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  - Popović, Branka
AU  - Jekić, Biljana
AU  - Novaković, Ivana
AU  - Luković, Ljiljana
AU  - Konstantinović, Vitomir
AU  - Babić, Marko
AU  - Milašin, Jelena
PY  - 2010
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1564
AB  - The aim of this study was to gain a better understanding of cancer genes contributing to oral squamous cell (OSCC) development and progression and correlate genetic changes to clinical parameters. Human papilloma virus (HPV) 16 detection is also included in the study. 60 samples of OSCC were analysed for erbB2 and c-myc amplification by dPCR, H-ras and p53 point mutations by PCR/SSCP. HPV was detected via amplification of its El and E6 genes. c-erbB2 was altered in 45%, c-myc in 35%, H-ras in 22% and p53 in 60% of samples. HPV was detected in 10% of cases. The frequency of p53 gene mutations showed a statistically significant association with tumour stage. Patients with c-erbB2 and H-ras alterations had lower survival than patients without these alterations. The number of detected genetic changes was remarkable but statistical association with tumour natural history was poor, indicating high clonal heterogeneity and multiple pathways of carcinogenesis.
PB  - Churchill Livingstone, Edinburgh
T2  - International Journal of Oral & Maxillofacial Surgery
T1  - Cancer genes alterations and HPV infection in oral squamous cell carcinoma
VL  - 39
IS  - 9
SP  - 909
EP  - 915
DO  - 10.1016/j.ijom.2010.05.007
ER  - 

@article{
author = "Popović, Branka and Jekić, Biljana and Novaković, Ivana and Luković, Ljiljana and Konstantinović, Vitomir and Babić, Marko and Milašin, Jelena",
year = "2010",
abstract = "The aim of this study was to gain a better understanding of cancer genes contributing to oral squamous cell (OSCC) development and progression and correlate genetic changes to clinical parameters. Human papilloma virus (HPV) 16 detection is also included in the study. 60 samples of OSCC were analysed for erbB2 and c-myc amplification by dPCR, H-ras and p53 point mutations by PCR/SSCP. HPV was detected via amplification of its El and E6 genes. c-erbB2 was altered in 45%, c-myc in 35%, H-ras in 22% and p53 in 60% of samples. HPV was detected in 10% of cases. The frequency of p53 gene mutations showed a statistically significant association with tumour stage. Patients with c-erbB2 and H-ras alterations had lower survival than patients without these alterations. The number of detected genetic changes was remarkable but statistical association with tumour natural history was poor, indicating high clonal heterogeneity and multiple pathways of carcinogenesis.",
publisher = "Churchill Livingstone, Edinburgh",
journal = "International Journal of Oral & Maxillofacial Surgery",
title = "Cancer genes alterations and HPV infection in oral squamous cell carcinoma",
volume = "39",
number = "9",
pages = "909-915",
doi = "10.1016/j.ijom.2010.05.007"
}

Popović, B., Jekić, B., Novaković, I., Luković, L., Konstantinović, V., Babić, M.,& Milašin, J.. (2010). Cancer genes alterations and HPV infection in oral squamous cell carcinoma. in International Journal of Oral & Maxillofacial Surgery
Churchill Livingstone, Edinburgh., 39(9), 909-915.
https://doi.org/10.1016/j.ijom.2010.05.007

Popović B, Jekić B, Novaković I, Luković L, Konstantinović V, Babić M, Milašin J. Cancer genes alterations and HPV infection in oral squamous cell carcinoma. in International Journal of Oral & Maxillofacial Surgery. 2010;39(9):909-915.
doi:10.1016/j.ijom.2010.05.007 .

Popović, Branka, Jekić, Biljana, Novaković, Ivana, Luković, Ljiljana, Konstantinović, Vitomir, Babić, Marko, Milašin, Jelena, "Cancer genes alterations and HPV infection in oral squamous cell carcinoma" in International Journal of Oral & Maxillofacial Surgery, 39, no. 9 (2010):909-915,
https://doi.org/10.1016/j.ijom.2010.05.007 . .

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  - Pastor, Tibor
AU  - Popović, Branka
AU  - Gvozdenović, Ana
AU  - Boro, Aleksandar
AU  - Petrović, Bojana
AU  - Novaković, Ivana
AU  - Puzović, Dragana
AU  - Luković, Ljiljana
AU  - Milašin, Jelena
PY  - 2009
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1502
AB  - Introduction. According to clinical and epidemiological studies, ovarian cancer ranks fifth in cancer deaths among women. The causes of ovarian cancer remain largely unknown but various factors may increase the risk of developing it, such as age, family history of cancer, childbearing status etc. This cancer results from a succession of genetic alterations involving oncogenes and tumour suppressor genes, which have a critical role in normal cell growth regulation. Mutations and/or overexpression of three oncogenes, c-erbB-2, c-Myc and K-ras, and of the tumour suppressor gene p53, have been frequently observed in a sporadic ovarian cancer. Objective. The aim of the present study was to analyze c-Myc and c-erbB-2 oncogene alterations, specifically amplification, as one of main mechanisms of their activation in ovarian cancers and to establish a possible association with the pathogenic process. Methods. DNA was isolated from 15 samples of malignant and 5 benign ovarian tumours, using proteinase K digestion, followed by phenol-chloroform isoamyl extraction and ethanol precipitation. C-Myc and c-erbB-2 amplification were detected by differential PCR. The level of gene copy increase was measured using the Scion image software. Results. The amplification of both c-Myc and c-erbB-2 was detected in 26.7% of ovarian epithelial carcinoma specimens. Only one tumour specimen concomitantly showed increased gene copy number for both studied genes. Interestingly, besides amplification, gene deletion was also detected (26.7% for c-erbB-2). Most of the ovarian carcinomas with alterations in c-Myc and c-erbB-2 belonged to advanced FIGO stages. Conclusion. The amplification of c-Myc and c-erbB-2 oncogenes in ovarian epithelial carcinomas is most probably a late event in the pathogenesis conferring these tumours a more aggressive biological behaviour. Similarly, gene deletions point to genomic instability in epithelial carcinomas in higher clinical stages as the result of clonal evolution and selection.
AB  - Uvod. Kliničke i epidemiološke studije su pokazale da je kancer jajnika peti po redu uzročnik smrti žena. Iako postoje mnogi predisponirajući faktori, kao što su starosna dob, porodična istorija kancera, sterilnost, broj rođene dece i dr., tačni uzroci nastanka tumora jajnika još nisu poznati. Zna se, međutim, da je kancer jajnika rezultat akumulacije različitih genskih alteracija, od kojih su najznačajnije mutacije, odnosno povišena ekspresija određenih onkogena, kao što su c-myc, c-erbB-2 i K-ras, i tumor-supresorskih gena, od kojih je najvažniji p53. Cilj rada. Cilj istraživanja je bio da se ispitaju alteracije c-myc i c-erbB-2 (pre svega njihove amplifikacije), najčešćeg mehanizma aktivacije ovih onkogena, u epitelnim karcinomima jajnika, i utvrde njihove potencijalne uloge u patogenezi ovog tipa neoplazmi u našoj populaciji. Metode rada. DNK je izolovana iz 15 uzoraka malignih tumora i pet uzoraka benignih tumora jajnika. Amplifikacije onkogena c-myc i c-erbB-2 ustanovljavane su metodom diferencijalne reakcije lančanog umnožavanja DNK (engl. differential polymerase chain reaction - dPCR). Nivo amplifikacije određen je nakon denzitometrijskog merenja traka na gelu primenom programa Scion image. Rezultati. Amplifikacija i gena c-myc i c-erbB-2 otkrivena je u četiri uzorka (26,7%) epitelnog karcinoma jajnika. Jedan od ispitivanih uzoraka je imao simultanu amplifikaciju oba gena. Većina uzoraka bila je visokog stadijuma prema kriterijumima Međunarodne federacije za ginekologiju i akušerstvo (International Federation of Gynecology and Obstetrics - FIGO). Zanimljivo je da je pored amplifikacije nezavisno ustanovljena i delecija gena c-erbB-2 u 26,7% karcinoma. Svi karcinomi sa delecijama su takođe pripadali visokim kliničkim stadijumima. Zaključak. Amplifikovani onkogeni c-myc i c-erbB-2 su odlika kasnih stadijuma epitelnih maligniteta i verovatno jedan od razloga njihovog agresivnog biološkog ponašanja. Slično tome, i delecija gena erb obeležava uznapredovale stadijume bolesti i ukazuje na genomsku nestabilnost koja se javlja u epitelnim karcinomima kao rezultat evolucije i selekcije različitih tumorskih klonova.
PB  - Srpsko lekarsko društvo, Beograd
T2  - Srpski arhiv za celokupno lekarstvo
T1  - Alterations of c-Myc and c-erbB-2 genes in ovarian tumours
T1  - Alteracije onkogena c-myc i c-erbB-2 u malignim tumorima jajnika
VL  - 137
IS  - 1-2
SP  - 47
EP  - 51
DO  - 10.2298/SARH0902047P
ER  - 

@article{
author = "Pastor, Tibor and Popović, Branka and Gvozdenović, Ana and Boro, Aleksandar and Petrović, Bojana and Novaković, Ivana and Puzović, Dragana and Luković, Ljiljana and Milašin, Jelena",
year = "2009",
abstract = "Introduction. According to clinical and epidemiological studies, ovarian cancer ranks fifth in cancer deaths among women. The causes of ovarian cancer remain largely unknown but various factors may increase the risk of developing it, such as age, family history of cancer, childbearing status etc. This cancer results from a succession of genetic alterations involving oncogenes and tumour suppressor genes, which have a critical role in normal cell growth regulation. Mutations and/or overexpression of three oncogenes, c-erbB-2, c-Myc and K-ras, and of the tumour suppressor gene p53, have been frequently observed in a sporadic ovarian cancer. Objective. The aim of the present study was to analyze c-Myc and c-erbB-2 oncogene alterations, specifically amplification, as one of main mechanisms of their activation in ovarian cancers and to establish a possible association with the pathogenic process. Methods. DNA was isolated from 15 samples of malignant and 5 benign ovarian tumours, using proteinase K digestion, followed by phenol-chloroform isoamyl extraction and ethanol precipitation. C-Myc and c-erbB-2 amplification were detected by differential PCR. The level of gene copy increase was measured using the Scion image software. Results. The amplification of both c-Myc and c-erbB-2 was detected in 26.7% of ovarian epithelial carcinoma specimens. Only one tumour specimen concomitantly showed increased gene copy number for both studied genes. Interestingly, besides amplification, gene deletion was also detected (26.7% for c-erbB-2). Most of the ovarian carcinomas with alterations in c-Myc and c-erbB-2 belonged to advanced FIGO stages. Conclusion. The amplification of c-Myc and c-erbB-2 oncogenes in ovarian epithelial carcinomas is most probably a late event in the pathogenesis conferring these tumours a more aggressive biological behaviour. Similarly, gene deletions point to genomic instability in epithelial carcinomas in higher clinical stages as the result of clonal evolution and selection., Uvod. Kliničke i epidemiološke studije su pokazale da je kancer jajnika peti po redu uzročnik smrti žena. Iako postoje mnogi predisponirajući faktori, kao što su starosna dob, porodična istorija kancera, sterilnost, broj rođene dece i dr., tačni uzroci nastanka tumora jajnika još nisu poznati. Zna se, međutim, da je kancer jajnika rezultat akumulacije različitih genskih alteracija, od kojih su najznačajnije mutacije, odnosno povišena ekspresija određenih onkogena, kao što su c-myc, c-erbB-2 i K-ras, i tumor-supresorskih gena, od kojih je najvažniji p53. Cilj rada. Cilj istraživanja je bio da se ispitaju alteracije c-myc i c-erbB-2 (pre svega njihove amplifikacije), najčešćeg mehanizma aktivacije ovih onkogena, u epitelnim karcinomima jajnika, i utvrde njihove potencijalne uloge u patogenezi ovog tipa neoplazmi u našoj populaciji. Metode rada. DNK je izolovana iz 15 uzoraka malignih tumora i pet uzoraka benignih tumora jajnika. Amplifikacije onkogena c-myc i c-erbB-2 ustanovljavane su metodom diferencijalne reakcije lančanog umnožavanja DNK (engl. differential polymerase chain reaction - dPCR). Nivo amplifikacije određen je nakon denzitometrijskog merenja traka na gelu primenom programa Scion image. Rezultati. Amplifikacija i gena c-myc i c-erbB-2 otkrivena je u četiri uzorka (26,7%) epitelnog karcinoma jajnika. Jedan od ispitivanih uzoraka je imao simultanu amplifikaciju oba gena. Većina uzoraka bila je visokog stadijuma prema kriterijumima Međunarodne federacije za ginekologiju i akušerstvo (International Federation of Gynecology and Obstetrics - FIGO). Zanimljivo je da je pored amplifikacije nezavisno ustanovljena i delecija gena c-erbB-2 u 26,7% karcinoma. Svi karcinomi sa delecijama su takođe pripadali visokim kliničkim stadijumima. Zaključak. Amplifikovani onkogeni c-myc i c-erbB-2 su odlika kasnih stadijuma epitelnih maligniteta i verovatno jedan od razloga njihovog agresivnog biološkog ponašanja. Slično tome, i delecija gena erb obeležava uznapredovale stadijume bolesti i ukazuje na genomsku nestabilnost koja se javlja u epitelnim karcinomima kao rezultat evolucije i selekcije različitih tumorskih klonova.",
publisher = "Srpsko lekarsko društvo, Beograd",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "Alterations of c-Myc and c-erbB-2 genes in ovarian tumours, Alteracije onkogena c-myc i c-erbB-2 u malignim tumorima jajnika",
volume = "137",
number = "1-2",
pages = "47-51",
doi = "10.2298/SARH0902047P"
}

Pastor, T., Popović, B., Gvozdenović, A., Boro, A., Petrović, B., Novaković, I., Puzović, D., Luković, L.,& Milašin, J.. (2009). Alterations of c-Myc and c-erbB-2 genes in ovarian tumours. in Srpski arhiv za celokupno lekarstvo
Srpsko lekarsko društvo, Beograd., 137(1-2), 47-51.
https://doi.org/10.2298/SARH0902047P

Pastor T, Popović B, Gvozdenović A, Boro A, Petrović B, Novaković I, Puzović D, Luković L, Milašin J. Alterations of c-Myc and c-erbB-2 genes in ovarian tumours. in Srpski arhiv za celokupno lekarstvo. 2009;137(1-2):47-51.
doi:10.2298/SARH0902047P .

Pastor, Tibor, Popović, Branka, Gvozdenović, Ana, Boro, Aleksandar, Petrović, Bojana, Novaković, Ivana, Puzović, Dragana, Luković, Ljiljana, Milašin, Jelena, "Alterations of c-Myc and c-erbB-2 genes in ovarian tumours" in Srpski arhiv za celokupno lekarstvo, 137, no. 1-2 (2009):47-51,
https://doi.org/10.2298/SARH0902047P . .

TY  - JOUR
AU  - Popović, Branka
AU  - Jekić, B.
AU  - Novaković, I.
AU  - Luković, Ljiljana
AU  - Tepavčević, Zvezdana
AU  - Jurišić, Vladimir
AU  - Vukadinović, Miroslav
AU  - Milašin, Jelena
PY  - 2007
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1329
AB  - Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II,III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, [sic].
PB  - Wiley-Blackwell, Hoboken
T2  - Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease
T1  - Bcl-2 expression in oral squamous cell carcinoma
VL  - 1095
SP  - 19
EP  - 25
DO  - 10.1196/annals.1397.003
ER  - 

@article{
author = "Popović, Branka and Jekić, B. and Novaković, I. and Luković, Ljiljana and Tepavčević, Zvezdana and Jurišić, Vladimir and Vukadinović, Miroslav and Milašin, Jelena",
year = "2007",
abstract = "Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II,III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, [sic].",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease",
title = "Bcl-2 expression in oral squamous cell carcinoma",
volume = "1095",
pages = "19-25",
doi = "10.1196/annals.1397.003"
}

Popović, B., Jekić, B., Novaković, I., Luković, L., Tepavčević, Z., Jurišić, V., Vukadinović, M.,& Milašin, J.. (2007). Bcl-2 expression in oral squamous cell carcinoma. in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease
Wiley-Blackwell, Hoboken., 1095, 19-25.
https://doi.org/10.1196/annals.1397.003

Popović B, Jekić B, Novaković I, Luković L, Tepavčević Z, Jurišić V, Vukadinović M, Milašin J. Bcl-2 expression in oral squamous cell carcinoma. in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease. 2007;1095:19-25.
doi:10.1196/annals.1397.003 .

Popović, Branka, Jekić, B., Novaković, I., Luković, Ljiljana, Tepavčević, Zvezdana, Jurišić, Vladimir, Vukadinović, Miroslav, Milašin, Jelena, "Bcl-2 expression in oral squamous cell carcinoma" in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease, 1095 (2007):19-25,
https://doi.org/10.1196/annals.1397.003 . .

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  - Ristanović, M.
AU  - Bunjevački, Vera
AU  - Tulić, C.
AU  - Novaković, I.
AU  - Perović, V.
AU  - Luković, Ljiljana
AU  - Milašin, Jelena
PY  - 2007
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1332
AB  - Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia: Aim: The aim of this study was to determine the prevalence and type of microdeletions of the Y chromosome of men with severe oligozoospermia-ICSI candidates in the Serbian population and to compare our findings with those from other parts of the world. Methods: In all patients spermiogram has been performed in order to determine the sperm concentration. Patients were subjected to detailed clinical, endocrinological and cytogenetic examinations. Microdeletion analysis was performed by polymerase chain reaction (PCR) on 203 patients with normal cytogenetic findings. The STS markers tested in each case were sY84, sY86 (AZFa); sY127, sY134 (AZFb); sY254, sY255 (AZFc). Results: at least one of the STS markers was deleted in I I of the 203 cases (5.4 %). Conclusion: AZFc microdeletions were identified with a rather high prevalence in men with severe oligozoospermia ICSI candidates in Serbian population.
PB  - Medecine Et Hygiene, Chene-Bourg
T2  - Genetic Counseling
T1  - Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia
VL  - 18
IS  - 3
SP  - 337
EP  - 342
UR  - https://hdl.handle.net/21.15107/rcub_smile_1332
ER  - 

@article{
author = "Ristanović, M. and Bunjevački, Vera and Tulić, C. and Novaković, I. and Perović, V. and Luković, Ljiljana and Milašin, Jelena",
year = "2007",
abstract = "Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia: Aim: The aim of this study was to determine the prevalence and type of microdeletions of the Y chromosome of men with severe oligozoospermia-ICSI candidates in the Serbian population and to compare our findings with those from other parts of the world. Methods: In all patients spermiogram has been performed in order to determine the sperm concentration. Patients were subjected to detailed clinical, endocrinological and cytogenetic examinations. Microdeletion analysis was performed by polymerase chain reaction (PCR) on 203 patients with normal cytogenetic findings. The STS markers tested in each case were sY84, sY86 (AZFa); sY127, sY134 (AZFb); sY254, sY255 (AZFc). Results: at least one of the STS markers was deleted in I I of the 203 cases (5.4 %). Conclusion: AZFc microdeletions were identified with a rather high prevalence in men with severe oligozoospermia ICSI candidates in Serbian population.",
publisher = "Medecine Et Hygiene, Chene-Bourg",
journal = "Genetic Counseling",
title = "Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia",
volume = "18",
number = "3",
pages = "337-342",
url = "https://hdl.handle.net/21.15107/rcub_smile_1332"
}

Ristanović, M., Bunjevački, V., Tulić, C., Novaković, I., Perović, V., Luković, L.,& Milašin, J.. (2007). Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia. in Genetic Counseling
Medecine Et Hygiene, Chene-Bourg., 18(3), 337-342.
https://hdl.handle.net/21.15107/rcub_smile_1332

Ristanović M, Bunjevački V, Tulić C, Novaković I, Perović V, Luković L, Milašin J. Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia. in Genetic Counseling. 2007;18(3):337-342.
https://hdl.handle.net/21.15107/rcub_smile_1332 .

Ristanović, M., Bunjevački, Vera, Tulić, C., Novaković, I., Perović, V., Luković, Ljiljana, Milašin, Jelena, "Prevalence of Y chromosome microdeletions in infertile men with severe oligozoospermia in Serbia" in Genetic Counseling, 18, no. 3 (2007):337-342,
https://hdl.handle.net/21.15107/rcub_smile_1332 .

TY  - JOUR
AU  - Petrović, Bojana
AU  - Perović, Milica
AU  - Novaković, Ivana
AU  - Atanacković, Jasmina
AU  - Popović, Branka
AU  - Luković, Ljiljana
AU  - Petković, Spasoje
PY  - 2006
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1271
AB  - Background/aim: Among the genes involved in ovarian carcinogenesis, there has been increased interest in tumor-suppressor genes p53 and BRCA1. Both of the genes make control of cell cycle, DNA repair and apoptosis. The p53 is a "genome guardian" inactivated in more than 50% of human cancers, while BRCA1 mutations are found mostly in breast and ovarian cancer. The aim of this investigation was to establish the frequency of loss of heterozygosity (LOH) in the regions of the genes p53 and BRCA1 in ovarian carcinomas, and to analyze the association of LOH with the disease stage and prognosis. Methods. We analyzed 20 patients with a confirmed diagnosis of epithelilal ovarian carcinoma. DNA for molecular-genetic analysis was extracted from the tumor tissue and blood as normal tissue of each person. Microsatellite markers of the regions of genes p53 and BRCA1 were amplified by PCR method. The determination of allelic status of microsatellites and detection of LOH was performed after PAA gel electroforesis. Results. Both of the analyzed microsatellite markers were informative in 13/20 (65%) cases. In the region of gene p53, LOH was established in 4/13 (30.7%) tumors. One of them had histological gradus G1, one had gradus G2, and two of them had gradus G3, while all were with the International Federation of Gynecology and Obstetrics (FIGO) IIIc stage. In the region of gene BRCA1, LOH was detected in 5/13 (38.5%) tumors. Four of them had histological gradus G2, and one had gradus G3, while by the (FIGO) classification one was with stage Ib, one was with stage IIIb, while the three were with stage IIIc. LOH in both of the analyzed regions was detected in one tumor (7.7%), with histological gradus G3 and the FIGO IIIc stage. Conclusion. The frequency of LOH in epthelial ovarian carcinomas was 30.7% and 38.5% for p53 and BRCA1 gene regions, respectively. Most of tumors with LOH had histological gradus G2 or G3, and the clinical FIGO stage IIIc, suggesting the association of this occurrence with a later phase of the disease.
AB  - Uvod/cilj: Među genima uključenim u proces ovarijumske karcinogeneze pažnju privlače tumor-supresor geni p53 i BRCA1. Oba gena kontrolišu ćelijski ciklus, reparaciju DNK i apoptozu. Dok je p53 univerzalni "čuvar genoma" čija se inaktivacija nalazi u više od 50% maligniteta čoveka, mutacije BRCA1 se nalaze pre svega kod karcinoma dojke i ovrijuma. Istraživanje je sprovedeno sa ciljem da se utvrdi učestalost gubitka heterozigotnosti (LOH) u regionima gena p53 i BRCA1 kod karcinoma ovarijuma i da se ispita njegova korelacija sa stadijumom i prognozom bolesti. Metode. Ispitivanjem je obuhvaćeno 20 bolesnica sa potvrđenom dijagnozom karcinoma ovarijuma. Za molekularno genetičku analizu DNK izolovana je iz tumorskog tkiva i krvi kao kontrolnog zdravog tkiva iste osobe. Mikrosatelitni markeri u regionu gena p53 i BRCA1 umnožavani su PCR metodom, a analiza alelskog statusa i pojave LOH je vršena nakon poliakril-amidinom (PAA) gel elektroforeze. Rezultati. Oba analizirana mikrosatelitna markera bila su informativna u po 13 do 20 slučajeva (65%). U regionu gena p53 nađen je LOH u 4 od 13 slučajeva (30,7%). Po jedan od ovih tumora bio je histološkog gradusa G1 i G2, a dva histološkog gradusa G3, dok je FIGO stadijum u svim slučajevima bio IIIc. U regionu gena BRCA1 LOH je nađen u 5 od 13 slučajeva (38,5%). Od ovih uzoraka četiri su bila histološkog gradusa G2, a jedan histološkog gradusa G3. Po FIGO klasifikaciji jedan uzorak sa LOH bio je u stadijumu Ic, jedan u stadijumu IIIb, dok su tri bila u stadijumu IIIc. Istovremeni gubitak heterozigotnosti za oba ispitivana gena detektovan je u jednom uzorku histološkog gradusa G3, u stadijumu IIIc, što čini 7,7%. Zaključak. Učestalost LOH kod karcinoma ovarijuma iznosila je 30,7% u regionu gena p53, odnosno 38,5% u regionu gena BRCA1. Najveći broj tumora sa LOH bio je histološkog gradusa G2 ili G3, u kliničkom stadijumu IIIc, pa se može zaključiti da je ova pojava povezana sa kasnijom fazom razvoja bolesti.
PB  - Vojnomedicinska akademija - Institut za naučne informacije, Beograd
T2  - Vojnosanitetski pregled
T1  - Analysis of loss of heterozygosity of the tumor suppressor genes p53 and BRCA1 in ovarial carcinomas
T1  - Analiza gubitka heterozigotnosti tumor-supresor gena p53 i BRCA1 kod karcinoma ovarijuma
VL  - 63
IS  - 9
SP  - 813
EP  - 818
DO  - 10.2298/VSP0609813P
ER  - 

@article{
author = "Petrović, Bojana and Perović, Milica and Novaković, Ivana and Atanacković, Jasmina and Popović, Branka and Luković, Ljiljana and Petković, Spasoje",
year = "2006",
abstract = "Background/aim: Among the genes involved in ovarian carcinogenesis, there has been increased interest in tumor-suppressor genes p53 and BRCA1. Both of the genes make control of cell cycle, DNA repair and apoptosis. The p53 is a "genome guardian" inactivated in more than 50% of human cancers, while BRCA1 mutations are found mostly in breast and ovarian cancer. The aim of this investigation was to establish the frequency of loss of heterozygosity (LOH) in the regions of the genes p53 and BRCA1 in ovarian carcinomas, and to analyze the association of LOH with the disease stage and prognosis. Methods. We analyzed 20 patients with a confirmed diagnosis of epithelilal ovarian carcinoma. DNA for molecular-genetic analysis was extracted from the tumor tissue and blood as normal tissue of each person. Microsatellite markers of the regions of genes p53 and BRCA1 were amplified by PCR method. The determination of allelic status of microsatellites and detection of LOH was performed after PAA gel electroforesis. Results. Both of the analyzed microsatellite markers were informative in 13/20 (65%) cases. In the region of gene p53, LOH was established in 4/13 (30.7%) tumors. One of them had histological gradus G1, one had gradus G2, and two of them had gradus G3, while all were with the International Federation of Gynecology and Obstetrics (FIGO) IIIc stage. In the region of gene BRCA1, LOH was detected in 5/13 (38.5%) tumors. Four of them had histological gradus G2, and one had gradus G3, while by the (FIGO) classification one was with stage Ib, one was with stage IIIb, while the three were with stage IIIc. LOH in both of the analyzed regions was detected in one tumor (7.7%), with histological gradus G3 and the FIGO IIIc stage. Conclusion. The frequency of LOH in epthelial ovarian carcinomas was 30.7% and 38.5% for p53 and BRCA1 gene regions, respectively. Most of tumors with LOH had histological gradus G2 or G3, and the clinical FIGO stage IIIc, suggesting the association of this occurrence with a later phase of the disease., Uvod/cilj: Među genima uključenim u proces ovarijumske karcinogeneze pažnju privlače tumor-supresor geni p53 i BRCA1. Oba gena kontrolišu ćelijski ciklus, reparaciju DNK i apoptozu. Dok je p53 univerzalni "čuvar genoma" čija se inaktivacija nalazi u više od 50% maligniteta čoveka, mutacije BRCA1 se nalaze pre svega kod karcinoma dojke i ovrijuma. Istraživanje je sprovedeno sa ciljem da se utvrdi učestalost gubitka heterozigotnosti (LOH) u regionima gena p53 i BRCA1 kod karcinoma ovarijuma i da se ispita njegova korelacija sa stadijumom i prognozom bolesti. Metode. Ispitivanjem je obuhvaćeno 20 bolesnica sa potvrđenom dijagnozom karcinoma ovarijuma. Za molekularno genetičku analizu DNK izolovana je iz tumorskog tkiva i krvi kao kontrolnog zdravog tkiva iste osobe. Mikrosatelitni markeri u regionu gena p53 i BRCA1 umnožavani su PCR metodom, a analiza alelskog statusa i pojave LOH je vršena nakon poliakril-amidinom (PAA) gel elektroforeze. Rezultati. Oba analizirana mikrosatelitna markera bila su informativna u po 13 do 20 slučajeva (65%). U regionu gena p53 nađen je LOH u 4 od 13 slučajeva (30,7%). Po jedan od ovih tumora bio je histološkog gradusa G1 i G2, a dva histološkog gradusa G3, dok je FIGO stadijum u svim slučajevima bio IIIc. U regionu gena BRCA1 LOH je nađen u 5 od 13 slučajeva (38,5%). Od ovih uzoraka četiri su bila histološkog gradusa G2, a jedan histološkog gradusa G3. Po FIGO klasifikaciji jedan uzorak sa LOH bio je u stadijumu Ic, jedan u stadijumu IIIb, dok su tri bila u stadijumu IIIc. Istovremeni gubitak heterozigotnosti za oba ispitivana gena detektovan je u jednom uzorku histološkog gradusa G3, u stadijumu IIIc, što čini 7,7%. Zaključak. Učestalost LOH kod karcinoma ovarijuma iznosila je 30,7% u regionu gena p53, odnosno 38,5% u regionu gena BRCA1. Najveći broj tumora sa LOH bio je histološkog gradusa G2 ili G3, u kliničkom stadijumu IIIc, pa se može zaključiti da je ova pojava povezana sa kasnijom fazom razvoja bolesti.",
publisher = "Vojnomedicinska akademija - Institut za naučne informacije, Beograd",
journal = "Vojnosanitetski pregled",
title = "Analysis of loss of heterozygosity of the tumor suppressor genes p53 and BRCA1 in ovarial carcinomas, Analiza gubitka heterozigotnosti tumor-supresor gena p53 i BRCA1 kod karcinoma ovarijuma",
volume = "63",
number = "9",
pages = "813-818",
doi = "10.2298/VSP0609813P"
}

Petrović, B., Perović, M., Novaković, I., Atanacković, J., Popović, B., Luković, L.,& Petković, S.. (2006). Analysis of loss of heterozygosity of the tumor suppressor genes p53 and BRCA1 in ovarial carcinomas. in Vojnosanitetski pregled
Vojnomedicinska akademija - Institut za naučne informacije, Beograd., 63(9), 813-818.
https://doi.org/10.2298/VSP0609813P

Petrović B, Perović M, Novaković I, Atanacković J, Popović B, Luković L, Petković S. Analysis of loss of heterozygosity of the tumor suppressor genes p53 and BRCA1 in ovarial carcinomas. in Vojnosanitetski pregled. 2006;63(9):813-818.
doi:10.2298/VSP0609813P .

Petrović, Bojana, Perović, Milica, Novaković, Ivana, Atanacković, Jasmina, Popović, Branka, Luković, Ljiljana, Petković, Spasoje, "Analysis of loss of heterozygosity of the tumor suppressor genes p53 and BRCA1 in ovarial carcinomas" in Vojnosanitetski pregled, 63, no. 9 (2006):813-818,
https://doi.org/10.2298/VSP0609813P . .