TY  - JOUR
AU  - Vejnović, Dubravka
AU  - Milić, Vera
AU  - Popović, Branka
AU  - Damnjanović, Tatjana
AU  - Maksimović, Nela
AU  - Bunjevački, Vera
AU  - Krajinović, Maja
AU  - Novaković, Ivana
AU  - Damjanov, Nemanja
AU  - Jekić, Biljana
PY  - 2019
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/2526
AB  - Background: Methotrexate (MTX), a folate analogue, is the most commonly used disease-modifying drug in the treatment of rheumatoid arthritis (RA). However, high interindividual differences in drug response are present among RA patients.Research design and methods: In a group of 234 RA patients treated with MTX, we investigated whether rs1650697 polymorphism in DHFR gene may have an impact on MTX efficacy and/or adverse drug effects (ADEs). Relative DAS28 values (rDAS28) were used for the estimation of MTX therapy and all ADEs were recorded. Patients were genotyped for selected polymorphism by real-time PCR method. Results: According to the European League Against Rheumatism criteria after 6 months of MTX therapy, 196 patients (83.8%) were classified as responders (25 (10.7%) were good and 171 (73.1%) were moderate) and 38 patients (16.2%) as nonresponders. ADEs were observed in 55 patients (23.5%). Conclusions: Our results showed that the presence of T allele might be protective against MTX hepatotoxicity measured by transaminase levels (p = 0.05). Furthermore, among patients who also received low-dose corticosteroids, we have found a lower rDAS value in patients with CC genotype (p = 0.039).
PB  - Taylor & Francis Ltd, Abingdon
T2  - Expert Opinion on Drug Metabolism & Toxicology
T1  - Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients
VL  - 15
IS  - 3
SP  - 253
EP  - 257
DO  - 10.1080/17425255.2019.1563594
ER  - 

@article{
author = "Vejnović, Dubravka and Milić, Vera and Popović, Branka and Damnjanović, Tatjana and Maksimović, Nela and Bunjevački, Vera and Krajinović, Maja and Novaković, Ivana and Damjanov, Nemanja and Jekić, Biljana",
year = "2019",
abstract = "Background: Methotrexate (MTX), a folate analogue, is the most commonly used disease-modifying drug in the treatment of rheumatoid arthritis (RA). However, high interindividual differences in drug response are present among RA patients.Research design and methods: In a group of 234 RA patients treated with MTX, we investigated whether rs1650697 polymorphism in DHFR gene may have an impact on MTX efficacy and/or adverse drug effects (ADEs). Relative DAS28 values (rDAS28) were used for the estimation of MTX therapy and all ADEs were recorded. Patients were genotyped for selected polymorphism by real-time PCR method. Results: According to the European League Against Rheumatism criteria after 6 months of MTX therapy, 196 patients (83.8%) were classified as responders (25 (10.7%) were good and 171 (73.1%) were moderate) and 38 patients (16.2%) as nonresponders. ADEs were observed in 55 patients (23.5%). Conclusions: Our results showed that the presence of T allele might be protective against MTX hepatotoxicity measured by transaminase levels (p = 0.05). Furthermore, among patients who also received low-dose corticosteroids, we have found a lower rDAS value in patients with CC genotype (p = 0.039).",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "Expert Opinion on Drug Metabolism & Toxicology",
title = "Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients",
volume = "15",
number = "3",
pages = "253-257",
doi = "10.1080/17425255.2019.1563594"
}

Vejnović, D., Milić, V., Popović, B., Damnjanović, T., Maksimović, N., Bunjevački, V., Krajinović, M., Novaković, I., Damjanov, N.,& Jekić, B.. (2019). Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients. in Expert Opinion on Drug Metabolism & Toxicology
Taylor & Francis Ltd, Abingdon., 15(3), 253-257.
https://doi.org/10.1080/17425255.2019.1563594

Vejnović D, Milić V, Popović B, Damnjanović T, Maksimović N, Bunjevački V, Krajinović M, Novaković I, Damjanov N, Jekić B. Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients. in Expert Opinion on Drug Metabolism & Toxicology. 2019;15(3):253-257.
doi:10.1080/17425255.2019.1563594 .

Vejnović, Dubravka, Milić, Vera, Popović, Branka, Damnjanović, Tatjana, Maksimović, Nela, Bunjevački, Vera, Krajinović, Maja, Novaković, Ivana, Damjanov, Nemanja, Jekić, Biljana, "Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients" in Expert Opinion on Drug Metabolism & Toxicology, 15, no. 3 (2019):253-257,
https://doi.org/10.1080/17425255.2019.1563594 . .

TY  - JOUR
AU  - Vejnović, Dubravka
AU  - Milić, Vera
AU  - Popović, Branka
AU  - Damnjanović, Tatjana
AU  - Maksimović, Nela
AU  - Bunjevački, Vera
AU  - Krajinović, Maja
AU  - Novaković, Ivana
AU  - Damjanov, Nemanja
AU  - Jekić, Biljana
PY  - 2019
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/2462
AB  - Background: Methotrexate (MTX), a folate analogue, is the most commonly used disease-modifying drug in the treatment of rheumatoid arthritis (RA). However, high interindividual differences in drug response are present among RA patients.Research design and methods: In a group of 234 RA patients treated with MTX, we investigated whether rs1650697 polymorphism in DHFR gene may have an impact on MTX efficacy and/or adverse drug effects (ADEs). Relative DAS28 values (rDAS28) were used for the estimation of MTX therapy and all ADEs were recorded. Patients were genotyped for selected polymorphism by real-time PCR method. Results: According to the European League Against Rheumatism criteria after 6 months of MTX therapy, 196 patients (83.8%) were classified as responders (25 (10.7%) were good and 171 (73.1%) were moderate) and 38 patients (16.2%) as nonresponders. ADEs were observed in 55 patients (23.5%). Conclusions: Our results showed that the presence of T allele might be protective against MTX hepatotoxicity measured by transaminase levels (p = 0.05). Furthermore, among patients who also received low-dose corticosteroids, we have found a lower rDAS value in patients with CC genotype (p = 0.039).
PB  - Taylor & Francis Ltd, Abingdon
T2  - Expert Opinion on Drug Metabolism & Toxicology
T1  - Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients
VL  - 15
IS  - 3
SP  - 253
EP  - 257
DO  - 10.1080/17425255.2019.1563594
ER  - 

@article{
author = "Vejnović, Dubravka and Milić, Vera and Popović, Branka and Damnjanović, Tatjana and Maksimović, Nela and Bunjevački, Vera and Krajinović, Maja and Novaković, Ivana and Damjanov, Nemanja and Jekić, Biljana",
year = "2019",
abstract = "Background: Methotrexate (MTX), a folate analogue, is the most commonly used disease-modifying drug in the treatment of rheumatoid arthritis (RA). However, high interindividual differences in drug response are present among RA patients.Research design and methods: In a group of 234 RA patients treated with MTX, we investigated whether rs1650697 polymorphism in DHFR gene may have an impact on MTX efficacy and/or adverse drug effects (ADEs). Relative DAS28 values (rDAS28) were used for the estimation of MTX therapy and all ADEs were recorded. Patients were genotyped for selected polymorphism by real-time PCR method. Results: According to the European League Against Rheumatism criteria after 6 months of MTX therapy, 196 patients (83.8%) were classified as responders (25 (10.7%) were good and 171 (73.1%) were moderate) and 38 patients (16.2%) as nonresponders. ADEs were observed in 55 patients (23.5%). Conclusions: Our results showed that the presence of T allele might be protective against MTX hepatotoxicity measured by transaminase levels (p = 0.05). Furthermore, among patients who also received low-dose corticosteroids, we have found a lower rDAS value in patients with CC genotype (p = 0.039).",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "Expert Opinion on Drug Metabolism & Toxicology",
title = "Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients",
volume = "15",
number = "3",
pages = "253-257",
doi = "10.1080/17425255.2019.1563594"
}

Vejnović, D., Milić, V., Popović, B., Damnjanović, T., Maksimović, N., Bunjevački, V., Krajinović, M., Novaković, I., Damjanov, N.,& Jekić, B.. (2019). Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients. in Expert Opinion on Drug Metabolism & Toxicology
Taylor & Francis Ltd, Abingdon., 15(3), 253-257.
https://doi.org/10.1080/17425255.2019.1563594

Vejnović D, Milić V, Popović B, Damnjanović T, Maksimović N, Bunjevački V, Krajinović M, Novaković I, Damjanov N, Jekić B. Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients. in Expert Opinion on Drug Metabolism & Toxicology. 2019;15(3):253-257.
doi:10.1080/17425255.2019.1563594 .

Vejnović, Dubravka, Milić, Vera, Popović, Branka, Damnjanović, Tatjana, Maksimović, Nela, Bunjevački, Vera, Krajinović, Maja, Novaković, Ivana, Damjanov, Nemanja, Jekić, Biljana, "Association of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patients" in Expert Opinion on Drug Metabolism & Toxicology, 15, no. 3 (2019):253-257,
https://doi.org/10.1080/17425255.2019.1563594 . .

TY  - JOUR
AU  - Jekić, Biljana
AU  - Luković, Ljiljana
AU  - Bunjevački, Vera
AU  - Milić, Vera
AU  - Novaković, Ivana
AU  - Damnjanović, Tatjana
AU  - Milašin, Jelena
AU  - Popović, Branka
AU  - Maksimović, Nela
AU  - Damjanov, Nemanja
AU  - Radunović, Goran
AU  - Kovacević, Ljiljana
AU  - Krajinović, Maja
PY  - 2013
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1839
AB  - Purpose Gamma-glutamyl hydrolase (GGH), cyclin D1 (CCND1) and thymidylate synthase (TS) genes encode enzymes that are involved in methotrexate (MTX) action. In a group of 184 RA patients treated with MTX, we have investigated whether selected polymorphisms in these genes modulate MTX efficacy and/or have impact on adverse drug effects (ADEs). Methods The efficacy of the MTX therapy has been estimated using the disease activity score in 28 joints (DAS28-ESR) based on EULAR criteria and relative DAS28 values (rDAS28). All adverse drug events were recorded. Patients were genotyped for selected polymorphisms of the GGH (-354 G>T and 452 C>T), CCND1 (870 A>G) and TYMS (variable number of tandem repeats, VNTR, and G to C substitution of triple repeat, 3R allele) gene. Association studies have been performed between obtained genotypes and the efficacy and toxicity of MTX. Results According to the EULAR response criteria, 146 RA patients (79.3 %) were classified as responders (good/moderate response) and 38 (20.7 %) as nonresponders (poor response). Higher frequency of the TYMS 3 G/3 G genotype has been found among non-responders as compared to individuals with remaining genotypes (p=0.02). ADEs were recorded in 53 patients. Among those patients eight experienced bone marrow toxicity, all of them carried GGH -354GG genotype (p=0.003). No other significant association were observed. Conclusion The 3 G/3 G genotype of the TYMS gene may indicate predisposition of poor response to MTX and GG genotype of GGH -354 T>G polymorphism may have high predictive value for myelosuppression in RA patients.
PB  - Springer Heidelberg, Heidelberg
T2  - European Journal of Clinical Pharmacology
T1  - Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients
VL  - 69
IS  - 3
SP  - 377
EP  - 383
DO  - 10.1007/s00228-012-1341-3
ER  - 

@article{
author = "Jekić, Biljana and Luković, Ljiljana and Bunjevački, Vera and Milić, Vera and Novaković, Ivana and Damnjanović, Tatjana and Milašin, Jelena and Popović, Branka and Maksimović, Nela and Damjanov, Nemanja and Radunović, Goran and Kovacević, Ljiljana and Krajinović, Maja",
year = "2013",
abstract = "Purpose Gamma-glutamyl hydrolase (GGH), cyclin D1 (CCND1) and thymidylate synthase (TS) genes encode enzymes that are involved in methotrexate (MTX) action. In a group of 184 RA patients treated with MTX, we have investigated whether selected polymorphisms in these genes modulate MTX efficacy and/or have impact on adverse drug effects (ADEs). Methods The efficacy of the MTX therapy has been estimated using the disease activity score in 28 joints (DAS28-ESR) based on EULAR criteria and relative DAS28 values (rDAS28). All adverse drug events were recorded. Patients were genotyped for selected polymorphisms of the GGH (-354 G>T and 452 C>T), CCND1 (870 A>G) and TYMS (variable number of tandem repeats, VNTR, and G to C substitution of triple repeat, 3R allele) gene. Association studies have been performed between obtained genotypes and the efficacy and toxicity of MTX. Results According to the EULAR response criteria, 146 RA patients (79.3 %) were classified as responders (good/moderate response) and 38 (20.7 %) as nonresponders (poor response). Higher frequency of the TYMS 3 G/3 G genotype has been found among non-responders as compared to individuals with remaining genotypes (p=0.02). ADEs were recorded in 53 patients. Among those patients eight experienced bone marrow toxicity, all of them carried GGH -354GG genotype (p=0.003). No other significant association were observed. Conclusion The 3 G/3 G genotype of the TYMS gene may indicate predisposition of poor response to MTX and GG genotype of GGH -354 T>G polymorphism may have high predictive value for myelosuppression in RA patients.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "European Journal of Clinical Pharmacology",
title = "Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients",
volume = "69",
number = "3",
pages = "377-383",
doi = "10.1007/s00228-012-1341-3"
}

Jekić, B., Luković, L., Bunjevački, V., Milić, V., Novaković, I., Damnjanović, T., Milašin, J., Popović, B., Maksimović, N., Damjanov, N., Radunović, G., Kovacević, L.,& Krajinović, M.. (2013). Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients. in European Journal of Clinical Pharmacology
Springer Heidelberg, Heidelberg., 69(3), 377-383.
https://doi.org/10.1007/s00228-012-1341-3

Jekić B, Luković L, Bunjevački V, Milić V, Novaković I, Damnjanović T, Milašin J, Popović B, Maksimović N, Damjanov N, Radunović G, Kovacević L, Krajinović M. Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients. in European Journal of Clinical Pharmacology. 2013;69(3):377-383.
doi:10.1007/s00228-012-1341-3 .

Jekić, Biljana, Luković, Ljiljana, Bunjevački, Vera, Milić, Vera, Novaković, Ivana, Damnjanović, Tatjana, Milašin, Jelena, Popović, Branka, Maksimović, Nela, Damjanov, Nemanja, Radunović, Goran, Kovacević, Ljiljana, Krajinović, Maja, "Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients" in European Journal of Clinical Pharmacology, 69, no. 3 (2013):377-383,
https://doi.org/10.1007/s00228-012-1341-3 . .

TY  - JOUR
AU  - Regueiro, Maria
AU  - Rivera, Luis
AU  - Damnjanović, Tatjana
AU  - Luković, Ljiljana
AU  - Milašin, Jelena
AU  - Herrera, Rene J.
PY  - 2012
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1745
AB  - Whether present-day European genetic variation and its distribution patterns can be attributed primarily to the initial peopling of Europe by anatomically modern humans during the Paleolithic, or to latter Near Eastern Neolithic input is still the subject of debate. Southeastern Europe has been a crossroads for several cultures since Paleolithic times and the Balkans, specifically, would have been part of the route used by Neolithic farmers to enter Europe. Given its geographic location in the heart of the Balkan Peninsula at the intersection of Central and Southeastern Europe, Serbia represents a key geographical location that may provide insight to elucidate the interactions between indigenous Paleolithic people and agricultural colonists from the Fertile Crescent In this study, we examine, for the first time, the Y-chromosome constitution of the general Serbian population. A total of 103 individuals were sampled and their DNA analyzed for 104 Y-chromosome bi-allelic markers and 17 associated STR loci. Our results indicate that approximately 58% of Serbian Y-chromosomes (I1-M253, I2a-P37.2 and R1a1a-M198) belong to lineages believed to be pre-Neolithic. On the other hand, the signature of putative Near Eastern Neolithic lineages, including E1b1b1a1-M78, G2a-P15, J1-M267, J2-M172 and R1b1a2-M269 accounts for 39% of the Y-chromosome. Haplogroup frequency distributions in Western and Eastern Europe reveal a spotted landscape of paleolithic Y chromosomes, undermining continental-wide generalizations. Furthermore, an examination of the distribution of Y-chromosome filiations in Europe indicates extreme levels of Paleolithic lineages in a region encompassing Serbia, Bosnia-Herzegovina and Croatia, possibly the result of Neolithic migrations encroaching on Paleolithic populations against the Adriatic Sea.
PB  - Elsevier, Amsterdam
T2  - Gene
T1  - High levels of Paleolithic Y-chromosome lineages characterize Serbia
VL  - 498
IS  - 1
SP  - 59
EP  - 67
DO  - 10.1016/j.gene.2012.01.030
ER  - 

@article{
author = "Regueiro, Maria and Rivera, Luis and Damnjanović, Tatjana and Luković, Ljiljana and Milašin, Jelena and Herrera, Rene J.",
year = "2012",
abstract = "Whether present-day European genetic variation and its distribution patterns can be attributed primarily to the initial peopling of Europe by anatomically modern humans during the Paleolithic, or to latter Near Eastern Neolithic input is still the subject of debate. Southeastern Europe has been a crossroads for several cultures since Paleolithic times and the Balkans, specifically, would have been part of the route used by Neolithic farmers to enter Europe. Given its geographic location in the heart of the Balkan Peninsula at the intersection of Central and Southeastern Europe, Serbia represents a key geographical location that may provide insight to elucidate the interactions between indigenous Paleolithic people and agricultural colonists from the Fertile Crescent In this study, we examine, for the first time, the Y-chromosome constitution of the general Serbian population. A total of 103 individuals were sampled and their DNA analyzed for 104 Y-chromosome bi-allelic markers and 17 associated STR loci. Our results indicate that approximately 58% of Serbian Y-chromosomes (I1-M253, I2a-P37.2 and R1a1a-M198) belong to lineages believed to be pre-Neolithic. On the other hand, the signature of putative Near Eastern Neolithic lineages, including E1b1b1a1-M78, G2a-P15, J1-M267, J2-M172 and R1b1a2-M269 accounts for 39% of the Y-chromosome. Haplogroup frequency distributions in Western and Eastern Europe reveal a spotted landscape of paleolithic Y chromosomes, undermining continental-wide generalizations. Furthermore, an examination of the distribution of Y-chromosome filiations in Europe indicates extreme levels of Paleolithic lineages in a region encompassing Serbia, Bosnia-Herzegovina and Croatia, possibly the result of Neolithic migrations encroaching on Paleolithic populations against the Adriatic Sea.",
publisher = "Elsevier, Amsterdam",
journal = "Gene",
title = "High levels of Paleolithic Y-chromosome lineages characterize Serbia",
volume = "498",
number = "1",
pages = "59-67",
doi = "10.1016/j.gene.2012.01.030"
}

Regueiro, M., Rivera, L., Damnjanović, T., Luković, L., Milašin, J.,& Herrera, R. J.. (2012). High levels of Paleolithic Y-chromosome lineages characterize Serbia. in Gene
Elsevier, Amsterdam., 498(1), 59-67.
https://doi.org/10.1016/j.gene.2012.01.030

Regueiro M, Rivera L, Damnjanović T, Luković L, Milašin J, Herrera RJ. High levels of Paleolithic Y-chromosome lineages characterize Serbia. in Gene. 2012;498(1):59-67.
doi:10.1016/j.gene.2012.01.030 .

Regueiro, Maria, Rivera, Luis, Damnjanović, Tatjana, Luković, Ljiljana, Milašin, Jelena, Herrera, Rene J., "High levels of Paleolithic Y-chromosome lineages characterize Serbia" in Gene, 498, no. 1 (2012):59-67,
https://doi.org/10.1016/j.gene.2012.01.030 . .

TY  - JOUR
AU  - Milić, Vera
AU  - Jekić, Biljana
AU  - Luković, Ljiljana
AU  - Bunjevački, Vera
AU  - Milašin, Jelena
AU  - Novaković, I.
AU  - Damnjanović, Tatjana
AU  - Popović, Branka
AU  - Maksimović, Nela
AU  - Damjanov, Nemanja
AU  - Radunović, Goran
AU  - Pejnović, Nada
AU  - Krajinović, Maja
PY  - 2012
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1741
AB  - Objectives Identifying genetic predictors of methotrexate (MTX) treatment response in patients with rheumatoid arthritis (RA) may have great importance for optimising drug doses required for clinical benefit without toxicity. In a group of 125 RA patients treated with MTX we investigated whether selected polymorphisms in genes relevant for MTX action (aminoimidazole-4-carboxiamide ribonucleotide transformylase, ATIC, and dihydrofolate reductase, DHFR) modulate disease activity and/or have impact on therapy side effects. Methods The efficacy of treatment was estimated both by the disease activity score in 28 joints (DAS28), based on EULAR criteria, and relative DAS28 (rDAS28) score. Adverse drug events (ADEs) were also recorded. RA patients were genotyped using the PCR-RFLP method, followed by an association study between ATIC -129T>G, DHFR -216T>C and DHFR -317A>G polymorphisms and the efficacy and toxicity of MTX. Results According to the EULAR response criteria, 96 RA patients (76.8%) were classified as responders (good/moderate response) and 29 (23.2%) as non-responders (poor response). rDAS28 values ranged from -0.01 to 0.80 (mean value 0.31 +/- 0.19). Among 125 patients enrolled in this study 39 experienced at least one side effect. The DHFR -317AA genotype was associated with the less favourable response (reduction in rDAS28 score, p=0.05). None of the analysed polymorphisms was associated with MTX toxicity. Conclusion RA patients with DHFR-317AA genotype had less favourable response to MTX Further studies in larger patient populations are necessary to confirm the relationship between the analysed polymorphisms and MTX treatment response.
PB  - Clinical & Exper Rheumatology, Pisa
T2  - Clinical & Experimental Rheumatology
T1  - Association of dihydrofolate reductase (DHFR)-317AA genotype with poor response to methotrexate in patients with rheumatoid arthritis
VL  - 30
IS  - 2
SP  - 178
EP  - 183
UR  - https://hdl.handle.net/21.15107/rcub_smile_1741
ER  - 

@article{
author = "Milić, Vera and Jekić, Biljana and Luković, Ljiljana and Bunjevački, Vera and Milašin, Jelena and Novaković, I. and Damnjanović, Tatjana and Popović, Branka and Maksimović, Nela and Damjanov, Nemanja and Radunović, Goran and Pejnović, Nada and Krajinović, Maja",
year = "2012",
abstract = "Objectives Identifying genetic predictors of methotrexate (MTX) treatment response in patients with rheumatoid arthritis (RA) may have great importance for optimising drug doses required for clinical benefit without toxicity. In a group of 125 RA patients treated with MTX we investigated whether selected polymorphisms in genes relevant for MTX action (aminoimidazole-4-carboxiamide ribonucleotide transformylase, ATIC, and dihydrofolate reductase, DHFR) modulate disease activity and/or have impact on therapy side effects. Methods The efficacy of treatment was estimated both by the disease activity score in 28 joints (DAS28), based on EULAR criteria, and relative DAS28 (rDAS28) score. Adverse drug events (ADEs) were also recorded. RA patients were genotyped using the PCR-RFLP method, followed by an association study between ATIC -129T>G, DHFR -216T>C and DHFR -317A>G polymorphisms and the efficacy and toxicity of MTX. Results According to the EULAR response criteria, 96 RA patients (76.8%) were classified as responders (good/moderate response) and 29 (23.2%) as non-responders (poor response). rDAS28 values ranged from -0.01 to 0.80 (mean value 0.31 +/- 0.19). Among 125 patients enrolled in this study 39 experienced at least one side effect. The DHFR -317AA genotype was associated with the less favourable response (reduction in rDAS28 score, p=0.05). None of the analysed polymorphisms was associated with MTX toxicity. Conclusion RA patients with DHFR-317AA genotype had less favourable response to MTX Further studies in larger patient populations are necessary to confirm the relationship between the analysed polymorphisms and MTX treatment response.",
publisher = "Clinical & Exper Rheumatology, Pisa",
journal = "Clinical & Experimental Rheumatology",
title = "Association of dihydrofolate reductase (DHFR)-317AA genotype with poor response to methotrexate in patients with rheumatoid arthritis",
volume = "30",
number = "2",
pages = "178-183",
url = "https://hdl.handle.net/21.15107/rcub_smile_1741"
}

Milić, V., Jekić, B., Luković, L., Bunjevački, V., Milašin, J., Novaković, I., Damnjanović, T., Popović, B., Maksimović, N., Damjanov, N., Radunović, G., Pejnović, N.,& Krajinović, M.. (2012). Association of dihydrofolate reductase (DHFR)-317AA genotype with poor response to methotrexate in patients with rheumatoid arthritis. in Clinical & Experimental Rheumatology
Clinical & Exper Rheumatology, Pisa., 30(2), 178-183.
https://hdl.handle.net/21.15107/rcub_smile_1741

Milić V, Jekić B, Luković L, Bunjevački V, Milašin J, Novaković I, Damnjanović T, Popović B, Maksimović N, Damjanov N, Radunović G, Pejnović N, Krajinović M. Association of dihydrofolate reductase (DHFR)-317AA genotype with poor response to methotrexate in patients with rheumatoid arthritis. in Clinical & Experimental Rheumatology. 2012;30(2):178-183.
https://hdl.handle.net/21.15107/rcub_smile_1741 .

Milić, Vera, Jekić, Biljana, Luković, Ljiljana, Bunjevački, Vera, Milašin, Jelena, Novaković, I., Damnjanović, Tatjana, Popović, Branka, Maksimović, Nela, Damjanov, Nemanja, Radunović, Goran, Pejnović, Nada, Krajinović, Maja, "Association of dihydrofolate reductase (DHFR)-317AA genotype with poor response to methotrexate in patients with rheumatoid arthritis" in Clinical & Experimental Rheumatology, 30, no. 2 (2012):178-183,
https://hdl.handle.net/21.15107/rcub_smile_1741 .

TY  - JOUR
AU  - Jekić, Biljana
AU  - Bunjevački, Vera
AU  - Dobričić, Valerija
AU  - Novaković, Ivana
AU  - Milašin, Jelena
AU  - Popović, Branka
AU  - Damnjanović, Tatjana
AU  - Maksimović, Nela
AU  - Perović, V.
AU  - Luković, Ljiljana
PY  - 2011
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1635
AB  - Myelodysplastic syndromes (MDS) are rare in children and only a few studies have analyzed their molecular mechanisms. The NPM1 gene encodes for nucleophosmin (NPM) which regulates hematopoiesis. Mutations in exon 12 of the NPM1 cause the nucleophosmin cytoplasmic dislocation and disrupt its functions. We have analyzed mutations of the NPM1 gene in archival bone marrow samples from 17 children with MDS and detected, in one patient, transition C to T in codon 293. To the best of our knowledge, this is the first analysis of NPM1 mutations in childhood MDS and the very first missense mutation of the NPM1 gene reported so far.
PB  - Srpsko biološko društvo, Beograd, i dr.
T2  - Archives of Biological Sciences
T1  - NPM1 gene mutations in children with Myelodysplastic syndromes
VL  - 63
IS  - 3
SP  - 649
EP  - 653
DO  - 10.2298/ABS1103649J
ER  - 

@article{
author = "Jekić, Biljana and Bunjevački, Vera and Dobričić, Valerija and Novaković, Ivana and Milašin, Jelena and Popović, Branka and Damnjanović, Tatjana and Maksimović, Nela and Perović, V. and Luković, Ljiljana",
year = "2011",
abstract = "Myelodysplastic syndromes (MDS) are rare in children and only a few studies have analyzed their molecular mechanisms. The NPM1 gene encodes for nucleophosmin (NPM) which regulates hematopoiesis. Mutations in exon 12 of the NPM1 cause the nucleophosmin cytoplasmic dislocation and disrupt its functions. We have analyzed mutations of the NPM1 gene in archival bone marrow samples from 17 children with MDS and detected, in one patient, transition C to T in codon 293. To the best of our knowledge, this is the first analysis of NPM1 mutations in childhood MDS and the very first missense mutation of the NPM1 gene reported so far.",
publisher = "Srpsko biološko društvo, Beograd, i dr.",
journal = "Archives of Biological Sciences",
title = "NPM1 gene mutations in children with Myelodysplastic syndromes",
volume = "63",
number = "3",
pages = "649-653",
doi = "10.2298/ABS1103649J"
}

Jekić, B., Bunjevački, V., Dobričić, V., Novaković, I., Milašin, J., Popović, B., Damnjanović, T., Maksimović, N., Perović, V.,& Luković, L.. (2011). NPM1 gene mutations in children with Myelodysplastic syndromes. in Archives of Biological Sciences
Srpsko biološko društvo, Beograd, i dr.., 63(3), 649-653.
https://doi.org/10.2298/ABS1103649J

Jekić B, Bunjevački V, Dobričić V, Novaković I, Milašin J, Popović B, Damnjanović T, Maksimović N, Perović V, Luković L. NPM1 gene mutations in children with Myelodysplastic syndromes. in Archives of Biological Sciences. 2011;63(3):649-653.
doi:10.2298/ABS1103649J .

Jekić, Biljana, Bunjevački, Vera, Dobričić, Valerija, Novaković, Ivana, Milašin, Jelena, Popović, Branka, Damnjanović, Tatjana, Maksimović, Nela, Perović, V., Luković, Ljiljana, "NPM1 gene mutations in children with Myelodysplastic syndromes" in Archives of Biological Sciences, 63, no. 3 (2011):649-653,
https://doi.org/10.2298/ABS1103649J . .

TY  - JOUR
AU  - Damnjanović, Tatjana
AU  - Milicević, Radomir
AU  - Novković, Tanja
AU  - Jovičić, Olivera
AU  - Bunjevački, Vera
AU  - Jekić, Biljana
AU  - Luković, Ljiljana
AU  - Novaković, Ivana
AU  - Redzić, Danka
AU  - Milašin, Jelena
PY  - 2010
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1582
AB  - Methylenetetrahydrofolate reductase (MTHFR) regulates the metabolism of folate and methionine, essential components of DNA synthesis and methylation. Polymorphisms in the MTHFR gene have been associated with susceptibility to some types of cancer. We investigated a possible association of MTHFR polymorphisms (677C > T and 1298A > C) and increased risk for acute lymphoblastic leukemia in 78 affected children. The frequencies of both MTHFR 677 genotypes and alleles were significantly different between patients and controls. A significant association between CT/TT individuals and reduced risk of acute lymphoblastic leukemia was found. The odds ratios were 0.53 (95% confidence interval, 032-0.89) and 0.30 (95% confidence interval, 0.12-0.81). Polymorphism 1298 did not show statistical difference between patients and controls.
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Journal of Pediatric Hematology Oncology
T1  - Association Between the Methylenetetrahydrofolate Reductase Polymorphisms and Risk of Acute Lymphoblastic Leukemia in Serbian Children
VL  - 32
IS  - 4
SP  - E148
EP  - E150
DO  - 10.1097/MPH.0b013e3181cbd252
ER  - 

@article{
author = "Damnjanović, Tatjana and Milicević, Radomir and Novković, Tanja and Jovičić, Olivera and Bunjevački, Vera and Jekić, Biljana and Luković, Ljiljana and Novaković, Ivana and Redzić, Danka and Milašin, Jelena",
year = "2010",
abstract = "Methylenetetrahydrofolate reductase (MTHFR) regulates the metabolism of folate and methionine, essential components of DNA synthesis and methylation. Polymorphisms in the MTHFR gene have been associated with susceptibility to some types of cancer. We investigated a possible association of MTHFR polymorphisms (677C > T and 1298A > C) and increased risk for acute lymphoblastic leukemia in 78 affected children. The frequencies of both MTHFR 677 genotypes and alleles were significantly different between patients and controls. A significant association between CT/TT individuals and reduced risk of acute lymphoblastic leukemia was found. The odds ratios were 0.53 (95% confidence interval, 032-0.89) and 0.30 (95% confidence interval, 0.12-0.81). Polymorphism 1298 did not show statistical difference between patients and controls.",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Journal of Pediatric Hematology Oncology",
title = "Association Between the Methylenetetrahydrofolate Reductase Polymorphisms and Risk of Acute Lymphoblastic Leukemia in Serbian Children",
volume = "32",
number = "4",
pages = "E148-E150",
doi = "10.1097/MPH.0b013e3181cbd252"
}

Damnjanović, T., Milicević, R., Novković, T., Jovičić, O., Bunjevački, V., Jekić, B., Luković, L., Novaković, I., Redzić, D.,& Milašin, J.. (2010). Association Between the Methylenetetrahydrofolate Reductase Polymorphisms and Risk of Acute Lymphoblastic Leukemia in Serbian Children. in Journal of Pediatric Hematology Oncology
Lippincott Williams & Wilkins, Philadelphia., 32(4), E148-E150.
https://doi.org/10.1097/MPH.0b013e3181cbd252

Damnjanović T, Milicević R, Novković T, Jovičić O, Bunjevački V, Jekić B, Luković L, Novaković I, Redzić D, Milašin J. Association Between the Methylenetetrahydrofolate Reductase Polymorphisms and Risk of Acute Lymphoblastic Leukemia in Serbian Children. in Journal of Pediatric Hematology Oncology. 2010;32(4):E148-E150.
doi:10.1097/MPH.0b013e3181cbd252 .

Damnjanović, Tatjana, Milicević, Radomir, Novković, Tanja, Jovičić, Olivera, Bunjevački, Vera, Jekić, Biljana, Luković, Ljiljana, Novaković, Ivana, Redzić, Danka, Milašin, Jelena, "Association Between the Methylenetetrahydrofolate Reductase Polymorphisms and Risk of Acute Lymphoblastic Leukemia in Serbian Children" in Journal of Pediatric Hematology Oncology, 32, no. 4 (2010):E148-E150,
https://doi.org/10.1097/MPH.0b013e3181cbd252 . .

TY  - JOUR
AU  - Damnjanović, Tatjana
AU  - Novaković, Ivana
AU  - Milašin, Jelena
AU  - Bunjevački, Vera
AU  - Jekić, Biljana
AU  - Cvijeticanin, Suzana
AU  - Luković, Ljiljana
PY  - 2007
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1365
AB  - The objective of this study was to assess indirectly the existence of X imprinting and its potential role in a number of clinical characteristics of Turner syndrome patients. Highly polymorphic X linked microsatellite markers were used to determine the origin of the single X chromosome in 13 patients with Turner syndrome. Ten (77%) patients retained the maternal X chromosome (X-m), while only three patients (23%) retained the paternal X chromosome (X-p). Fisher exact statistical test was used for the association of X chromosome origin with the clinical phenotype. No significant difference was found between the two groups of patients regarding the following phenotype characteristics: lymphoedema. at birth, short neck, low posterior hairline, eye anomalies (ptosis, epicanthal folds, hypertelorism, strabismus), multiple pigmented naevi, cardiac and renal anomalies. Absence association between the X chromosome origin and Turner phenotype was confirmed by a meta-analysis combining five studies, including this one. It was only neck webbing that showed a trend of association with X-m.
T2  - Korean Journal of Genetics
T1  - LeX chromosome imprinting in turner syndrome
VL  - 29
IS  - 3
SP  - 291
EP  - 295
UR  - https://hdl.handle.net/21.15107/rcub_smile_1365
ER  - 

@article{
author = "Damnjanović, Tatjana and Novaković, Ivana and Milašin, Jelena and Bunjevački, Vera and Jekić, Biljana and Cvijeticanin, Suzana and Luković, Ljiljana",
year = "2007",
abstract = "The objective of this study was to assess indirectly the existence of X imprinting and its potential role in a number of clinical characteristics of Turner syndrome patients. Highly polymorphic X linked microsatellite markers were used to determine the origin of the single X chromosome in 13 patients with Turner syndrome. Ten (77%) patients retained the maternal X chromosome (X-m), while only three patients (23%) retained the paternal X chromosome (X-p). Fisher exact statistical test was used for the association of X chromosome origin with the clinical phenotype. No significant difference was found between the two groups of patients regarding the following phenotype characteristics: lymphoedema. at birth, short neck, low posterior hairline, eye anomalies (ptosis, epicanthal folds, hypertelorism, strabismus), multiple pigmented naevi, cardiac and renal anomalies. Absence association between the X chromosome origin and Turner phenotype was confirmed by a meta-analysis combining five studies, including this one. It was only neck webbing that showed a trend of association with X-m.",
journal = "Korean Journal of Genetics",
title = "LeX chromosome imprinting in turner syndrome",
volume = "29",
number = "3",
pages = "291-295",
url = "https://hdl.handle.net/21.15107/rcub_smile_1365"
}

Damnjanović, T., Novaković, I., Milašin, J., Bunjevački, V., Jekić, B., Cvijeticanin, S.,& Luković, L.. (2007). LeX chromosome imprinting in turner syndrome. in Korean Journal of Genetics, 29(3), 291-295.
https://hdl.handle.net/21.15107/rcub_smile_1365

Damnjanović T, Novaković I, Milašin J, Bunjevački V, Jekić B, Cvijeticanin S, Luković L. LeX chromosome imprinting in turner syndrome. in Korean Journal of Genetics. 2007;29(3):291-295.
https://hdl.handle.net/21.15107/rcub_smile_1365 .

Damnjanović, Tatjana, Novaković, Ivana, Milašin, Jelena, Bunjevački, Vera, Jekić, Biljana, Cvijeticanin, Suzana, Luković, Ljiljana, "LeX chromosome imprinting in turner syndrome" in Korean Journal of Genetics, 29, no. 3 (2007):291-295,
https://hdl.handle.net/21.15107/rcub_smile_1365 .

TY  - JOUR
AU  - Jekić, B.
AU  - Novaković, I.
AU  - Luković, L
AU  - Kuzmanović, M
AU  - Popović, Branka
AU  - Milašin, Jelena
AU  - Bunjevacki, G
AU  - Damnjanović, Tatjana
AU  - Cvjetičanin, S
AU  - Bunjevački, Vera
PY  - 2006
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1314
AB  - Myelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisims underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed nnutations of these genes in a cohort of 35 children with MDS. Single-strand conformation polymorphism polymerase chain reaction analysis performed on FMS codon 969 and TP53 exons 5-9 showed no mutations in the analyzed sequences. Our results Suggest that molecular mechanisms of MDS evolution in children are different from those in adults.
PB  - Elsevier Science Inc, New York
T2  - Cancer Genetics & Cytogenetics
T1  - Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome
VL  - 166
IS  - 2
SP  - 163
EP  - 165
DO  - 10.1016/j.cancergencyto.2005.11.003
ER  - 

@article{
author = "Jekić, B. and Novaković, I. and Luković, L and Kuzmanović, M and Popović, Branka and Milašin, Jelena and Bunjevacki, G and Damnjanović, Tatjana and Cvjetičanin, S and Bunjevački, Vera",
year = "2006",
abstract = "Myelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisims underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed nnutations of these genes in a cohort of 35 children with MDS. Single-strand conformation polymorphism polymerase chain reaction analysis performed on FMS codon 969 and TP53 exons 5-9 showed no mutations in the analyzed sequences. Our results Suggest that molecular mechanisms of MDS evolution in children are different from those in adults.",
publisher = "Elsevier Science Inc, New York",
journal = "Cancer Genetics & Cytogenetics",
title = "Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome",
volume = "166",
number = "2",
pages = "163-165",
doi = "10.1016/j.cancergencyto.2005.11.003"
}

Jekić, B., Novaković, I., Luković, L., Kuzmanović, M., Popović, B., Milašin, J., Bunjevacki, G., Damnjanović, T., Cvjetičanin, S.,& Bunjevački, V.. (2006). Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. in Cancer Genetics & Cytogenetics
Elsevier Science Inc, New York., 166(2), 163-165.
https://doi.org/10.1016/j.cancergencyto.2005.11.003

Jekić B, Novaković I, Luković L, Kuzmanović M, Popović B, Milašin J, Bunjevacki G, Damnjanović T, Cvjetičanin S, Bunjevački V. Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. in Cancer Genetics & Cytogenetics. 2006;166(2):163-165.
doi:10.1016/j.cancergencyto.2005.11.003 .

Jekić, B., Novaković, I., Luković, L, Kuzmanović, M, Popović, Branka, Milašin, Jelena, Bunjevacki, G, Damnjanović, Tatjana, Cvjetičanin, S, Bunjevački, Vera, "Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome" in Cancer Genetics & Cytogenetics, 166, no. 2 (2006):163-165,
https://doi.org/10.1016/j.cancergencyto.2005.11.003 . .