TY  - JOUR
AU  - Jelovac, Marina
AU  - Kotur, Nikola
AU  - Ristivojević, Bojan
AU  - Pavlović, Djordje
AU  - Spasovski, Vesna
AU  - Damjanov, Nemanja
AU  - Pavlović, Sonja
AU  - Zukić, Branka
PY  - 2023
UR  - https://www.mdpi.com/1422-0067/24/10/8538
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1859
AB  - Systemic sclerosis (SSc) is a rare connective tissue disorder with highest morbidity and mortality among rheumatologic diseases. Disease progression is highly heterogeneous between patients, implying a strong need for individualization of therapy. Four pharmacogenetic variants, namely TPMT rs1800460, TPMT rs1142345, MTHFR rs1801133 and SLCO1B1 rs4149056 were tested for association with severe disease outcomes in 102 patients with SSc from Serbia treated either with immunosuppressants azathioprine (AZA) and methotrexate (MTX) or with other types of medications. Genotyping was performed using PCR-RFLP and direct Sanger sequencing. R software was used for statistical analysis and development of polygenic risk score (PRS) model. Association was found between MTHFR rs1801133 and higher risk for elevated systolic pressure in all patients except those prescribed with MTX, and higher risk for kidney insufficiency in patients prescribed with other types of drugs. In patients treated with MTX, variant SLCO1B1 rs4149056 was protective against kidney insufficiency. For patients receiving MTX a trend was shown for having a higher PRS rank and elevated systolic pressure. Our results open a door wide for more extensive research on pharmacogenomics markers in patients with SSc. Altogether, pharmacogenomics markers could predict the outcome of patients with SSc and help in prevention of adverse drug reactions.
T2  - International Journal of Molecular Sciences
T2  - International Journal of Molecular Sciences
T1  - Can Pharmacogenetic Variants in TPMT, MTHFR and SLCO1B1 Genes Be Used as Potential Markers of Outcome Prediction in Systemic Sclerosis Patients?
IS  - 10
SP  - 8538
VL  - 24
DO  - 10.3390/ijms24108538
ER  - 

@article{
author = "Jelovac, Marina and Kotur, Nikola and Ristivojević, Bojan and Pavlović, Djordje and Spasovski, Vesna and Damjanov, Nemanja and Pavlović, Sonja and Zukić, Branka",
year = "2023",
abstract = "Systemic sclerosis (SSc) is a rare connective tissue disorder with highest morbidity and mortality among rheumatologic diseases. Disease progression is highly heterogeneous between patients, implying a strong need for individualization of therapy. Four pharmacogenetic variants, namely TPMT rs1800460, TPMT rs1142345, MTHFR rs1801133 and SLCO1B1 rs4149056 were tested for association with severe disease outcomes in 102 patients with SSc from Serbia treated either with immunosuppressants azathioprine (AZA) and methotrexate (MTX) or with other types of medications. Genotyping was performed using PCR-RFLP and direct Sanger sequencing. R software was used for statistical analysis and development of polygenic risk score (PRS) model. Association was found between MTHFR rs1801133 and higher risk for elevated systolic pressure in all patients except those prescribed with MTX, and higher risk for kidney insufficiency in patients prescribed with other types of drugs. In patients treated with MTX, variant SLCO1B1 rs4149056 was protective against kidney insufficiency. For patients receiving MTX a trend was shown for having a higher PRS rank and elevated systolic pressure. Our results open a door wide for more extensive research on pharmacogenomics markers in patients with SSc. Altogether, pharmacogenomics markers could predict the outcome of patients with SSc and help in prevention of adverse drug reactions.",
journal = "International Journal of Molecular Sciences, International Journal of Molecular Sciences",
title = "Can Pharmacogenetic Variants in TPMT, MTHFR and SLCO1B1 Genes Be Used as Potential Markers of Outcome Prediction in Systemic Sclerosis Patients?",
number = "10",
pages = "8538",
volume = "24",
doi = "10.3390/ijms24108538"
}

Jelovac, M., Kotur, N., Ristivojević, B., Pavlović, D., Spasovski, V., Damjanov, N., Pavlović, S.,& Zukić, B.. (2023). Can Pharmacogenetic Variants in TPMT, MTHFR and SLCO1B1 Genes Be Used as Potential Markers of Outcome Prediction in Systemic Sclerosis Patients?. in International Journal of Molecular Sciences, 24(10), 8538.
https://doi.org/10.3390/ijms24108538

Jelovac M, Kotur N, Ristivojević B, Pavlović D, Spasovski V, Damjanov N, Pavlović S, Zukić B. Can Pharmacogenetic Variants in TPMT, MTHFR and SLCO1B1 Genes Be Used as Potential Markers of Outcome Prediction in Systemic Sclerosis Patients?. in International Journal of Molecular Sciences. 2023;24(10):8538.
doi:10.3390/ijms24108538 .

Jelovac, Marina, Kotur, Nikola, Ristivojević, Bojan, Pavlović, Djordje, Spasovski, Vesna, Damjanov, Nemanja, Pavlović, Sonja, Zukić, Branka, "Can Pharmacogenetic Variants in TPMT, MTHFR and SLCO1B1 Genes Be Used as Potential Markers of Outcome Prediction in Systemic Sclerosis Patients?" in International Journal of Molecular Sciences, 24, no. 10 (2023):8538,
https://doi.org/10.3390/ijms24108538 . .

TY  - CONF
AU  - Jelovac, Marina
AU  - Kotur, Nikola
AU  - Ristivojević, Bojan
AU  - Pavlović, Đorđe
AU  - Spasovski, Vesna
AU  - Damjanov, Nemanja
AU  - Pavlović, Sonja
AU  - Zukić, Branka
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2119
AB  - Introduction: Systemic sclerosis(SSc) is a rare autoimmune disorder that affects connective tissues and
hasthe highest morbidity and mortality among rheumatologic diseases. Clinical presentations as well as
disease progression are highly heterogeneous between patients, implying a strong need for individualization of therapy.
Methods: Four pharmacogenetic variants, namely TPMT rs1800460, TPMT rs1142345, MTHFR rs1801133
and SLCO1B1 rs4149056 were tested for association with severe disease outcomes in 102 patients with
SSc from Serbia treated either with immunosuppressants azathioprine (AZA) and methotrexate (MTX) or
with other types of medications. Genotyping was performed using PCR-RFLP and direct Sanger sequencing. R software was used for statistical analysis and development of polygenic risk score (PRS)
model.
Results: Association wasfound between MTHFR rs1801133 and higher risk for elevated systolic pressure
in all patients except those prescribed with MTX, and higher risk for kidney insufficiency in patients prescribed with other types of drugs. In patients treated with MTX, variant SLCO1B1 rs4149056 was protective against kidney insufficiency. For patients receiving MTX a trend was shown for having a higher PRS
rank and elevated systolic pressure.
Conclusion: Our results open a door wide for more extensive research on pharmacogenomics markers
in patients with SSc. Altogether, pharmacogenomics markers could predict the outcome of patients with
SSc and help in prevention of adverse drug reactions
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Can pharmacogenetic variants in TPMT, MTHFR and SLCO1B1 genes be used as potential markers of outcome prediction in systemic sclerosis patients?
EP  - 64
SP  - 64
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2119
ER  - 

@conference{
author = "Jelovac, Marina and Kotur, Nikola and Ristivojević, Bojan and Pavlović, Đorđe and Spasovski, Vesna and Damjanov, Nemanja and Pavlović, Sonja and Zukić, Branka",
year = "2023",
abstract = "Introduction: Systemic sclerosis(SSc) is a rare autoimmune disorder that affects connective tissues and
hasthe highest morbidity and mortality among rheumatologic diseases. Clinical presentations as well as
disease progression are highly heterogeneous between patients, implying a strong need for individualization of therapy.
Methods: Four pharmacogenetic variants, namely TPMT rs1800460, TPMT rs1142345, MTHFR rs1801133
and SLCO1B1 rs4149056 were tested for association with severe disease outcomes in 102 patients with
SSc from Serbia treated either with immunosuppressants azathioprine (AZA) and methotrexate (MTX) or
with other types of medications. Genotyping was performed using PCR-RFLP and direct Sanger sequencing. R software was used for statistical analysis and development of polygenic risk score (PRS)
model.
Results: Association wasfound between MTHFR rs1801133 and higher risk for elevated systolic pressure
in all patients except those prescribed with MTX, and higher risk for kidney insufficiency in patients prescribed with other types of drugs. In patients treated with MTX, variant SLCO1B1 rs4149056 was protective against kidney insufficiency. For patients receiving MTX a trend was shown for having a higher PRS
rank and elevated systolic pressure.
Conclusion: Our results open a door wide for more extensive research on pharmacogenomics markers
in patients with SSc. Altogether, pharmacogenomics markers could predict the outcome of patients with
SSc and help in prevention of adverse drug reactions",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Can pharmacogenetic variants in TPMT, MTHFR and SLCO1B1 genes be used as potential markers of outcome prediction in systemic sclerosis patients?",
pages = "64-64",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2119"
}

Jelovac, M., Kotur, N., Ristivojević, B., Pavlović, Đ., Spasovski, V., Damjanov, N., Pavlović, S.,& Zukić, B.. (2023). Can pharmacogenetic variants in TPMT, MTHFR and SLCO1B1 genes be used as potential markers of outcome prediction in systemic sclerosis patients?. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 64-64.
https://hdl.handle.net/21.15107/rcub_imagine_2119

Jelovac M, Kotur N, Ristivojević B, Pavlović Đ, Spasovski V, Damjanov N, Pavlović S, Zukić B. Can pharmacogenetic variants in TPMT, MTHFR and SLCO1B1 genes be used as potential markers of outcome prediction in systemic sclerosis patients?. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:64-64.
https://hdl.handle.net/21.15107/rcub_imagine_2119 .

Jelovac, Marina, Kotur, Nikola, Ristivojević, Bojan, Pavlović, Đorđe, Spasovski, Vesna, Damjanov, Nemanja, Pavlović, Sonja, Zukić, Branka, "Can pharmacogenetic variants in TPMT, MTHFR and SLCO1B1 genes be used as potential markers of outcome prediction in systemic sclerosis patients?" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):64-64,
https://hdl.handle.net/21.15107/rcub_imagine_2119 .

TY  - JOUR
AU  - Colić, Jelena
AU  - Pruner, Iva
AU  - Damjanov, Nemanja
AU  - Pekmezović, Tatjana
AU  - Sefik-Bukilica, Mirjana
AU  - Antović, Aleksandra
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1534
AB  - J Rheumatol 2022; doi: 10.3899/jrheum.210931

In the Methods section, under the subheading “Follow-up and study outcome,” the last sentence should be as follows: “All new DUs were recorded by contacting all 39 patients once every 1–3 months during follow-up.” The error does not affect the results or conclusions of the study.

This correction only applies to the April 1 First Release. The correct text appears in the print and online issues.
PB  - J Rheumatol Publ Co, Toronto
T2  - Journal of Rheumatology
T1  - Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)
EP  - 440
IS  - 5
SP  - 440
VL  - 49
DO  - 10.3899/jrheum.210931.C1
ER  - 

@article{
author = "Colić, Jelena and Pruner, Iva and Damjanov, Nemanja and Pekmezović, Tatjana and Sefik-Bukilica, Mirjana and Antović, Aleksandra",
year = "2022",
abstract = "J Rheumatol 2022; doi: 10.3899/jrheum.210931

In the Methods section, under the subheading “Follow-up and study outcome,” the last sentence should be as follows: “All new DUs were recorded by contacting all 39 patients once every 1–3 months during follow-up.” The error does not affect the results or conclusions of the study.

This correction only applies to the April 1 First Release. The correct text appears in the print and online issues.",
publisher = "J Rheumatol Publ Co, Toronto",
journal = "Journal of Rheumatology",
title = "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)",
pages = "440-440",
number = "5",
volume = "49",
doi = "10.3899/jrheum.210931.C1"
}

Colić, J., Pruner, I., Damjanov, N., Pekmezović, T., Sefik-Bukilica, M.,& Antović, A.. (2022). Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022). in Journal of Rheumatology
J Rheumatol Publ Co, Toronto., 49(5), 440-440.
https://doi.org/10.3899/jrheum.210931.C1

Colić J, Pruner I, Damjanov N, Pekmezović T, Sefik-Bukilica M, Antović A. Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022). in Journal of Rheumatology. 2022;49(5):440-440.
doi:10.3899/jrheum.210931.C1 .

Colić, Jelena, Pruner, Iva, Damjanov, Nemanja, Pekmezović, Tatjana, Sefik-Bukilica, Mirjana, Antović, Aleksandra, "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)" in Journal of Rheumatology, 49, no. 5 (2022):440-440,
https://doi.org/10.3899/jrheum.210931.C1 . .

TY  - JOUR
AU  - Colić, Jelena
AU  - Pruner, Iva
AU  - Damjanov, Nemanja
AU  - Pekmezović, Tatjana
AU  - Sefik-Bukilica, Mirjana
AU  - Antović, Aleksandra
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1536
AB  - Objective. To assess thrombin generation, fibrin formation, and structure together with the fibrinolytic status in patients with systemic sclerosis (SSc) in relation to the occurrence of digital ulcers (DUs) during the course of disease. Methods. We studied variables of endothelial dysfunction, thrombin generation, overall hemostatic potential, and fibrin clot turbidity in plasma from 58 patients with SSc (39 with DU history and 19 DU-naive) and 46 matched healthy controls (HCs). Fibrin structure was visualized using scanning electron microscopy (SEM). Finally, 39 patients with a history of DUs were followed for 1.5 years and the predictive value of all investigated markers for new DU onset was explored. Results. Significantly enhanced endogenous thrombin potential (ETP) and prolonged clot lysis time (CLT) were found in patients with DUs compared to HCs. CLT was prolonged in patients with DUs compared to those without, showing good validity in identifying DUs with an area under the curve of 0.7 (95% CI 0.6-0.8). The levels of ETP and intercellular adhesion molecule 1 were independently associated with CLT. Over the follow-up period, 20 patients developed new DUs. CLT was prolonged (P  lt  0.001) in patients with new DU episodes, especially those with recurrent DUs. Regression analysis showed that the Raynaud phenomenon visual analog scale and CLT were predictors of new DUs (OR 1.1, 95% CI 1.0-1.1 and OR 1.2, 95% CI 1.1-1.3, respectively). SEM confirmed denser fibrin clots in patients with new DUs. Conclusion. Our results suggest that impaired fibrinolysis might have an emerging role in underlying digital vasculopathy and its progression in SSc.
PB  - Toronto : J Rheumatol Publ Co.
T2  - Journal of Rheumatology
T1  - Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis
EP  - 606
IS  - 6
SP  - 598
VL  - 49
DO  - 10.3899/jrheum.210931
ER  - 

@article{
author = "Colić, Jelena and Pruner, Iva and Damjanov, Nemanja and Pekmezović, Tatjana and Sefik-Bukilica, Mirjana and Antović, Aleksandra",
year = "2022",
abstract = "Objective. To assess thrombin generation, fibrin formation, and structure together with the fibrinolytic status in patients with systemic sclerosis (SSc) in relation to the occurrence of digital ulcers (DUs) during the course of disease. Methods. We studied variables of endothelial dysfunction, thrombin generation, overall hemostatic potential, and fibrin clot turbidity in plasma from 58 patients with SSc (39 with DU history and 19 DU-naive) and 46 matched healthy controls (HCs). Fibrin structure was visualized using scanning electron microscopy (SEM). Finally, 39 patients with a history of DUs were followed for 1.5 years and the predictive value of all investigated markers for new DU onset was explored. Results. Significantly enhanced endogenous thrombin potential (ETP) and prolonged clot lysis time (CLT) were found in patients with DUs compared to HCs. CLT was prolonged in patients with DUs compared to those without, showing good validity in identifying DUs with an area under the curve of 0.7 (95% CI 0.6-0.8). The levels of ETP and intercellular adhesion molecule 1 were independently associated with CLT. Over the follow-up period, 20 patients developed new DUs. CLT was prolonged (P  lt  0.001) in patients with new DU episodes, especially those with recurrent DUs. Regression analysis showed that the Raynaud phenomenon visual analog scale and CLT were predictors of new DUs (OR 1.1, 95% CI 1.0-1.1 and OR 1.2, 95% CI 1.1-1.3, respectively). SEM confirmed denser fibrin clots in patients with new DUs. Conclusion. Our results suggest that impaired fibrinolysis might have an emerging role in underlying digital vasculopathy and its progression in SSc.",
publisher = "Toronto : J Rheumatol Publ Co.",
journal = "Journal of Rheumatology",
title = "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis",
pages = "606-598",
number = "6",
volume = "49",
doi = "10.3899/jrheum.210931"
}

Colić, J., Pruner, I., Damjanov, N., Pekmezović, T., Sefik-Bukilica, M.,& Antović, A.. (2022). Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis. in Journal of Rheumatology
Toronto : J Rheumatol Publ Co.., 49(6), 598-606.
https://doi.org/10.3899/jrheum.210931

Colić J, Pruner I, Damjanov N, Pekmezović T, Sefik-Bukilica M, Antović A. Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis. in Journal of Rheumatology. 2022;49(6):598-606.
doi:10.3899/jrheum.210931 .

Colić, Jelena, Pruner, Iva, Damjanov, Nemanja, Pekmezović, Tatjana, Sefik-Bukilica, Mirjana, Antović, Aleksandra, "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis" in Journal of Rheumatology, 49, no. 6 (2022):598-606,
https://doi.org/10.3899/jrheum.210931 . .

TY  - CONF
AU  - Zeković, Ana
AU  - Vreca, Misa
AU  - Spasovski, Vesna
AU  - Skodrić-Trifunović, Vesna
AU  - Marković-Denić, Ljiljana
AU  - Anđelković, Marina
AU  - Pavlović, Sonja
AU  - Damjanov, Nemanja
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1262
PB  - BMJ Publishing Group, London
C3  - Annals of the Rheumatic Diseases
T1  - Relationship between interleukin-23 and gastrointestinal involvement in patients with systemic sclerosis
EP  - 1229
SP  - 1228
VL  - 78
DO  - 10.1136/annrheumdis-2019-eular.2289
ER  - 

@conference{
author = "Zeković, Ana and Vreca, Misa and Spasovski, Vesna and Skodrić-Trifunović, Vesna and Marković-Denić, Ljiljana and Anđelković, Marina and Pavlović, Sonja and Damjanov, Nemanja",
year = "2019",
publisher = "BMJ Publishing Group, London",
journal = "Annals of the Rheumatic Diseases",
title = "Relationship between interleukin-23 and gastrointestinal involvement in patients with systemic sclerosis",
pages = "1229-1228",
volume = "78",
doi = "10.1136/annrheumdis-2019-eular.2289"
}

Zeković, A., Vreca, M., Spasovski, V., Skodrić-Trifunović, V., Marković-Denić, L., Anđelković, M., Pavlović, S.,& Damjanov, N.. (2019). Relationship between interleukin-23 and gastrointestinal involvement in patients with systemic sclerosis. in Annals of the Rheumatic Diseases
BMJ Publishing Group, London., 78, 1228-1229.
https://doi.org/10.1136/annrheumdis-2019-eular.2289

Zeković A, Vreca M, Spasovski V, Skodrić-Trifunović V, Marković-Denić L, Anđelković M, Pavlović S, Damjanov N. Relationship between interleukin-23 and gastrointestinal involvement in patients with systemic sclerosis. in Annals of the Rheumatic Diseases. 2019;78:1228-1229.
doi:10.1136/annrheumdis-2019-eular.2289 .

Zeković, Ana, Vreca, Misa, Spasovski, Vesna, Skodrić-Trifunović, Vesna, Marković-Denić, Ljiljana, Anđelković, Marina, Pavlović, Sonja, Damjanov, Nemanja, "Relationship between interleukin-23 and gastrointestinal involvement in patients with systemic sclerosis" in Annals of the Rheumatic Diseases, 78 (2019):1228-1229,
https://doi.org/10.1136/annrheumdis-2019-eular.2289 . .

TY  - JOUR
AU  - Vreca, Misa
AU  - Anđelković, Marina
AU  - Tošić, Nataša
AU  - Zeković, Ana
AU  - Damjanov, Nemanja
AU  - Pavlović, Sonja
AU  - Spasovski, Vesna
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1135
AB  - Systemic sclerosis (SSc) is a heterogeneous multisystem autoimmune disease with unknown etiology. Numerous studies have indicated that the disease heterogeneity implies various genetic abnormalities. Considering that SSc is characterized by a strong sex bias and that the position of IRAK1 gene is on the X chromosome, we assume that variations in IRAK1 gene could explain female predominance of SSc. It was previously described that miR-146a has a role in 'fine-tuning' regulation of the TLR/NF-kB signaling pathway through down-regulation of IRAK1 gene. The aim of the present study was to analyze both variants and expression level of IRAK1 and miR-146a genes in terms of susceptibility to SSc and clinical presentation of SSc patients. We analyzed variants IRAK1 rs3027898 C  gt  A and miR-146a rs2910164 C  gt  G in 102 SSc patients and 66 healthy subjects. Genotyping was performed by Sanger sequencing. Expression level of IRAK1 mRNA and miR-146a in PBMCs was performed in subset of 50 patients and 13 healthy controls by RT-qPCR. Our results showed that there was no association between IRAK1 rs3027898 and the risk of SSc in women. However, the analysis of genotype distribution of the mir-146a rs2910164 C  gt  G variant indicated that CC genotype shows strong association with lung fibrosis and active form of the disease. When expression level of IRAK1 gene was analyzed, we detected significant downregulation of IRAK1 mRNA in SSc patients compared to controls, as well as in male compared to female patients, in patients with ACAS autoantibodies and in patients with severe skin involvement. Regarding the expression level of miR-146a, we have found significantly reduced expression in SSc patients, in patients with skin involvement and in male SSc patients. The results from this study indicate that expression of IRAK1 gene could explain phenotypic heterogeneity of SSc and may be involved in the pathogenesis of SSc due to its differential expression in certain subgroups. Our results also suggested that miR-146a rs2910164 CC genotype may be predisposing factor for development lung fibrosis and more progressive form of SSc. Results from relative expression analysis of miR-146a demonstrated that changes in the level of this miRNA may have an impact on development and clinical course of SSc.
PB  - Elsevier Science Bv, Amsterdam
T2  - Immunology Letters
T1  - Impact of alterations in X-linked IRAK1gene and miR-146a on susceptibility and clinical manifestations in patients with systemic sclerosis
EP  - 8
SP  - 1
VL  - 204
DO  - 10.1016/j.imlet.2018.10.002
ER  - 

@article{
author = "Vreca, Misa and Anđelković, Marina and Tošić, Nataša and Zeković, Ana and Damjanov, Nemanja and Pavlović, Sonja and Spasovski, Vesna",
year = "2018",
abstract = "Systemic sclerosis (SSc) is a heterogeneous multisystem autoimmune disease with unknown etiology. Numerous studies have indicated that the disease heterogeneity implies various genetic abnormalities. Considering that SSc is characterized by a strong sex bias and that the position of IRAK1 gene is on the X chromosome, we assume that variations in IRAK1 gene could explain female predominance of SSc. It was previously described that miR-146a has a role in 'fine-tuning' regulation of the TLR/NF-kB signaling pathway through down-regulation of IRAK1 gene. The aim of the present study was to analyze both variants and expression level of IRAK1 and miR-146a genes in terms of susceptibility to SSc and clinical presentation of SSc patients. We analyzed variants IRAK1 rs3027898 C  gt  A and miR-146a rs2910164 C  gt  G in 102 SSc patients and 66 healthy subjects. Genotyping was performed by Sanger sequencing. Expression level of IRAK1 mRNA and miR-146a in PBMCs was performed in subset of 50 patients and 13 healthy controls by RT-qPCR. Our results showed that there was no association between IRAK1 rs3027898 and the risk of SSc in women. However, the analysis of genotype distribution of the mir-146a rs2910164 C  gt  G variant indicated that CC genotype shows strong association with lung fibrosis and active form of the disease. When expression level of IRAK1 gene was analyzed, we detected significant downregulation of IRAK1 mRNA in SSc patients compared to controls, as well as in male compared to female patients, in patients with ACAS autoantibodies and in patients with severe skin involvement. Regarding the expression level of miR-146a, we have found significantly reduced expression in SSc patients, in patients with skin involvement and in male SSc patients. The results from this study indicate that expression of IRAK1 gene could explain phenotypic heterogeneity of SSc and may be involved in the pathogenesis of SSc due to its differential expression in certain subgroups. Our results also suggested that miR-146a rs2910164 CC genotype may be predisposing factor for development lung fibrosis and more progressive form of SSc. Results from relative expression analysis of miR-146a demonstrated that changes in the level of this miRNA may have an impact on development and clinical course of SSc.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Immunology Letters",
title = "Impact of alterations in X-linked IRAK1gene and miR-146a on susceptibility and clinical manifestations in patients with systemic sclerosis",
pages = "8-1",
volume = "204",
doi = "10.1016/j.imlet.2018.10.002"
}

Vreca, M., Anđelković, M., Tošić, N., Zeković, A., Damjanov, N., Pavlović, S.,& Spasovski, V.. (2018). Impact of alterations in X-linked IRAK1gene and miR-146a on susceptibility and clinical manifestations in patients with systemic sclerosis. in Immunology Letters
Elsevier Science Bv, Amsterdam., 204, 1-8.
https://doi.org/10.1016/j.imlet.2018.10.002

Vreca M, Anđelković M, Tošić N, Zeković A, Damjanov N, Pavlović S, Spasovski V. Impact of alterations in X-linked IRAK1gene and miR-146a on susceptibility and clinical manifestations in patients with systemic sclerosis. in Immunology Letters. 2018;204:1-8.
doi:10.1016/j.imlet.2018.10.002 .

Vreca, Misa, Anđelković, Marina, Tošić, Nataša, Zeković, Ana, Damjanov, Nemanja, Pavlović, Sonja, Spasovski, Vesna, "Impact of alterations in X-linked IRAK1gene and miR-146a on susceptibility and clinical manifestations in patients with systemic sclerosis" in Immunology Letters, 204 (2018):1-8,
https://doi.org/10.1016/j.imlet.2018.10.002 . .

TY  - JOUR
AU  - Vreca, Misa
AU  - Zeković, Ana
AU  - Damjanov, Nemanja
AU  - Anđelković, Marina
AU  - Ugrin, Milena
AU  - Pavlović, Sonja
AU  - Spasovski, Vesna
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1194
AB  - Systemic sclerosis (SSc) is a rare, chronic, multisystem autoimmune disease clinically characterized by progressive fibrosis of the skin and internal organs. The basic mechanism appears to involve endothelial cell injury, overproduction of extracellular matrix proteins, and aberrant immune activation. So far, there have been a few attempts to find genetic biomarkers for monitoring disease activity or for correlation with certain symptoms. In order to reveal reliable biomarkers, we analyzed the expression of four genes representing three important signaling pathways, TLR7, TLR9, and JAK2-STAT3. Using RT-qPCR technique, we analyzed the expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells of 50 SSc patients and 13 healthy individuals. We detected significant upregulation of TLR7 gene expression in a group of SSc patients compared to non-SSc group. Receiver operating characteristic (ROC) analysis showed that TLR7 expression efficiently discriminates SSc cases from healthy individuals. High TLR7 expression positively correlated with the late form of disease, active SSc, and the presence of digital ulcers. Decreased levels of TLR9 and JAK2 mRNA were found in the patient's cohort in comparison to non-SSc individuals, but showed no correlation with specific clinical outcomes. The expression level of the STAT3 gene did not differ between the analyzed groups. This is the first study on the expression of TLR7, TLR9, and STAT3 genes in SSc patients. Our results show that TLR7, TLR9, and JAK2 genes are potential biomarkers for SSc. The results obtained in this study could contribute to better classification, monitoring, and outcome prediction of patients with SSc based on genetics.
PB  - Springer Heidelberg, Heidelberg
T2  - Journal of Applied Genetics
T1  - Expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells from patients with systemic sclerosis
EP  - 66
IS  - 1
SP  - 59
VL  - 59
DO  - 10.1007/s13353-017-0415-4
ER  - 

@article{
author = "Vreca, Misa and Zeković, Ana and Damjanov, Nemanja and Anđelković, Marina and Ugrin, Milena and Pavlović, Sonja and Spasovski, Vesna",
year = "2018",
abstract = "Systemic sclerosis (SSc) is a rare, chronic, multisystem autoimmune disease clinically characterized by progressive fibrosis of the skin and internal organs. The basic mechanism appears to involve endothelial cell injury, overproduction of extracellular matrix proteins, and aberrant immune activation. So far, there have been a few attempts to find genetic biomarkers for monitoring disease activity or for correlation with certain symptoms. In order to reveal reliable biomarkers, we analyzed the expression of four genes representing three important signaling pathways, TLR7, TLR9, and JAK2-STAT3. Using RT-qPCR technique, we analyzed the expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells of 50 SSc patients and 13 healthy individuals. We detected significant upregulation of TLR7 gene expression in a group of SSc patients compared to non-SSc group. Receiver operating characteristic (ROC) analysis showed that TLR7 expression efficiently discriminates SSc cases from healthy individuals. High TLR7 expression positively correlated with the late form of disease, active SSc, and the presence of digital ulcers. Decreased levels of TLR9 and JAK2 mRNA were found in the patient's cohort in comparison to non-SSc individuals, but showed no correlation with specific clinical outcomes. The expression level of the STAT3 gene did not differ between the analyzed groups. This is the first study on the expression of TLR7, TLR9, and STAT3 genes in SSc patients. Our results show that TLR7, TLR9, and JAK2 genes are potential biomarkers for SSc. The results obtained in this study could contribute to better classification, monitoring, and outcome prediction of patients with SSc based on genetics.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "Journal of Applied Genetics",
title = "Expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells from patients with systemic sclerosis",
pages = "66-59",
number = "1",
volume = "59",
doi = "10.1007/s13353-017-0415-4"
}

Vreca, M., Zeković, A., Damjanov, N., Anđelković, M., Ugrin, M., Pavlović, S.,& Spasovski, V.. (2018). Expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells from patients with systemic sclerosis. in Journal of Applied Genetics
Springer Heidelberg, Heidelberg., 59(1), 59-66.
https://doi.org/10.1007/s13353-017-0415-4

Vreca M, Zeković A, Damjanov N, Anđelković M, Ugrin M, Pavlović S, Spasovski V. Expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells from patients with systemic sclerosis. in Journal of Applied Genetics. 2018;59(1):59-66.
doi:10.1007/s13353-017-0415-4 .

Vreca, Misa, Zeković, Ana, Damjanov, Nemanja, Anđelković, Marina, Ugrin, Milena, Pavlović, Sonja, Spasovski, Vesna, "Expression of TLR7, TLR9, JAK2, and STAT3 genes in peripheral blood mononuclear cells from patients with systemic sclerosis" in Journal of Applied Genetics, 59, no. 1 (2018):59-66,
https://doi.org/10.1007/s13353-017-0415-4 . .

TY  - JOUR
AU  - Zeković, Ana
AU  - Vreca, Misa
AU  - Spasovski, Vesna
AU  - Anđelković, Marina
AU  - Pavlović, Sonja
AU  - Damjanov, Nemanja
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1102
AB  - Genetic predisposition to systemic sclerosis (SSc) has still not been fully revealed. Interleukin-6 (IL-6) is a mediator of T cell proliferation and fibrotic events in SSc. Polymorphisms in the IL-6 are found to be important in susceptibility to development of SSc. We aimed to assess the frequency of -174 C/G of IL-6 gene polymorphism in SSc patients and healthy controls, as well as correlation with disease manifestations. In the case-control study, 102 patients with SSc and 93 controls were included. PCR-RFLP method was performed for genotyping promotor variants -174 C/G of IL-6 gene. The expression level of IL-6 was determined by qRT-PCR on subset of 50 patients and 13 healthy controls with different IL-6 genotypes. We used UCLA GIT 2.0 questionnaire to assess gastrointestinal involvement in SSc patients. The expression level of IL-6 gene was significantly higher in patients with SSc in comparison with healthy controls (p  lt  0.05). Carriers of C-allele of IL-6 gene compared to those with G allele, showed higher expression of IL-6 gene (95.8 vs. 41.2, p  lt  0.05), higher GIT total score (0.85 vs. 0.5, p  lt  0.05) and higher distension scale score (1.4 +/- 0.9 vs. 0.78 +/- 0.8, p = 0.05). No significant differences in genotype distribution and allele frequency were observed between patients and controls. The expression of IL6 gene varies significantly during the course of SSc. The IL-6 gene variant -174 C/G (presence of C-allele) is associated with higher IL-6 gene expression and greater GIT impairment in patients with SSc.
PB  - Springer London Ltd, London
T2  - Clinical Rheumatology
T1  - Association between the-174 C/G polymorphism in the interleukin-6 (IL-6) gene and gastrointestinal involvement in patients with systemic sclerosis
EP  - 2454
IS  - 9
SP  - 2447
VL  - 37
DO  - 10.1007/s10067-018-4163-6
ER  - 

@article{
author = "Zeković, Ana and Vreca, Misa and Spasovski, Vesna and Anđelković, Marina and Pavlović, Sonja and Damjanov, Nemanja",
year = "2018",
abstract = "Genetic predisposition to systemic sclerosis (SSc) has still not been fully revealed. Interleukin-6 (IL-6) is a mediator of T cell proliferation and fibrotic events in SSc. Polymorphisms in the IL-6 are found to be important in susceptibility to development of SSc. We aimed to assess the frequency of -174 C/G of IL-6 gene polymorphism in SSc patients and healthy controls, as well as correlation with disease manifestations. In the case-control study, 102 patients with SSc and 93 controls were included. PCR-RFLP method was performed for genotyping promotor variants -174 C/G of IL-6 gene. The expression level of IL-6 was determined by qRT-PCR on subset of 50 patients and 13 healthy controls with different IL-6 genotypes. We used UCLA GIT 2.0 questionnaire to assess gastrointestinal involvement in SSc patients. The expression level of IL-6 gene was significantly higher in patients with SSc in comparison with healthy controls (p  lt  0.05). Carriers of C-allele of IL-6 gene compared to those with G allele, showed higher expression of IL-6 gene (95.8 vs. 41.2, p  lt  0.05), higher GIT total score (0.85 vs. 0.5, p  lt  0.05) and higher distension scale score (1.4 +/- 0.9 vs. 0.78 +/- 0.8, p = 0.05). No significant differences in genotype distribution and allele frequency were observed between patients and controls. The expression of IL6 gene varies significantly during the course of SSc. The IL-6 gene variant -174 C/G (presence of C-allele) is associated with higher IL-6 gene expression and greater GIT impairment in patients with SSc.",
publisher = "Springer London Ltd, London",
journal = "Clinical Rheumatology",
title = "Association between the-174 C/G polymorphism in the interleukin-6 (IL-6) gene and gastrointestinal involvement in patients with systemic sclerosis",
pages = "2454-2447",
number = "9",
volume = "37",
doi = "10.1007/s10067-018-4163-6"
}

Zeković, A., Vreca, M., Spasovski, V., Anđelković, M., Pavlović, S.,& Damjanov, N.. (2018). Association between the-174 C/G polymorphism in the interleukin-6 (IL-6) gene and gastrointestinal involvement in patients with systemic sclerosis. in Clinical Rheumatology
Springer London Ltd, London., 37(9), 2447-2454.
https://doi.org/10.1007/s10067-018-4163-6

Zeković A, Vreca M, Spasovski V, Anđelković M, Pavlović S, Damjanov N. Association between the-174 C/G polymorphism in the interleukin-6 (IL-6) gene and gastrointestinal involvement in patients with systemic sclerosis. in Clinical Rheumatology. 2018;37(9):2447-2454.
doi:10.1007/s10067-018-4163-6 .

Zeković, Ana, Vreca, Misa, Spasovski, Vesna, Anđelković, Marina, Pavlović, Sonja, Damjanov, Nemanja, "Association between the-174 C/G polymorphism in the interleukin-6 (IL-6) gene and gastrointestinal involvement in patients with systemic sclerosis" in Clinical Rheumatology, 37, no. 9 (2018):2447-2454,
https://doi.org/10.1007/s10067-018-4163-6 . .

TY  - JOUR
AU  - Jančić, Ivan
AU  - Šefik-Bukilica, Mirjana
AU  - Živojinović, Slađana
AU  - Damjanov, Nemanja
AU  - Spasovski, Vesna
AU  - Kotur, Nikola
AU  - Karan-Đurašević, Teodora
AU  - Pavlović, Sonja
AU  - Bufan, Biljana
AU  - Arsenović-Ranin, Nevena
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/837
AB  - Uvod: Genetički faktori su značajni za predviđanje ishoda lečenja bolesnika sa reumatoidnim artritisom (RA). Cilj studije bio je da se ispita uticaj-308G/A TNF-α (rs 1800629) i -174G/C IL-6 (rs1800795) promotorskih polimorfizama na terapijski odgovor na etanercept. Metode: U studiju su bila uključena 73 pacijenta sa aktivnim RA. Terapijski odgovor je procenjivan posle 6 i 12 meseci terapije po kriterijumima Evropske lige protiv reumatizma. Genotipizacija pacijenata za polimorfizme -308G/A TNF-α i -174G/C IL-6 urađena je PCR-RFLP metodom i procenjivan je uticaj genotipova na odgovor na etanercept. Rezultati: Nije bilo razlike u procentu respondera (pacijenti kod kojih se DAS28 popravio  gt  1,2) između pacijenata sa TNF-α -308GG, GA i AA genotipom ni posle 6 ni posle 12 meseci tretmana. Posle 12 meseci lečenja procenat respondera je bio značajno veći kod pacijenata sa IL-6 -174GG u odnosu na pacijente sa GC ili CC genotipom (p= 0,006, x2 test). Poređenje pacijenata prema kombinovanim IL-6/TNF-α genotipovima pokazalo je da je IL-6 -174GG / TNF-α -308GG genotip učestaliji kod respondera u odnosu na druge kombinovane genotipove (p= 0.022, x2 test). Tačnije, svi pacijenti sa kombinovanim IL-6 -174GG / TNF-α -308GG genotipom bili su responderi posle 12 meseci terapije etanerceptom. Zaključak: Studija pokazuje da bolesnici sa genotipovima koji se povezuju sa manjom produkcijom TNF-α i IL-6 najbolje odgovaraju na terapiju etanerceptom.
AB  - Background: The study was undertaken to assess the influence of functional -308G /A TNF-α (rs 1800629) and -174G/C IL-6 (rs1800795) promoter polymorphisms on the therapeutic response to etanercept, a TNF-α blocker, in patients with rheumatoid arthritis (RA). Methods: Seventy-three patients suffering from active RA were studied, at baseline and 6 and 12 months after therapy. The therapeutic response was estimated according to the European League Against Rheumatism response criteria. Patients were genotyped for -308G /A TNF-α and -174G/C IL-6 polymorphisms by the PCR-RFLP method, and the influence of genotype on etanercept response was assessed. Results: No difference in the percentage of responders (patients who had DAS28 improvement  gt  1.2) between patients with the TNF-α -308GG and GA and AA genotype was detected after 6 and 12 months of treatment. After 12 months of treatment the percentage of responders was significantly increased in patients with the IL-6 -174GG genotype compared with those with the GC or CC genotype (p=0.006 by Chi-square test). Evaluation of the patients according to their combined IL-6/TNF-α genotypes showed that patients with the IL-6 -174GG / TNF-α -308GG genotype were more frequent among the responders compared to those with other combined genotypes (p=0.022 by Chisquare test). More precisely, all patients with the combined IL-6 -174GG / TNF-α -308GG genotype were responders after 12 months of etanercept treatment. Conclusions: The study suggests that patients who are genetically low TNF-α and IL-6 producers are the best responders to etanercept therapy.
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu
T1  - Influence of promoter polymorphisms of the TNF-α (-308G/A) and IL-6 (-174G/C) genes on therapeutic response to etanercept in rheumatoid arthritis
EP  - 421
IS  - 4
SP  - 414
VL  - 34
DO  - 10.2478/jomb-2014-0060
ER  - 

@article{
author = "Jančić, Ivan and Šefik-Bukilica, Mirjana and Živojinović, Slađana and Damjanov, Nemanja and Spasovski, Vesna and Kotur, Nikola and Karan-Đurašević, Teodora and Pavlović, Sonja and Bufan, Biljana and Arsenović-Ranin, Nevena",
year = "2015",
abstract = "Uvod: Genetički faktori su značajni za predviđanje ishoda lečenja bolesnika sa reumatoidnim artritisom (RA). Cilj studije bio je da se ispita uticaj-308G/A TNF-α (rs 1800629) i -174G/C IL-6 (rs1800795) promotorskih polimorfizama na terapijski odgovor na etanercept. Metode: U studiju su bila uključena 73 pacijenta sa aktivnim RA. Terapijski odgovor je procenjivan posle 6 i 12 meseci terapije po kriterijumima Evropske lige protiv reumatizma. Genotipizacija pacijenata za polimorfizme -308G/A TNF-α i -174G/C IL-6 urađena je PCR-RFLP metodom i procenjivan je uticaj genotipova na odgovor na etanercept. Rezultati: Nije bilo razlike u procentu respondera (pacijenti kod kojih se DAS28 popravio  gt  1,2) između pacijenata sa TNF-α -308GG, GA i AA genotipom ni posle 6 ni posle 12 meseci tretmana. Posle 12 meseci lečenja procenat respondera je bio značajno veći kod pacijenata sa IL-6 -174GG u odnosu na pacijente sa GC ili CC genotipom (p= 0,006, x2 test). Poređenje pacijenata prema kombinovanim IL-6/TNF-α genotipovima pokazalo je da je IL-6 -174GG / TNF-α -308GG genotip učestaliji kod respondera u odnosu na druge kombinovane genotipove (p= 0.022, x2 test). Tačnije, svi pacijenti sa kombinovanim IL-6 -174GG / TNF-α -308GG genotipom bili su responderi posle 12 meseci terapije etanerceptom. Zaključak: Studija pokazuje da bolesnici sa genotipovima koji se povezuju sa manjom produkcijom TNF-α i IL-6 najbolje odgovaraju na terapiju etanerceptom., Background: The study was undertaken to assess the influence of functional -308G /A TNF-α (rs 1800629) and -174G/C IL-6 (rs1800795) promoter polymorphisms on the therapeutic response to etanercept, a TNF-α blocker, in patients with rheumatoid arthritis (RA). Methods: Seventy-three patients suffering from active RA were studied, at baseline and 6 and 12 months after therapy. The therapeutic response was estimated according to the European League Against Rheumatism response criteria. Patients were genotyped for -308G /A TNF-α and -174G/C IL-6 polymorphisms by the PCR-RFLP method, and the influence of genotype on etanercept response was assessed. Results: No difference in the percentage of responders (patients who had DAS28 improvement  gt  1.2) between patients with the TNF-α -308GG and GA and AA genotype was detected after 6 and 12 months of treatment. After 12 months of treatment the percentage of responders was significantly increased in patients with the IL-6 -174GG genotype compared with those with the GC or CC genotype (p=0.006 by Chi-square test). Evaluation of the patients according to their combined IL-6/TNF-α genotypes showed that patients with the IL-6 -174GG / TNF-α -308GG genotype were more frequent among the responders compared to those with other combined genotypes (p=0.022 by Chisquare test). More precisely, all patients with the combined IL-6 -174GG / TNF-α -308GG genotype were responders after 12 months of etanercept treatment. Conclusions: The study suggests that patients who are genetically low TNF-α and IL-6 producers are the best responders to etanercept therapy.",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu, Influence of promoter polymorphisms of the TNF-α (-308G/A) and IL-6 (-174G/C) genes on therapeutic response to etanercept in rheumatoid arthritis",
pages = "421-414",
number = "4",
volume = "34",
doi = "10.2478/jomb-2014-0060"
}

Jančić, I., Šefik-Bukilica, M., Živojinović, S., Damjanov, N., Spasovski, V., Kotur, N., Karan-Đurašević, T., Pavlović, S., Bufan, B.,& Arsenović-Ranin, N.. (2015). Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 34(4), 414-421.
https://doi.org/10.2478/jomb-2014-0060

Jančić I, Šefik-Bukilica M, Živojinović S, Damjanov N, Spasovski V, Kotur N, Karan-Đurašević T, Pavlović S, Bufan B, Arsenović-Ranin N. Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu. in Journal of Medical Biochemistry. 2015;34(4):414-421.
doi:10.2478/jomb-2014-0060 .

Jančić, Ivan, Šefik-Bukilica, Mirjana, Živojinović, Slađana, Damjanov, Nemanja, Spasovski, Vesna, Kotur, Nikola, Karan-Đurašević, Teodora, Pavlović, Sonja, Bufan, Biljana, Arsenović-Ranin, Nevena, "Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu" in Journal of Medical Biochemistry, 34, no. 4 (2015):414-421,
https://doi.org/10.2478/jomb-2014-0060 . .

TY  - JOUR
AU  - Jancić, Ivan
AU  - Arsenović-Ranin, Nevena
AU  - Sefik-Bukilica, Mirjana
AU  - Živojinović, Slađana
AU  - Damjanov, Nemanja
AU  - Spasovski, Vesna
AU  - Srzentić Dražilov, Sanja
AU  - Stanković, Biljana
AU  - Pavlović, Sonja
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/645
AB  - To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement  gt  1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-alpha) blockers in RA.
PB  - Springer Heidelberg, Heidelberg
T2  - Rheumatology International
T1  - -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis
EP  - 1486
IS  - 6
SP  - 1481
VL  - 33
DO  - 10.1007/s00296-012-2586-y
ER  - 

@article{
author = "Jancić, Ivan and Arsenović-Ranin, Nevena and Sefik-Bukilica, Mirjana and Živojinović, Slađana and Damjanov, Nemanja and Spasovski, Vesna and Srzentić Dražilov, Sanja and Stanković, Biljana and Pavlović, Sonja",
year = "2013",
abstract = "To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement  gt  1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-alpha) blockers in RA.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "Rheumatology International",
title = "-174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis",
pages = "1486-1481",
number = "6",
volume = "33",
doi = "10.1007/s00296-012-2586-y"
}

Jancić, I., Arsenović-Ranin, N., Sefik-Bukilica, M., Živojinović, S., Damjanov, N., Spasovski, V., Srzentić Dražilov, S., Stanković, B.,& Pavlović, S.. (2013). -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis. in Rheumatology International
Springer Heidelberg, Heidelberg., 33(6), 1481-1486.
https://doi.org/10.1007/s00296-012-2586-y

Jancić I, Arsenović-Ranin N, Sefik-Bukilica M, Živojinović S, Damjanov N, Spasovski V, Srzentić Dražilov S, Stanković B, Pavlović S. -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis. in Rheumatology International. 2013;33(6):1481-1486.
doi:10.1007/s00296-012-2586-y .

Jancić, Ivan, Arsenović-Ranin, Nevena, Sefik-Bukilica, Mirjana, Živojinović, Slađana, Damjanov, Nemanja, Spasovski, Vesna, Srzentić Dražilov, Sanja, Stanković, Biljana, Pavlović, Sonja, "-174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis" in Rheumatology International, 33, no. 6 (2013):1481-1486,
https://doi.org/10.1007/s00296-012-2586-y . .