PiMZ and PiMS phenotypes in LC patients were not deficient in the classical sense. AAT levels were 90 and 134%, respectively, when compared to PiMM phenotype in the control group. Conclusion: Our findings revealed that moderate deficiency of AAT is not risk factor for LC development. Although polymorphism of AAT was not associated with risk of LC, further research of this antiprotease and antiapoptotic protein could clarify its role in carcinogenesis, given its high concentration in LC patients, even in AATD patients.",
publisher = "Balkan Union of Oncology (B.U.ON.)",
journal = "Journal of Buon",
title = "Phenotypes and serum level of alpha-1-antitrypsin in lung cancer",
pages = "676-672",
number = "4",
volume = "16",
url = "https://hdl.handle.net/21.15107/rcub_imagine_520"
}

Topić, A., Ljujić, M., Petrović-Stanojević, N., Dopudja-Pantić, V.,& Radojković, D.. (2011). Phenotypes and serum level of alpha-1-antitrypsin in lung cancer. in Journal of Buon
Balkan Union of Oncology (B.U.ON.)., 16(4), 672-676.
https://hdl.handle.net/21.15107/rcub_imagine_520

Topić A, Ljujić M, Petrović-Stanojević N, Dopudja-Pantić V, Radojković D. Phenotypes and serum level of alpha-1-antitrypsin in lung cancer. in Journal of Buon. 2011;16(4):672-676.
https://hdl.handle.net/21.15107/rcub_imagine_520 .

Topić, Aleksandra, Ljujić, Mila, Petrović-Stanojević, Nataša, Dopudja-Pantić, V., Radojković, Dragica, "Phenotypes and serum level of alpha-1-antitrypsin in lung cancer" in Journal of Buon, 16, no. 4 (2011):672-676,
https://hdl.handle.net/21.15107/rcub_imagine_520 .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nestorović, A. R.
AU  - Tomović, A. M.
AU  - Petrović-Stanojević, Nataša
AU  - Anđelić-Jelić, M. S.
AU  - Dopudja-Pantić, V. B.
AU  - Nagorni-Obradović, Lj. M.
AU  - Mitić-Milikić, M. M.
AU  - Radojković, Dragica
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/385
AB  - Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are a major cause of morbidity and mortality worldwide. In both diseases airways inflammation plays an important role. Functional promoter polymorphism, at the position -308, of tumor necrosis factor (TNF)-alpha represents attractive potential susceptibilty marker for both diseases. In order to investigate the role of this polymorphism in COPD and LC, a case-control study was performed. The patient groups consisted of 97 subjects with COPD and 70 subjects with LC, while the control group encompassed 102 subjects. Results of our study showed significant decrease of heterozygote for TNF-alpha-308*1/*2 gene variant in COPD group in comparison to controls (p=0.043). According to our results heterozygous carriers of TNF-alpha-308*1/*2 polymorphism had a 2.3-fold decreased risk for COPD development (CR=0.44,95%CI=0.20-0.97). In patients with lung cancer we also observed a trend of decreased distribution of TNF-alpha-308*1/*2 heterozygotes, but statistical significance was not achieved. To our knowledge, this is the first study implicating decreased frequency of TNF-alpha-308*1/*2 gene variant in patients with COPD and LC. Although these results need to be confirmed on larger cohort, they represent a new and interesting finding, not reported in other populations tested so far.
PB  - Aepress Sro, Bratislava
T2  - Neoplasma
T1  - TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer
EP  - 352
IS  - 4
SP  - 348
VL  - 56
DO  - 10.4149/neo_2009_04_348
ER  - 

@article{
author = "Stanković, Marija and Nestorović, A. R. and Tomović, A. M. and Petrović-Stanojević, Nataša and Anđelić-Jelić, M. S. and Dopudja-Pantić, V. B. and Nagorni-Obradović, Lj. M. and Mitić-Milikić, M. M. and Radojković, Dragica",
year = "2009",
abstract = "Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are a major cause of morbidity and mortality worldwide. In both diseases airways inflammation plays an important role. Functional promoter polymorphism, at the position -308, of tumor necrosis factor (TNF)-alpha represents attractive potential susceptibilty marker for both diseases. In order to investigate the role of this polymorphism in COPD and LC, a case-control study was performed. The patient groups consisted of 97 subjects with COPD and 70 subjects with LC, while the control group encompassed 102 subjects. Results of our study showed significant decrease of heterozygote for TNF-alpha-308*1/*2 gene variant in COPD group in comparison to controls (p=0.043). According to our results heterozygous carriers of TNF-alpha-308*1/*2 polymorphism had a 2.3-fold decreased risk for COPD development (CR=0.44,95%CI=0.20-0.97). In patients with lung cancer we also observed a trend of decreased distribution of TNF-alpha-308*1/*2 heterozygotes, but statistical significance was not achieved. To our knowledge, this is the first study implicating decreased frequency of TNF-alpha-308*1/*2 gene variant in patients with COPD and LC. Although these results need to be confirmed on larger cohort, they represent a new and interesting finding, not reported in other populations tested so far.",
publisher = "Aepress Sro, Bratislava",
journal = "Neoplasma",
title = "TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer",
pages = "352-348",
number = "4",
volume = "56",
doi = "10.4149/neo_2009_04_348"
}

Stanković, M., Nestorović, A. R., Tomović, A. M., Petrović-Stanojević, N., Anđelić-Jelić, M. S., Dopudja-Pantić, V. B., Nagorni-Obradović, Lj. M., Mitić-Milikić, M. M.,& Radojković, D.. (2009). TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer. in Neoplasma
Aepress Sro, Bratislava., 56(4), 348-352.
https://doi.org/10.4149/neo_2009_04_348

Stanković M, Nestorović AR, Tomović AM, Petrović-Stanojević N, Anđelić-Jelić MS, Dopudja-Pantić VB, Nagorni-Obradović LM, Mitić-Milikić MM, Radojković D. TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer. in Neoplasma. 2009;56(4):348-352.
doi:10.4149/neo_2009_04_348 .

Stanković, Marija, Nestorović, A. R., Tomović, A. M., Petrović-Stanojević, Nataša, Anđelić-Jelić, M. S., Dopudja-Pantić, V. B., Nagorni-Obradović, Lj. M., Mitić-Milikić, M. M., Radojković, Dragica, "TNF-alpha-308 promotor polymorphism in patients with chronic obstructive pulmonary disease and lung cancer" in Neoplasma, 56, no. 4 (2009):348-352,
https://doi.org/10.4149/neo_2009_04_348 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Rakićević, Ljiljana
AU  - Tomović, Andrija
AU  - Mitić-Milikić, Marija
AU  - Nagorni-Obradović, Ljudmila
AU  - Grujić, Milan
AU  - Petrović-Stanojević, Nataša
AU  - Anđelić-Jelić, Marina
AU  - Dopudja-Pantić, Vesna
AU  - Radojković, Dragica
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/356
AB  - Background: The excess of matrix metalloproteinases (MMPs) might be associated with the airways destruction or dilatation in bronchiectasis. The functional promoter polymorphisms of MMPI and MMP9 genes, involved in the extracellular matrix remodeling, might increase the expression of MMPs leading to the development of bronchiectasis. Methods: Detection of MMP1 G-1607GG and MMP9 C-1562T gene variants was performed on 37 patients with idiopathic disseminated bronchiectasis and 102 control subjects. We also described a novel method for simple and rapid detection of MMP1 G-1607GG polymorphism. Results: The frequency of -1607GG allele was significantly higher in the group of patients than in control subjects (P = 0.014). The heterozygote genotype showed association with bronchiectasis (odds ratio, 5.3; 95% confidence intervals, 1.4-20.0). The association was even stronger in homozygotes for -1607GG allele (odds ration, 8.7; 95% confidence intervals, 1.9-41.0). The allelic and genotype frequencies of MMP9 C-1562T variant did not show significant differences between the groups. Conclusions: This is the first report concerning a role of MMP1 G-1607GG and MMP9 C-1562T variants in pathogenesis of idiopathic disseminated bronchiectasis. The results of our study revealed the association of -1607GG allele and the lack of association of MMP9 C-1562T variant with the disease.
PB  - BMJ Publishing Group
T2  - Journal of Investigative Medicine
T1  - Matrix Metalloproteinases Gene Variants in Idiopathic Disseminated Bronchiectasis
EP  - 503
IS  - 3
SP  - 500
VL  - 57
DO  - 10.2310/JIM.0b013e318198277c
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Divac Rankov, Aleksandra and Rakićević, Ljiljana and Tomović, Andrija and Mitić-Milikić, Marija and Nagorni-Obradović, Ljudmila and Grujić, Milan and Petrović-Stanojević, Nataša and Anđelić-Jelić, Marina and Dopudja-Pantić, Vesna and Radojković, Dragica",
year = "2009",
abstract = "Background: The excess of matrix metalloproteinases (MMPs) might be associated with the airways destruction or dilatation in bronchiectasis. The functional promoter polymorphisms of MMPI and MMP9 genes, involved in the extracellular matrix remodeling, might increase the expression of MMPs leading to the development of bronchiectasis. Methods: Detection of MMP1 G-1607GG and MMP9 C-1562T gene variants was performed on 37 patients with idiopathic disseminated bronchiectasis and 102 control subjects. We also described a novel method for simple and rapid detection of MMP1 G-1607GG polymorphism. Results: The frequency of -1607GG allele was significantly higher in the group of patients than in control subjects (P = 0.014). The heterozygote genotype showed association with bronchiectasis (odds ratio, 5.3; 95% confidence intervals, 1.4-20.0). The association was even stronger in homozygotes for -1607GG allele (odds ration, 8.7; 95% confidence intervals, 1.9-41.0). The allelic and genotype frequencies of MMP9 C-1562T variant did not show significant differences between the groups. Conclusions: This is the first report concerning a role of MMP1 G-1607GG and MMP9 C-1562T variants in pathogenesis of idiopathic disseminated bronchiectasis. The results of our study revealed the association of -1607GG allele and the lack of association of MMP9 C-1562T variant with the disease.",
publisher = "BMJ Publishing Group",
journal = "Journal of Investigative Medicine",
title = "Matrix Metalloproteinases Gene Variants in Idiopathic Disseminated Bronchiectasis",
pages = "503-500",
number = "3",
volume = "57",
doi = "10.2310/JIM.0b013e318198277c"
}

Stanković, M., Nikolić, A., Divac Rankov, A., Rakićević, L., Tomović, A., Mitić-Milikić, M., Nagorni-Obradović, L., Grujić, M., Petrović-Stanojević, N., Anđelić-Jelić, M., Dopudja-Pantić, V.,& Radojković, D.. (2009). Matrix Metalloproteinases Gene Variants in Idiopathic Disseminated Bronchiectasis. in Journal of Investigative Medicine
BMJ Publishing Group., 57(3), 500-503.
https://doi.org/10.2310/JIM.0b013e318198277c

Stanković M, Nikolić A, Divac Rankov A, Rakićević L, Tomović A, Mitić-Milikić M, Nagorni-Obradović L, Grujić M, Petrović-Stanojević N, Anđelić-Jelić M, Dopudja-Pantić V, Radojković D. Matrix Metalloproteinases Gene Variants in Idiopathic Disseminated Bronchiectasis. in Journal of Investigative Medicine. 2009;57(3):500-503.
doi:10.2310/JIM.0b013e318198277c .

Stanković, Marija, Nikolić, Aleksandra, Divac Rankov, Aleksandra, Rakićević, Ljiljana, Tomović, Andrija, Mitić-Milikić, Marija, Nagorni-Obradović, Ljudmila, Grujić, Milan, Petrović-Stanojević, Nataša, Anđelić-Jelić, Marina, Dopudja-Pantić, Vesna, Radojković, Dragica, "Matrix Metalloproteinases Gene Variants in Idiopathic Disseminated Bronchiectasis" in Journal of Investigative Medicine, 57, no. 3 (2009):500-503,
https://doi.org/10.2310/JIM.0b013e318198277c . .

TY  - JOUR
AU  - Nisević, Ivan
AU  - Dinić, Jelena
AU  - Nikolić, Aleksandra
AU  - Đorđević, Valentina
AU  - Lukić, Snežana
AU  - Ugljesić, Milenko
AU  - Anđelić-Jelić, Marina
AU  - Petrović-Stanojević, Nataša
AU  - Radojković, Dragica
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/325
AB  - Chronic pancreatitis and pancreatic adenocarcinoma are extensively studied as common and potentially lethal disorders. However, their Causes and genetic background in most cases remain unclear. The C677T polymorphism in 5',10'-methylenetetrahydrofolate reductase (MTHFR) gene may modulate the risk of pancreatic disorders. In this Study, we tested whether MTHFR C677T polymorphism is associated with chronic pancreatitis and pancreatic adenocarcinoma in the Serbian population. DNA was extracted from blood samples of 51 chronic pancreatitis patients, 21 pancreatic adenocarcinoma patients, and a control group consisting of 50 healthy smokers. The MTHFR C677T polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Although, no statistically significant differences were observed in the distribution of MTHFR genotype or allele frequencies between patients and control groups, the results showed an increased frequency of homozygotes for MTHFR C677T polymorphisrn in chronic pancreatitis patients ( 14%) and a decreased frequency in pancreatic adenocarcinoma patients (5%) in comparison to the control group (8%). We speculate that the MTHFR C677T polymorphism Could act as a possible risk factor for chronic pancreatitis and a possible protective factor in pancreatic adenocarcinoma. This observation needs further investigation in prospective Studies on a larger number of patients, in which the effect of other genetic and environmental factors should also be taken into consideration.
PB  - Wiley, Hoboken
T2  - Cell Biochemistry and Function
T1  - MTHFR C677T polymorphism in chronic pancreatitis and pancreatic adenocarcinoma
EP  - 663
IS  - 6
SP  - 659
VL  - 26
DO  - 10.1002/cbf.1487
ER  - 

@article{
author = "Nisević, Ivan and Dinić, Jelena and Nikolić, Aleksandra and Đorđević, Valentina and Lukić, Snežana and Ugljesić, Milenko and Anđelić-Jelić, Marina and Petrović-Stanojević, Nataša and Radojković, Dragica",
year = "2008",
abstract = "Chronic pancreatitis and pancreatic adenocarcinoma are extensively studied as common and potentially lethal disorders. However, their Causes and genetic background in most cases remain unclear. The C677T polymorphism in 5',10'-methylenetetrahydrofolate reductase (MTHFR) gene may modulate the risk of pancreatic disorders. In this Study, we tested whether MTHFR C677T polymorphism is associated with chronic pancreatitis and pancreatic adenocarcinoma in the Serbian population. DNA was extracted from blood samples of 51 chronic pancreatitis patients, 21 pancreatic adenocarcinoma patients, and a control group consisting of 50 healthy smokers. The MTHFR C677T polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Although, no statistically significant differences were observed in the distribution of MTHFR genotype or allele frequencies between patients and control groups, the results showed an increased frequency of homozygotes for MTHFR C677T polymorphisrn in chronic pancreatitis patients ( 14%) and a decreased frequency in pancreatic adenocarcinoma patients (5%) in comparison to the control group (8%). We speculate that the MTHFR C677T polymorphism Could act as a possible risk factor for chronic pancreatitis and a possible protective factor in pancreatic adenocarcinoma. This observation needs further investigation in prospective Studies on a larger number of patients, in which the effect of other genetic and environmental factors should also be taken into consideration.",
publisher = "Wiley, Hoboken",
journal = "Cell Biochemistry and Function",
title = "MTHFR C677T polymorphism in chronic pancreatitis and pancreatic adenocarcinoma",
pages = "663-659",
number = "6",
volume = "26",
doi = "10.1002/cbf.1487"
}

Nisević, I., Dinić, J., Nikolić, A., Đorđević, V., Lukić, S., Ugljesić, M., Anđelić-Jelić, M., Petrović-Stanojević, N.,& Radojković, D.. (2008). MTHFR C677T polymorphism in chronic pancreatitis and pancreatic adenocarcinoma. in Cell Biochemistry and Function
Wiley, Hoboken., 26(6), 659-663.
https://doi.org/10.1002/cbf.1487

Nisević I, Dinić J, Nikolić A, Đorđević V, Lukić S, Ugljesić M, Anđelić-Jelić M, Petrović-Stanojević N, Radojković D. MTHFR C677T polymorphism in chronic pancreatitis and pancreatic adenocarcinoma. in Cell Biochemistry and Function. 2008;26(6):659-663.
doi:10.1002/cbf.1487 .

Nisević, Ivan, Dinić, Jelena, Nikolić, Aleksandra, Đorđević, Valentina, Lukić, Snežana, Ugljesić, Milenko, Anđelić-Jelić, Marina, Petrović-Stanojević, Nataša, Radojković, Dragica, "MTHFR C677T polymorphism in chronic pancreatitis and pancreatic adenocarcinoma" in Cell Biochemistry and Function, 26, no. 6 (2008):659-663,
https://doi.org/10.1002/cbf.1487 . .

TY  - JOUR
AU  - Stanković, Marija
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Tomović, Andrija
AU  - Petrović-Stanojević, Nataša
AU  - Anđelić, Marina
AU  - Dopudja-Pantić, Vesna
AU  - Surlan, Mirjana
AU  - Vujicić, Ivan
AU  - Ponomarev, Dimitrije
AU  - Mitić-Milikić, Marija
AU  - Kušić-Tišma, Jelena
AU  - Radojković, Dragica
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/316
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
EP  - 362
IS  - 3
SP  - 357
VL  - 12
DO  - 10.1089/gte.2007.0069
ER  - 

@article{
author = "Stanković, Marija and Nikolić, Aleksandra and Divac Rankov, Aleksandra and Tomović, Andrija and Petrović-Stanojević, Nataša and Anđelić, Marina and Dopudja-Pantić, Vesna and Surlan, Mirjana and Vujicić, Ivan and Ponomarev, Dimitrije and Mitić-Milikić, Marija and Kušić-Tišma, 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",
pages = "362-357",
number = "3",
volume = "12",
doi = "10.1089/gte.2007.0069"
}

Stanković, M., Nikolić, A., Divac Rankov, A., Tomović, A., Petrović-Stanojević, N., Anđelić, M., Dopudja-Pantić, V., Surlan, M., Vujicić, I., Ponomarev, D., Mitić-Milikić, M., Kušić-Tišma, 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 Rankov A, Tomović A, Petrović-Stanojević N, Anđelić M, Dopudja-Pantić V, Surlan M, Vujicić I, Ponomarev D, Mitić-Milikić M, Kušić-Tišma 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 Rankov, Aleksandra, Tomović, Andrija, Petrović-Stanojević, Nataša, Anđelić, Marina, Dopudja-Pantić, Vesna, Surlan, Mirjana, Vujicić, Ivan, Ponomarev, Dimitrije, Mitić-Milikić, Marija, Kušić-Tišma, 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  - JOUR
AU  - Ljujić, Mila
AU  - Topić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Petrović-Stanojević, Nataša
AU  - Surlan, Mirjana
AU  - Mitić-Milikić, Maria
AU  - Radojković, Dragica
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/340
AB  - Laboratory diagnosis of alpha-1-antitrypsin (AAT) deficiency is routinely performed by phenotyping methods, which include measurement of serum alpha-1-antitrypsin concentration and isoelectric focusing (IEF). Several DNA-based methods are also used for AAT deficiency testing, but they still have not become part of routine diagnostics. The aim of the study was to identify AAT variants using 2 different methods, isoelectric focusing and denaturing gradient gel electrophoresis (DGGE), and to compare obtained results as well as practical application of these 2 methods. The study has encompassed 27 emphysema patients. In all patients, AAT phenotypization was conducted using IEF, whereas genotypization was performed by DGGE. Variations detected by DGGE were characterized by DNA sequencing. Mutations in the AAT gene were detected in 6 patients. Three patients were homozygous for the Z allele, whereas I patient was heterozygous. In 2 patients, novel AAT variants, G320R and V321F, were detected. When results obtained by IEF and DGGE were compared, it was observed that IEF results were inconclusive or misinterpreted in 5 cases (18.5%). Both methods proved to be reliable for detection of the Z alleles, whereas discrepancy existed for M4 allele and rare variants. Therefore, the optimal strategy for diagnostics of AAT deficiency should encompass detection of the most common AAT variants by IEF and screening for the less common variants by DGGE in combination with sequencing.
PB  - Elsevier Science Inc, New York
T2  - Translational Research
T1  - Lsoelectric focusing phenotyping and denaturing gradient gel electrophoresis genotyping: a comparison of two methods in detection of alpha-1-antitrypsin variants
EP  - 259
IS  - 5
SP  - 255
VL  - 151
DO  - 10.1016/j.trsl.2008.02.002
ER  - 

@article{
author = "Ljujić, Mila and Topić, Aleksandra and Divac Rankov, Aleksandra and Nikolić, Aleksandra and Petrović-Stanojević, Nataša and Surlan, Mirjana and Mitić-Milikić, Maria and Radojković, Dragica",
year = "2008",
abstract = "Laboratory diagnosis of alpha-1-antitrypsin (AAT) deficiency is routinely performed by phenotyping methods, which include measurement of serum alpha-1-antitrypsin concentration and isoelectric focusing (IEF). Several DNA-based methods are also used for AAT deficiency testing, but they still have not become part of routine diagnostics. The aim of the study was to identify AAT variants using 2 different methods, isoelectric focusing and denaturing gradient gel electrophoresis (DGGE), and to compare obtained results as well as practical application of these 2 methods. The study has encompassed 27 emphysema patients. In all patients, AAT phenotypization was conducted using IEF, whereas genotypization was performed by DGGE. Variations detected by DGGE were characterized by DNA sequencing. Mutations in the AAT gene were detected in 6 patients. Three patients were homozygous for the Z allele, whereas I patient was heterozygous. In 2 patients, novel AAT variants, G320R and V321F, were detected. When results obtained by IEF and DGGE were compared, it was observed that IEF results were inconclusive or misinterpreted in 5 cases (18.5%). Both methods proved to be reliable for detection of the Z alleles, whereas discrepancy existed for M4 allele and rare variants. Therefore, the optimal strategy for diagnostics of AAT deficiency should encompass detection of the most common AAT variants by IEF and screening for the less common variants by DGGE in combination with sequencing.",
publisher = "Elsevier Science Inc, New York",
journal = "Translational Research",
title = "Lsoelectric focusing phenotyping and denaturing gradient gel electrophoresis genotyping: a comparison of two methods in detection of alpha-1-antitrypsin variants",
pages = "259-255",
number = "5",
volume = "151",
doi = "10.1016/j.trsl.2008.02.002"
}

Ljujić, M., Topić, A., Divac Rankov, A., Nikolić, A., Petrović-Stanojević, N., Surlan, M., Mitić-Milikić, M.,& Radojković, D.. (2008). Lsoelectric focusing phenotyping and denaturing gradient gel electrophoresis genotyping: a comparison of two methods in detection of alpha-1-antitrypsin variants. in Translational Research
Elsevier Science Inc, New York., 151(5), 255-259.
https://doi.org/10.1016/j.trsl.2008.02.002

Ljujić M, Topić A, Divac Rankov A, Nikolić A, Petrović-Stanojević N, Surlan M, Mitić-Milikić M, Radojković D. Lsoelectric focusing phenotyping and denaturing gradient gel electrophoresis genotyping: a comparison of two methods in detection of alpha-1-antitrypsin variants. in Translational Research. 2008;151(5):255-259.
doi:10.1016/j.trsl.2008.02.002 .

Ljujić, Mila, Topić, Aleksandra, Divac Rankov, Aleksandra, Nikolić, Aleksandra, Petrović-Stanojević, Nataša, Surlan, Mirjana, Mitić-Milikić, Maria, Radojković, Dragica, "Lsoelectric focusing phenotyping and denaturing gradient gel electrophoresis genotyping: a comparison of two methods in detection of alpha-1-antitrypsin variants" in Translational Research, 151, no. 5 (2008):255-259,
https://doi.org/10.1016/j.trsl.2008.02.002 . .

TY  - CONF
AU  - Nikolić, Aleksandra
AU  - Nisević, I
AU  - Dinić, J.
AU  - Lukić, S.
AU  - Anđelić, M.
AU  - Petrović-Stanojević, Nataša
AU  - Đorđević, Valentina
AU  - Rakićević, Ljiljana
AU  - Ugljesić, M.
AU  - Radojković, Dragica
PY  - 2007
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/288
PB  - Oxford Univ Press, Oxford
C3  - Annals of Oncology
T1  - Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer
EP  - VII65
SP  - VII64
VL  - 18
UR  - https://hdl.handle.net/21.15107/rcub_imagine_288
ER  - 

@conference{
author = "Nikolić, Aleksandra and Nisević, I and Dinić, J. and Lukić, S. and Anđelić, M. and Petrović-Stanojević, Nataša and Đorđević, Valentina 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",
pages = "VII65-VII64",
volume = "18",
url = "https://hdl.handle.net/21.15107/rcub_imagine_288"
}

Nikolić, A., Nisević, I., Dinić, J., Lukić, S., Anđelić, 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_imagine_288

Nikolić A, Nisević I, Dinić J, Lukić S, Anđelić 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_imagine_288 .

Nikolić, Aleksandra, Nisević, I, Dinić, J., Lukić, S., Anđelić, M., Petrović-Stanojević, Nataša, Đorđević, Valentina, 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_imagine_288 .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Mitić-Milikić, M
AU  - Nagorni-Obradović, L
AU  - Petrović-Stanojević, Nataša
AU  - Dopudja-Pantić, V
AU  - Nadaskić, R
AU  - Savić, A
AU  - Radojković, Dragica
PY  - 2005
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/211
PB  - BMJ Publishing Group, London
T2  - Thorax
T1  - CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: a controversial issue
EP  - 85
IS  - 1
SP  - 85
VL  - 60
UR  - https://hdl.handle.net/21.15107/rcub_imagine_211
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Nikolić, Aleksandra and Mitić-Milikić, M and Nagorni-Obradović, L and Petrović-Stanojević, Nataša and Dopudja-Pantić, V and Nadaskić, R and Savić, A and Radojković, Dragica",
year = "2005",
publisher = "BMJ Publishing Group, London",
journal = "Thorax",
title = "CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: a controversial issue",
pages = "85-85",
number = "1",
volume = "60",
url = "https://hdl.handle.net/21.15107/rcub_imagine_211"
}

Divac Rankov, A., Nikolić, A., Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, N., Dopudja-Pantić, V., Nadaskić, R., Savić, A.,& Radojković, D.. (2005). CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: a controversial issue. in Thorax
BMJ Publishing Group, London., 60(1), 85-85.
https://hdl.handle.net/21.15107/rcub_imagine_211

Divac Rankov A, Nikolić A, Mitić-Milikić M, Nagorni-Obradović L, Petrović-Stanojević N, Dopudja-Pantić V, Nadaskić R, Savić A, Radojković D. CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: a controversial issue. in Thorax. 2005;60(1):85-85.
https://hdl.handle.net/21.15107/rcub_imagine_211 .

Divac Rankov, Aleksandra, Nikolić, Aleksandra, Mitić-Milikić, M, Nagorni-Obradović, L, Petrović-Stanojević, Nataša, Dopudja-Pantić, V, Nadaskić, R, Savić, A, Radojković, Dragica, "CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: a controversial issue" in Thorax, 60, no. 1 (2005):85-85,
https://hdl.handle.net/21.15107/rcub_imagine_211 .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Mitić-Milikić, M.
AU  - Nagorni-Obradović, L.
AU  - Petrović-Stanojević, Nataša
AU  - Dopudja-Pantić, V.
AU  - Nadaskić, R.
AU  - Savić, A.
AU  - Radojković, Dragica
PY  - 2005
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/215
PB  - BMJ Publishing Group
T2  - Thorax
T1  - CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: A controversial issue [2]
IS  - 1
SP  - 85
VL  - 60
UR  - https://hdl.handle.net/21.15107/rcub_imagine_215
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Nikolić, Aleksandra and Mitić-Milikić, M. and Nagorni-Obradović, L. and Petrović-Stanojević, Nataša and Dopudja-Pantić, V. and Nadaskić, R. and Savić, A. and Radojković, Dragica",
year = "2005",
publisher = "BMJ Publishing Group",
journal = "Thorax",
title = "CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: A controversial issue [2]",
number = "1",
pages = "85",
volume = "60",
url = "https://hdl.handle.net/21.15107/rcub_imagine_215"
}

Divac Rankov, A., Nikolić, A., Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, N., Dopudja-Pantić, V., Nadaskić, R., Savić, A.,& Radojković, D.. (2005). CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: A controversial issue [2]. in Thorax
BMJ Publishing Group., 60(1), 85.
https://hdl.handle.net/21.15107/rcub_imagine_215

Divac Rankov A, Nikolić A, Mitić-Milikić M, Nagorni-Obradović L, Petrović-Stanojević N, Dopudja-Pantić V, Nadaskić R, Savić A, Radojković D. CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: A controversial issue [2]. in Thorax. 2005;60(1):85.
https://hdl.handle.net/21.15107/rcub_imagine_215 .

Divac Rankov, Aleksandra, Nikolić, Aleksandra, Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, Nataša, Dopudja-Pantić, V., Nadaskić, R., Savić, A., Radojković, Dragica, "CFTR mutations and polymorphisms in adults with disseminated bronchiectasis: A controversial issue [2]" in Thorax, 60, no. 1 (2005):85,
https://hdl.handle.net/21.15107/rcub_imagine_215 .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Mitić-Milikić, M.
AU  - Nagorni-Obradović, L.
AU  - Petrović-Stanojević, Nataša
AU  - Dopudja-Pantić, V.
AU  - Nadaskić, R.
AU  - Savić, A.
AU  - Radojković, Dragica
PY  - 2004
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/199
AB  - We performed the complete screening of the CFTR gene in a group of 31 patients with COPD in order to investigate the impact of mutations and polymorphisms in the CFTR gene. The cumulative frequency of CFTR mutations (17.74%) was significantly higher than in our general population (P  lt 0.0001). The R75Q was significantly overrepresented in COPD patients (8.06%; P =0.002). In all patients carrying the R75Q chronic bronchitis was a dominant symptom of COPD, and all were homozygous for the V470 allele. These findings suggest that R75Q mutation could be characteristic CFTR variant for COPD patients.
PB  - Elsevier
T2  - Journal of Cystic Fibrosis
T1  - High frequency of the R75Q CFTR variation in patients with chronic obstructive pulmonary disease
EP  - 191
IS  - 3
SP  - 189
VL  - 3
DO  - 10.1016/j.jcf.2004.05.049
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Nikolić, Aleksandra and Mitić-Milikić, M. and Nagorni-Obradović, L. and Petrović-Stanojević, Nataša and Dopudja-Pantić, V. and Nadaskić, R. and Savić, A. and Radojković, Dragica",
year = "2004",
abstract = "We performed the complete screening of the CFTR gene in a group of 31 patients with COPD in order to investigate the impact of mutations and polymorphisms in the CFTR gene. The cumulative frequency of CFTR mutations (17.74%) was significantly higher than in our general population (P  lt 0.0001). The R75Q was significantly overrepresented in COPD patients (8.06%; P =0.002). In all patients carrying the R75Q chronic bronchitis was a dominant symptom of COPD, and all were homozygous for the V470 allele. These findings suggest that R75Q mutation could be characteristic CFTR variant for COPD patients.",
publisher = "Elsevier",
journal = "Journal of Cystic Fibrosis",
title = "High frequency of the R75Q CFTR variation in patients with chronic obstructive pulmonary disease",
pages = "191-189",
number = "3",
volume = "3",
doi = "10.1016/j.jcf.2004.05.049"
}

Divac Rankov, A., Nikolić, A., Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, N., Dopudja-Pantić, V., Nadaskić, R., Savić, A.,& Radojković, D.. (2004). High frequency of the R75Q CFTR variation in patients with chronic obstructive pulmonary disease. in Journal of Cystic Fibrosis
Elsevier., 3(3), 189-191.
https://doi.org/10.1016/j.jcf.2004.05.049

Divac Rankov A, Nikolić A, Mitić-Milikić M, Nagorni-Obradović L, Petrović-Stanojević N, Dopudja-Pantić V, Nadaskić R, Savić A, Radojković D. High frequency of the R75Q CFTR variation in patients with chronic obstructive pulmonary disease. in Journal of Cystic Fibrosis. 2004;3(3):189-191.
doi:10.1016/j.jcf.2004.05.049 .

Divac Rankov, Aleksandra, Nikolić, Aleksandra, Mitić-Milikić, M., Nagorni-Obradović, L., Petrović-Stanojević, Nataša, Dopudja-Pantić, V., Nadaskić, R., Savić, A., Radojković, Dragica, "High frequency of the R75Q CFTR variation in patients with chronic obstructive pulmonary disease" in Journal of Cystic Fibrosis, 3, no. 3 (2004):189-191,
https://doi.org/10.1016/j.jcf.2004.05.049 . .