TY  - THES
AU  - Stanković, Biljana
PY  - 2015
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=2312
UR  - https://nardus.mpn.gov.rs/handle/123456789/4171
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:10223/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024962482
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/39
AB  - Hronične inflamatorne bolesti creva (HIBC) predstavljaju rastući globalni zdravstveni problem, posebno u belim populacijama, uključujući i srpsku populaciju. Ova studija obuhvatila je dva tipa HIBC - inflamatornu bolest creva (IBC), koju čine Kronova bolest (KB) i ulcerozni kolitis (UK); i celijačnu bolest (CB). HIBC su kompleksne bolesti u čijoj, još uvek potpuno nerazjašnjenoj etiologiji učestvuju genetički, sredinski i imunološki faktori. Razvoj IBC je rezultat poremećenog imunološkog odgovora na crevnu mikrofloru kod genetički podložnih osoba. Ustanovljen je veliki broj asocijacija između IBC i varijanti u genima čiji proteinski produkti učestvuju u nespecifičnom imunskom odgovoru. Oštećenje intestinalne mukoze kod pacijenata sa IBC dešava se kao posledica deregulacije inflamatornih i apoptotskih procesa koji utiču na dugovečnost T ćelija i integritet epitelijalne barijere. Protein NF-κB je jedan od ključnih regulatora transkripcije gena eksprimiranih tokom ovih patogenetskih promena. U mukozi pacijenata sa KB dolazi do formiranja granuloma, limfoidnih mikrostruktura karakterističnih i za druge inflamatorne bolesti, među kojima je reumatoidni artritis (RA). Zbog toga su KB i RA klasifikovane kao granulomatozne bolesti. U poređenju sa brojnim, još uvek nedovoljno definisanim genetičkim faktorima rizika za razvoj IBC, nasledna komponenta u razvoju CB je dobro okarakterisana i najviše je povezana sa specifičnim varijantama gena HLA-DQ. Jedan od ciljeva ove studije je bio da ispita asocijaciju između HIBC i određenih genetičkih varijanti. Tačnije, analizirana je povezanost IBC sa varijantama u genima NOD2, TLR4, TNF-α, IL-6, IL-1β i IL-1RN, i ispitan je njihov prediktivni značaj za pojavu IBC. Varijanta u genu IL-6 ispitana je kao faktor rizika za nastanak dve granulomatozne bolesti, KB i RA. Takođe, analizirana je distribucija genotipova HLA-DQ u grupi pedijatrijskih pacijenata obolelih od CB i procenjen je rizik za pojavu CB koju ovi genotipovi nose. Sledeći cilj je bila analiza nivoa transkripcije proinflamatornih gena IL-6 i TNF-α, i apoptotskih gena Bcl-2, Bax, Fas i FasL u intestinalnoj mukozi i perifernoj krvi pacijenata obolelih od KB, kako bi se definisali ekspresioni profili gena uključenih u patogenezu KB i ispitao njihov dijagnostički potencijal. Poslednji cilj u okviru istaživanja vezanog za IBC odnosio se na analizu DNK vezujuće aktivnosti NF-κB iz jedarnih ekstrakata intestinalne mukoze pacijenata obolelih od KB...
AB  - Chronic inflammatory bowel diseases (CIBDs) remain an expanding global health problem, particularly in most Caucasian populations, including Serbian. The focus of this study included two types of chronic inflammatory bowel diseases - inflammatory bowel disease (IBD), which comprises Crohn’s disease (CrD) and ulcerative colitis (UC); and celiac disease (CD). These are complex diseases with various genetic, environmental and immunological risk factors, whose etiologies are not yet fully resolved. The development of IBD is a result of abnormal immune response that occurs in genetically susceptible individuals against the enteric flora. Many studies have investigated associations between IBD occurrence and variants in genes that encode proteins involved in nonspecific immune response. Intestinal mucosal damage in CrD patients occurs as a result of the deregulation of inflammatory and apoptotic processes, which influence T cell longevity and epithelial barrier integrity. Regulatory protein NF-κB has a key role in the transcription of genes whose products are involved in these pathogenic events. Another property of CrD is formation of granulomas, which can also occur in other diseases, such as rheumatoid arthritis (RA). For that reason, CrD and RA are categorized as granulomatous diseases. Compared with numerous, still insufficiently defined genetic risk factors for the development of IBD, a genetic component in CD development is well characterized and mostly associated with specific variants of HLA-DQ genes. One of the aims of this study was to evaluate disease-gene associations. More precisely, we examined IBD associations with several genetic variants - variants in NOD2, TLR4, TNF-α, IL-6, IL-1β and IL-1RN genes, and investigated their contribution in the prediction of IBD occurrence. Additionally, we analyzed variant in IL-6 gene as a risk factor for two types of granulomatous diseases, CrD and RA. Also, we inspected the distribution of HLA-DQ genotypes in the group of pediatric celiac patients and estimated the risk of CD development that these genotypes confer. Another aim was the analysis of mRNA level of proinflammatory IL-6 and TNF-α, and apoptotic Bcl-2, Bax, Fas and FasL genes in intestinal mucosa, as well as in the peripheral blood of CrD patients, in order to reveal the expression patterns involved in the pathogenesis of CrD...
PB  - Univerzitet u Beogradu, Biološki fakultet
T1  - Molekularni markeri hronične inflamacije i apoptoze kod inflamatornih bolesti creva
T1  - Molecular markers of chronic inflammation and apoptosis in inflammatory bowel diseases
UR  - https://hdl.handle.net/21.15107/rcub_nardus_4171
ER  - 

@phdthesis{
author = "Stanković, Biljana",
year = "2015",
abstract = "Hronične inflamatorne bolesti creva (HIBC) predstavljaju rastući globalni zdravstveni problem, posebno u belim populacijama, uključujući i srpsku populaciju. Ova studija obuhvatila je dva tipa HIBC - inflamatornu bolest creva (IBC), koju čine Kronova bolest (KB) i ulcerozni kolitis (UK); i celijačnu bolest (CB). HIBC su kompleksne bolesti u čijoj, još uvek potpuno nerazjašnjenoj etiologiji učestvuju genetički, sredinski i imunološki faktori. Razvoj IBC je rezultat poremećenog imunološkog odgovora na crevnu mikrofloru kod genetički podložnih osoba. Ustanovljen je veliki broj asocijacija između IBC i varijanti u genima čiji proteinski produkti učestvuju u nespecifičnom imunskom odgovoru. Oštećenje intestinalne mukoze kod pacijenata sa IBC dešava se kao posledica deregulacije inflamatornih i apoptotskih procesa koji utiču na dugovečnost T ćelija i integritet epitelijalne barijere. Protein NF-κB je jedan od ključnih regulatora transkripcije gena eksprimiranih tokom ovih patogenetskih promena. U mukozi pacijenata sa KB dolazi do formiranja granuloma, limfoidnih mikrostruktura karakterističnih i za druge inflamatorne bolesti, među kojima je reumatoidni artritis (RA). Zbog toga su KB i RA klasifikovane kao granulomatozne bolesti. U poređenju sa brojnim, još uvek nedovoljno definisanim genetičkim faktorima rizika za razvoj IBC, nasledna komponenta u razvoju CB je dobro okarakterisana i najviše je povezana sa specifičnim varijantama gena HLA-DQ. Jedan od ciljeva ove studije je bio da ispita asocijaciju između HIBC i određenih genetičkih varijanti. Tačnije, analizirana je povezanost IBC sa varijantama u genima NOD2, TLR4, TNF-α, IL-6, IL-1β i IL-1RN, i ispitan je njihov prediktivni značaj za pojavu IBC. Varijanta u genu IL-6 ispitana je kao faktor rizika za nastanak dve granulomatozne bolesti, KB i RA. Takođe, analizirana je distribucija genotipova HLA-DQ u grupi pedijatrijskih pacijenata obolelih od CB i procenjen je rizik za pojavu CB koju ovi genotipovi nose. Sledeći cilj je bila analiza nivoa transkripcije proinflamatornih gena IL-6 i TNF-α, i apoptotskih gena Bcl-2, Bax, Fas i FasL u intestinalnoj mukozi i perifernoj krvi pacijenata obolelih od KB, kako bi se definisali ekspresioni profili gena uključenih u patogenezu KB i ispitao njihov dijagnostički potencijal. Poslednji cilj u okviru istaživanja vezanog za IBC odnosio se na analizu DNK vezujuće aktivnosti NF-κB iz jedarnih ekstrakata intestinalne mukoze pacijenata obolelih od KB..., Chronic inflammatory bowel diseases (CIBDs) remain an expanding global health problem, particularly in most Caucasian populations, including Serbian. The focus of this study included two types of chronic inflammatory bowel diseases - inflammatory bowel disease (IBD), which comprises Crohn’s disease (CrD) and ulcerative colitis (UC); and celiac disease (CD). These are complex diseases with various genetic, environmental and immunological risk factors, whose etiologies are not yet fully resolved. The development of IBD is a result of abnormal immune response that occurs in genetically susceptible individuals against the enteric flora. Many studies have investigated associations between IBD occurrence and variants in genes that encode proteins involved in nonspecific immune response. Intestinal mucosal damage in CrD patients occurs as a result of the deregulation of inflammatory and apoptotic processes, which influence T cell longevity and epithelial barrier integrity. Regulatory protein NF-κB has a key role in the transcription of genes whose products are involved in these pathogenic events. Another property of CrD is formation of granulomas, which can also occur in other diseases, such as rheumatoid arthritis (RA). For that reason, CrD and RA are categorized as granulomatous diseases. Compared with numerous, still insufficiently defined genetic risk factors for the development of IBD, a genetic component in CD development is well characterized and mostly associated with specific variants of HLA-DQ genes. One of the aims of this study was to evaluate disease-gene associations. More precisely, we examined IBD associations with several genetic variants - variants in NOD2, TLR4, TNF-α, IL-6, IL-1β and IL-1RN genes, and investigated their contribution in the prediction of IBD occurrence. Additionally, we analyzed variant in IL-6 gene as a risk factor for two types of granulomatous diseases, CrD and RA. Also, we inspected the distribution of HLA-DQ genotypes in the group of pediatric celiac patients and estimated the risk of CD development that these genotypes confer. Another aim was the analysis of mRNA level of proinflammatory IL-6 and TNF-α, and apoptotic Bcl-2, Bax, Fas and FasL genes in intestinal mucosa, as well as in the peripheral blood of CrD patients, in order to reveal the expression patterns involved in the pathogenesis of CrD...",
publisher = "Univerzitet u Beogradu, Biološki fakultet",
title = "Molekularni markeri hronične inflamacije i apoptoze kod inflamatornih bolesti creva, Molecular markers of chronic inflammation and apoptosis in inflammatory bowel diseases",
url = "https://hdl.handle.net/21.15107/rcub_nardus_4171"
}

Stanković, B.. (2015). Molekularni markeri hronične inflamacije i apoptoze kod inflamatornih bolesti creva. 
Univerzitet u Beogradu, Biološki fakultet..
https://hdl.handle.net/21.15107/rcub_nardus_4171

Stanković B. Molekularni markeri hronične inflamacije i apoptoze kod inflamatornih bolesti creva. 2015;.
https://hdl.handle.net/21.15107/rcub_nardus_4171 .

Stanković, Biljana, "Molekularni markeri hronične inflamacije i apoptoze kod inflamatornih bolesti creva" (2015),
https://hdl.handle.net/21.15107/rcub_nardus_4171 .

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

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

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

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

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

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Kojić, Snežana
AU  - Knezević, Srbislav
AU  - Krivokapić, Zoran
AU  - Ristanović, Momcilo
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/543
AB  - Background: The tumor suppressor gene SMAD4 (DPC4) encodes for the common intracellular mediator of the TGF-beta superfamily pathway, which regulates numerous cellular processes, such as cell proliferation, cell differentiation, apoptosis, cell fate and migration. This study was aimed to investigate the presence of genetic variants in SMAD4 gene promoter in malignant pancreatic and colorectal tissue and to analyze their functional consequences. Methods: The study was performed on genomic DNA isolated from malignant tissue samples obtained on surgery from 50 patients with pancreatic carcinoma and 50 patients with colorectal cancer. Screening for mutations within an 800 bp-long fragment of the SMAD4 gene promoter was performed by DNA sequencing and two mononucleotide repeats, at positions -462 and -4, were found to be polymorphic in malignant tissue. The exact number of thymidines in the tracts -462T(15) and -4T(12) was determined by PCR with fluorescently labeled primers followed by capillary electrophoresis. Functional analysis of -462T(15)/-4T(12) haplotypes was performed by luciferase reporter assays. Results: Haplotype -462T(14)/-4T(10) was found in 85% of pancreatic cancer tissues, but it was not present in any of colorectal cancer tissues. Statistically significant reduction (p  lt  0.001) in activity was observed in the haplotype -462T(14)/-4T(10) in comparison with the haplotypes -462T(15)/-4T(12) and -462T(14)/-4T(11). Conclusion: Results of this study indicate that novel genetic variant -4T(10) in the SMAD4 gene promoter affects its activity and that element -4T(12) may play a role in transcriptional regulation of SMAD4 gene expression. Obtained results, though preliminary, also indicate that SMAD4 gene promoter haplotype -462T(14)/-4T(10) may represent a genetic marker of potential relevance for pancreatic and colorectal cancer. The findings of this study should be confirmed by further investigation in these two and other tumors, on larger number of patients and with different tumor stages. Translational research aimed at investigating potential application of mononucleotide repeats -462T(15) and -4T(12) in SMAD4 gene promoter as molecular markers in cancer may also prove useful.
PB  - Elsevier Sci Ltd, Oxford
T2  - Cancer Epidemiology
T1  - Structural and functional analysis of SMAD4 gene promoter in malignant pancreatic and colorectal tissues: Detection of two novel polymorphic nucleotide repeats
EP  - 271
IS  - 3
SP  - 265
VL  - 35
DO  - 10.1016/j.canep.2010.10.002
ER  - 

@article{
author = "Nikolić, Aleksandra and Kojić, Snežana and Knezević, Srbislav and Krivokapić, Zoran and Ristanović, Momcilo and Radojković, Dragica",
year = "2011",
abstract = "Background: The tumor suppressor gene SMAD4 (DPC4) encodes for the common intracellular mediator of the TGF-beta superfamily pathway, which regulates numerous cellular processes, such as cell proliferation, cell differentiation, apoptosis, cell fate and migration. This study was aimed to investigate the presence of genetic variants in SMAD4 gene promoter in malignant pancreatic and colorectal tissue and to analyze their functional consequences. Methods: The study was performed on genomic DNA isolated from malignant tissue samples obtained on surgery from 50 patients with pancreatic carcinoma and 50 patients with colorectal cancer. Screening for mutations within an 800 bp-long fragment of the SMAD4 gene promoter was performed by DNA sequencing and two mononucleotide repeats, at positions -462 and -4, were found to be polymorphic in malignant tissue. The exact number of thymidines in the tracts -462T(15) and -4T(12) was determined by PCR with fluorescently labeled primers followed by capillary electrophoresis. Functional analysis of -462T(15)/-4T(12) haplotypes was performed by luciferase reporter assays. Results: Haplotype -462T(14)/-4T(10) was found in 85% of pancreatic cancer tissues, but it was not present in any of colorectal cancer tissues. Statistically significant reduction (p  lt  0.001) in activity was observed in the haplotype -462T(14)/-4T(10) in comparison with the haplotypes -462T(15)/-4T(12) and -462T(14)/-4T(11). Conclusion: Results of this study indicate that novel genetic variant -4T(10) in the SMAD4 gene promoter affects its activity and that element -4T(12) may play a role in transcriptional regulation of SMAD4 gene expression. Obtained results, though preliminary, also indicate that SMAD4 gene promoter haplotype -462T(14)/-4T(10) may represent a genetic marker of potential relevance for pancreatic and colorectal cancer. The findings of this study should be confirmed by further investigation in these two and other tumors, on larger number of patients and with different tumor stages. Translational research aimed at investigating potential application of mononucleotide repeats -462T(15) and -4T(12) in SMAD4 gene promoter as molecular markers in cancer may also prove useful.",
publisher = "Elsevier Sci Ltd, Oxford",
journal = "Cancer Epidemiology",
title = "Structural and functional analysis of SMAD4 gene promoter in malignant pancreatic and colorectal tissues: Detection of two novel polymorphic nucleotide repeats",
pages = "271-265",
number = "3",
volume = "35",
doi = "10.1016/j.canep.2010.10.002"
}

Nikolić, A., Kojić, S., Knezević, S., Krivokapić, Z., Ristanović, M.,& Radojković, D.. (2011). Structural and functional analysis of SMAD4 gene promoter in malignant pancreatic and colorectal tissues: Detection of two novel polymorphic nucleotide repeats. in Cancer Epidemiology
Elsevier Sci Ltd, Oxford., 35(3), 265-271.
https://doi.org/10.1016/j.canep.2010.10.002

Nikolić A, Kojić S, Knezević S, Krivokapić Z, Ristanović M, Radojković D. Structural and functional analysis of SMAD4 gene promoter in malignant pancreatic and colorectal tissues: Detection of two novel polymorphic nucleotide repeats. in Cancer Epidemiology. 2011;35(3):265-271.
doi:10.1016/j.canep.2010.10.002 .

Nikolić, Aleksandra, Kojić, Snežana, Knezević, Srbislav, Krivokapić, Zoran, Ristanović, Momcilo, Radojković, Dragica, "Structural and functional analysis of SMAD4 gene promoter in malignant pancreatic and colorectal tissues: Detection of two novel polymorphic nucleotide repeats" in Cancer Epidemiology, 35, no. 3 (2011):265-271,
https://doi.org/10.1016/j.canep.2010.10.002 . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Miković, Željko
AU  - Rakićević, Ljiljana
AU  - Srzentić, Snežana
AU  - Mandić, Vesna
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/484
AB  - Uvod. Prisustvo urođene trombofilije predstavlja dodatni faktor rizika od nastanka venskog tromboembolizma u trudnoći, ali i komplikacija same trudnoće kao što su ponavljani gubitak trudnoće, abrupcija placente, intrauterino zaostajanje u rastu i razvoju, te rana preeklampsija. Trudnice sa trombofilijom, a posebno one sa nedostatkom antitrombina, u riziku su od nastanka obe vrste komplikacija u trudnoći. Prikaz bolesnice. U radu je prikazana trudnica sa urođenim nedostatkom antitrombina u toku njene prve trudnoće, čija majka je četiri puta imala duboke venske tromboze, tokom trudnoće i puerperijuma. Uz redovno laboratorijsko praćenje hemostaznih parametara i redovne akušerske kontrole sa praćenjem važnog parametra placentne vaskularizacije, čitava trudnoća protekla je bez komplikacija. Profilaktička terapija niskomolekularnim heparinom uvedena je od 20. nedelje trudnoće, a supstituciona terapija primenom koncentrata antitrombina, neposredno pre porođaja. Porođaj je protekao bez komplikacija i u 37. nedelji rođena je zdrava muška beba telesne težine 3,6 kg i dužine 52 cm, sa Abgar skorom 9/10. Zaključak. Pravovremeno postavljena dijagnoza trombofilije, redovne akušerske kontrole i praćenje hemostaznih parametara u toku trudnoće, kao i primena adekvatne profilaktičke i supstitucione terapije, doprinele su prevenciji mogućih maternalnih ili komplikacija same trudnoće kod bolesnice sa urođenim nedostatkom antitrombina.
AB  - Background. Presence of inherited thrombophilia is an additional risk factor for maternal thromboembolism and certain adverse pregnancy outcomes, including recurrent fetal loss, placental abruption, intrauterine growth restriction and earlyonset severe preeclampsia. Pregnant women with thrombophilia, especially those with antithrombin (AT) deficiency, are at high risk of both kinds of complications. Case report. We presented a pregnant women with congenital antithrombin deficiency in the first pregnancy, whose mother had had four times pregnancy-related deep vein thrombosis, and antithrombin deficiency. With the regular laboratory monitoring of hemostatic parameters and gynaecology surveillance including the follow-up of placental vascular flow, the whole pregnancy proceeded without complications. The prophylactic therapy with low molecular weight heparin was introduced from the 20th week of gestation and one dose of substitution therapy with antithrombin concentrate was administrated before delivery. Pregnancy and labour were terminated without complications at the 37th week of gestation, resulting in the delivery of a healthy male newborn of 3.6 kg body weight, 52 cm long, and with the Apgar scores of 9/10. Conclusion. A timely made diagnosis of thrombophilia, accompanied with regular obstetrics check-ups and follow-ups of hemostatic parameters during pregnancy, as well as the use of adequate prophylactic and substitution therapy, are the successful tools for the prevention of possible maternal complications and pregnancy itself in our patient with congenital AT deficiency.
PB  - Vojnomedicinska akademija - Institut za naučne informacije, Beograd
T2  - Vojnosanitetski pregled
T1  - Uspešan ishod trudnoće kod bolesnice sa urođenim nedostatkom antitrombina
T1  - A successful outcome of pregnancy in a patient with congenital antithrombin deficiency
EP  - 177
IS  - 2
SP  - 175
VL  - 68
DO  - 10.2298/VSP1102175K
ER  - 

@article{
author = "Kovač, Mirjana and Miković, Željko and Rakićević, Ljiljana and Srzentić, Snežana and Mandić, Vesna and Đorđević, Valentina and Radojković, Dragica",
year = "2011",
abstract = "Uvod. Prisustvo urođene trombofilije predstavlja dodatni faktor rizika od nastanka venskog tromboembolizma u trudnoći, ali i komplikacija same trudnoće kao što su ponavljani gubitak trudnoće, abrupcija placente, intrauterino zaostajanje u rastu i razvoju, te rana preeklampsija. Trudnice sa trombofilijom, a posebno one sa nedostatkom antitrombina, u riziku su od nastanka obe vrste komplikacija u trudnoći. Prikaz bolesnice. U radu je prikazana trudnica sa urođenim nedostatkom antitrombina u toku njene prve trudnoće, čija majka je četiri puta imala duboke venske tromboze, tokom trudnoće i puerperijuma. Uz redovno laboratorijsko praćenje hemostaznih parametara i redovne akušerske kontrole sa praćenjem važnog parametra placentne vaskularizacije, čitava trudnoća protekla je bez komplikacija. Profilaktička terapija niskomolekularnim heparinom uvedena je od 20. nedelje trudnoće, a supstituciona terapija primenom koncentrata antitrombina, neposredno pre porođaja. Porođaj je protekao bez komplikacija i u 37. nedelji rođena je zdrava muška beba telesne težine 3,6 kg i dužine 52 cm, sa Abgar skorom 9/10. Zaključak. Pravovremeno postavljena dijagnoza trombofilije, redovne akušerske kontrole i praćenje hemostaznih parametara u toku trudnoće, kao i primena adekvatne profilaktičke i supstitucione terapije, doprinele su prevenciji mogućih maternalnih ili komplikacija same trudnoće kod bolesnice sa urođenim nedostatkom antitrombina., Background. Presence of inherited thrombophilia is an additional risk factor for maternal thromboembolism and certain adverse pregnancy outcomes, including recurrent fetal loss, placental abruption, intrauterine growth restriction and earlyonset severe preeclampsia. Pregnant women with thrombophilia, especially those with antithrombin (AT) deficiency, are at high risk of both kinds of complications. Case report. We presented a pregnant women with congenital antithrombin deficiency in the first pregnancy, whose mother had had four times pregnancy-related deep vein thrombosis, and antithrombin deficiency. With the regular laboratory monitoring of hemostatic parameters and gynaecology surveillance including the follow-up of placental vascular flow, the whole pregnancy proceeded without complications. The prophylactic therapy with low molecular weight heparin was introduced from the 20th week of gestation and one dose of substitution therapy with antithrombin concentrate was administrated before delivery. Pregnancy and labour were terminated without complications at the 37th week of gestation, resulting in the delivery of a healthy male newborn of 3.6 kg body weight, 52 cm long, and with the Apgar scores of 9/10. Conclusion. A timely made diagnosis of thrombophilia, accompanied with regular obstetrics check-ups and follow-ups of hemostatic parameters during pregnancy, as well as the use of adequate prophylactic and substitution therapy, are the successful tools for the prevention of possible maternal complications and pregnancy itself in our patient with congenital AT deficiency.",
publisher = "Vojnomedicinska akademija - Institut za naučne informacije, Beograd",
journal = "Vojnosanitetski pregled",
title = "Uspešan ishod trudnoće kod bolesnice sa urođenim nedostatkom antitrombina, A successful outcome of pregnancy in a patient with congenital antithrombin deficiency",
pages = "177-175",
number = "2",
volume = "68",
doi = "10.2298/VSP1102175K"
}

Kovač, M., Miković, Ž., Rakićević, L., Srzentić, S., Mandić, V., Đorđević, V.,& Radojković, D.. (2011). Uspešan ishod trudnoće kod bolesnice sa urođenim nedostatkom antitrombina. in Vojnosanitetski pregled
Vojnomedicinska akademija - Institut za naučne informacije, Beograd., 68(2), 175-177.
https://doi.org/10.2298/VSP1102175K

Kovač M, Miković Ž, Rakićević L, Srzentić S, Mandić V, Đorđević V, Radojković D. Uspešan ishod trudnoće kod bolesnice sa urođenim nedostatkom antitrombina. in Vojnosanitetski pregled. 2011;68(2):175-177.
doi:10.2298/VSP1102175K .

Kovač, Mirjana, Miković, Željko, Rakićević, Ljiljana, Srzentić, Snežana, Mandić, Vesna, Đorđević, Valentina, Radojković, Dragica, "Uspešan ishod trudnoće kod bolesnice sa urođenim nedostatkom antitrombina" in Vojnosanitetski pregled, 68, no. 2 (2011):175-177,
https://doi.org/10.2298/VSP1102175K . .

TY  - JOUR
AU  - Lukić, Snežana
AU  - Nikolić, Aleksandra
AU  - Alempijević, Tamara
AU  - Popović, Dragan
AU  - Sokic Milutinović, Aleksandra
AU  - Ugljesić, Milenko
AU  - Knezević, Srbislav
AU  - Milicić, Biljana
AU  - Dinić, Dragica
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/489
AB  - The purpose of this study was to determine the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and to investigate its role as a potential risk factor in patients with chronic pancreatitis and pancreatic cancer. Deletion polymorphism of the 287-bp fragment of intron 16 of the ACE gene results in higher levels of circulating enzyme and therefore may represent a risk factor for disease development. The study included 55 patients with chronic pancreatitis, 45 patients with pancreatic cancer and 128 healthy subjects. The presence of I and D variants in the ACE gene was analyzed by a polymerase chain reaction (PCR) method. Distribution of ACE ID genotypes was analyzed by means of logistic regression. When chronic pancreatitis and pancreatic cancer groups were compared in the univariate analysis, the following factors were identified as statistically significant predictors of pancreatic disease: age, gender, smoking, fat intake, ACE II genotype and ACE DD genotype. However, in the multivariate analysis, only age, gender and smoking were singled out as predictors for the occurrence of pancreatic disease. Our findings indicate that the ACE I/D polymorphism could play a role in the development of chronic pancreatitis and pancreatic cancer through interaction with other genetic and environmental factors.
PB  - Karger, Basel
T2  - Digestive Surgery
T1  - Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer
EP  - 262
IS  - 4
SP  - 258
VL  - 28
DO  - 10.1159/000328666
ER  - 

@article{
author = "Lukić, Snežana and Nikolić, Aleksandra and Alempijević, Tamara and Popović, Dragan and Sokic Milutinović, Aleksandra and Ugljesić, Milenko and Knezević, Srbislav and Milicić, Biljana and Dinić, Dragica and Radojković, Dragica",
year = "2011",
abstract = "The purpose of this study was to determine the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and to investigate its role as a potential risk factor in patients with chronic pancreatitis and pancreatic cancer. Deletion polymorphism of the 287-bp fragment of intron 16 of the ACE gene results in higher levels of circulating enzyme and therefore may represent a risk factor for disease development. The study included 55 patients with chronic pancreatitis, 45 patients with pancreatic cancer and 128 healthy subjects. The presence of I and D variants in the ACE gene was analyzed by a polymerase chain reaction (PCR) method. Distribution of ACE ID genotypes was analyzed by means of logistic regression. When chronic pancreatitis and pancreatic cancer groups were compared in the univariate analysis, the following factors were identified as statistically significant predictors of pancreatic disease: age, gender, smoking, fat intake, ACE II genotype and ACE DD genotype. However, in the multivariate analysis, only age, gender and smoking were singled out as predictors for the occurrence of pancreatic disease. Our findings indicate that the ACE I/D polymorphism could play a role in the development of chronic pancreatitis and pancreatic cancer through interaction with other genetic and environmental factors.",
publisher = "Karger, Basel",
journal = "Digestive Surgery",
title = "Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer",
pages = "262-258",
number = "4",
volume = "28",
doi = "10.1159/000328666"
}

Lukić, S., Nikolić, A., Alempijević, T., Popović, D., Sokic Milutinović, A., Ugljesić, M., Knezević, S., Milicić, B., Dinić, D.,& Radojković, D.. (2011). Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer. in Digestive Surgery
Karger, Basel., 28(4), 258-262.
https://doi.org/10.1159/000328666

Lukić S, Nikolić A, Alempijević T, Popović D, Sokic Milutinović A, Ugljesić M, Knezević S, Milicić B, Dinić D, Radojković D. Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer. in Digestive Surgery. 2011;28(4):258-262.
doi:10.1159/000328666 .

Lukić, Snežana, Nikolić, Aleksandra, Alempijević, Tamara, Popović, Dragan, Sokic Milutinović, Aleksandra, Ugljesić, Milenko, Knezević, Srbislav, Milicić, Biljana, Dinić, Dragica, Radojković, Dragica, "Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer" in Digestive Surgery, 28, no. 4 (2011):258-262,
https://doi.org/10.1159/000328666 . .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Stanković, Marija
AU  - Nišević, Ivan
AU  - Lukić, Snežana
AU  - Anđelić-Jelić, Marina
AU  - Popović, Dragan
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/509
AB  - Cilj ove studije bio je da se odredi učestalost polimorfizma Ile105Val u genu za glutation S-transferazu P1 (GSTP1) i proceni njegov uticaj na rizik za obolevanje od pankreasnih bolesti u srpskoj populaciji. Studija je obuhvatila 157 pacijenata sa najčešćim bolestima pankreasa: 47 sa karcinomom pankreasa, 50 sa hroničnim pankreatitisom i 60 sa dijabetes melitusom tipa 2, kao i 107 zdravih ispitanika. Prisustvo polimorfizma Ile105Val u genu za GSTP1 je analizirano metodom PCR-RFLP (Polymerase Chain Reaction - Restriction Fragment Length Polymorphism). Učestalost alela 105Val je bila niža kod pacijenata sa karcinomom pankreasa (24,5%) i hroničnim pankreatitisom (24,0%) i neznatno povišena kod pacijenata sa dijabe tes melitusom tipa 2 (31,7%) u odnosu na učestalost kod zdra vih ispitanika (29,9%), ali razlike nisu bile statistički zna čaj ne. Učestalost pojedinih genotipova polimorfizma Ile105Val se razlikovala među analiziranim grupama, ali razlike takođe nisu bile statistički značajne. Samo nekoliko studija se do sada bavilo ulogom GSTP1 Ile105Val polimorfizma u bolestima pankreasa i uglavnom su dale oprečne rezultate. Značaj GSTP1 Ile105Val polimorfizma za bolesti pankreasa još uvek nije razjašnjen i potrebna su dalja istraživanja da bi se ispitala njegova uloga u pankreasnom tkivu. .
AB  - The aim of the current preliminary case-control study was to identify glutathione S-transferase P1 (GSTP1) Ile105Val allele and genotype frequency and to evaluate its impact on susceptibility to pancreatic diseases in a Serbian population. This study has encom passed 157 patients with three major types of chronic pancreatic pathology: 47 with pancreatic cancer, 50 with chronic pancreatitis and 60 with type 2 diabetes mellitus, as well as 107 healthy individuals. The presence of GSTP1 Ile105Val polymorphism was analyzed using a PCR-RFLP method. Allele 105Val was less frequent in patients with pancreatic cancer (24.5%) and chronic pancreatitis (24.0%) and slightly more frequent in patients with type 2 diabetes mellitus (31.7%) in comparison to healthy individuals (29.9%), but the differences were not statistically significant. Distribution of Ile105Val polymorphism genotypes differed between the analyzed groups, but differences were also not statistically significant. There are only a few studies regarding the role of GSTP1 Ile105Val polymorphism in pancreatic diseases and their results are inconsistent. The significance of GSTP1 Ile105Val polymorphism for pan creatic pathology remains unclear and further studies are needed in order to elucidate its role in pancreatic diseases. .
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - Polimorfizam GSTP1 Ile105Val u srpskoj populaciji sa pankreasnim oboljenjima
T1  - GSTP1 Ile105Val polymorphism in Serbian patients with pancreatic diseases
EP  - 125
IS  - 2
SP  - 121
VL  - 30
DO  - 10.2478/v10011-011-0001-y
ER  - 

@article{
author = "Nikolić, Aleksandra and Stanković, Marija and Nišević, Ivan and Lukić, Snežana and Anđelić-Jelić, Marina and Popović, Dragan and Radojković, Dragica",
year = "2011",
abstract = "Cilj ove studije bio je da se odredi učestalost polimorfizma Ile105Val u genu za glutation S-transferazu P1 (GSTP1) i proceni njegov uticaj na rizik za obolevanje od pankreasnih bolesti u srpskoj populaciji. Studija je obuhvatila 157 pacijenata sa najčešćim bolestima pankreasa: 47 sa karcinomom pankreasa, 50 sa hroničnim pankreatitisom i 60 sa dijabetes melitusom tipa 2, kao i 107 zdravih ispitanika. Prisustvo polimorfizma Ile105Val u genu za GSTP1 je analizirano metodom PCR-RFLP (Polymerase Chain Reaction - Restriction Fragment Length Polymorphism). Učestalost alela 105Val je bila niža kod pacijenata sa karcinomom pankreasa (24,5%) i hroničnim pankreatitisom (24,0%) i neznatno povišena kod pacijenata sa dijabe tes melitusom tipa 2 (31,7%) u odnosu na učestalost kod zdra vih ispitanika (29,9%), ali razlike nisu bile statistički zna čaj ne. Učestalost pojedinih genotipova polimorfizma Ile105Val se razlikovala među analiziranim grupama, ali razlike takođe nisu bile statistički značajne. Samo nekoliko studija se do sada bavilo ulogom GSTP1 Ile105Val polimorfizma u bolestima pankreasa i uglavnom su dale oprečne rezultate. Značaj GSTP1 Ile105Val polimorfizma za bolesti pankreasa još uvek nije razjašnjen i potrebna su dalja istraživanja da bi se ispitala njegova uloga u pankreasnom tkivu. ., The aim of the current preliminary case-control study was to identify glutathione S-transferase P1 (GSTP1) Ile105Val allele and genotype frequency and to evaluate its impact on susceptibility to pancreatic diseases in a Serbian population. This study has encom passed 157 patients with three major types of chronic pancreatic pathology: 47 with pancreatic cancer, 50 with chronic pancreatitis and 60 with type 2 diabetes mellitus, as well as 107 healthy individuals. The presence of GSTP1 Ile105Val polymorphism was analyzed using a PCR-RFLP method. Allele 105Val was less frequent in patients with pancreatic cancer (24.5%) and chronic pancreatitis (24.0%) and slightly more frequent in patients with type 2 diabetes mellitus (31.7%) in comparison to healthy individuals (29.9%), but the differences were not statistically significant. Distribution of Ile105Val polymorphism genotypes differed between the analyzed groups, but differences were also not statistically significant. There are only a few studies regarding the role of GSTP1 Ile105Val polymorphism in pancreatic diseases and their results are inconsistent. The significance of GSTP1 Ile105Val polymorphism for pan creatic pathology remains unclear and further studies are needed in order to elucidate its role in pancreatic diseases. .",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Polimorfizam GSTP1 Ile105Val u srpskoj populaciji sa pankreasnim oboljenjima, GSTP1 Ile105Val polymorphism in Serbian patients with pancreatic diseases",
pages = "125-121",
number = "2",
volume = "30",
doi = "10.2478/v10011-011-0001-y"
}

Nikolić, A., Stanković, M., Nišević, I., Lukić, S., Anđelić-Jelić, M., Popović, D.,& Radojković, D.. (2011). Polimorfizam GSTP1 Ile105Val u srpskoj populaciji sa pankreasnim oboljenjima. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 30(2), 121-125.
https://doi.org/10.2478/v10011-011-0001-y

Nikolić A, Stanković M, Nišević I, Lukić S, Anđelić-Jelić M, Popović D, Radojković D. Polimorfizam GSTP1 Ile105Val u srpskoj populaciji sa pankreasnim oboljenjima. in Journal of Medical Biochemistry. 2011;30(2):121-125.
doi:10.2478/v10011-011-0001-y .

Nikolić, Aleksandra, Stanković, Marija, Nišević, Ivan, Lukić, Snežana, Anđelić-Jelić, Marina, Popović, Dragan, Radojković, Dragica, "Polimorfizam GSTP1 Ile105Val u srpskoj populaciji sa pankreasnim oboljenjima" in Journal of Medical Biochemistry, 30, no. 2 (2011):121-125,
https://doi.org/10.2478/v10011-011-0001-y . .

TY  - JOUR
AU  - Kojić, Snežana
AU  - Radojković, Dragica
AU  - Faulkner, Georgine
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/493
AB  - Remodeling is a stringently controlled process that enables adequate response of muscle cells to constant physical stresses. In this process, different kinds of stimuli have to be sensed and converted into biochemical signals that ultimately lead to alterations of muscle phenotype. Several multiprotein complexes located in the sarcomere and organized on the titin molecular spring have been identified as stress sensors and signal transducers. In this review, we focus on Ankrd1/CARP and Ankrd2/Arpp proteins, which belong to the muscle ankyrin repeat protein family (MARP) involved in a mechano-signaling pathway that links myofibrillar stress response to muscle gene expression. Apart from the mechanosensory function, they have an important role in transcriptional regulation, myofibrillar assembly, cardiogenesis and myogenesis. Their altered expression has been demonstrated in neuromuscular disorders, cardiovascular diseases, as well as in tumors, suggesting a role in pathological processes. Although analyzed in a limited number of patients, there is a considerable body of evidence that MARP proteins could be suitable candidates for prognostic and diagnostic biomarkers.
PB  - Taylor & Francis Ltd, Abingdon
T2  - Critical Reviews in Clinical Laboratory Sciences
T1  - Muscle ankyrin repeat proteins: their role in striated muscle function in health and disease
EP  - 294
IS  - 5-6
SP  - 269
VL  - 48
DO  - 10.3109/10408363.2011.643857
ER  - 

@article{
author = "Kojić, Snežana and Radojković, Dragica and Faulkner, Georgine",
year = "2011",
abstract = "Remodeling is a stringently controlled process that enables adequate response of muscle cells to constant physical stresses. In this process, different kinds of stimuli have to be sensed and converted into biochemical signals that ultimately lead to alterations of muscle phenotype. Several multiprotein complexes located in the sarcomere and organized on the titin molecular spring have been identified as stress sensors and signal transducers. In this review, we focus on Ankrd1/CARP and Ankrd2/Arpp proteins, which belong to the muscle ankyrin repeat protein family (MARP) involved in a mechano-signaling pathway that links myofibrillar stress response to muscle gene expression. Apart from the mechanosensory function, they have an important role in transcriptional regulation, myofibrillar assembly, cardiogenesis and myogenesis. Their altered expression has been demonstrated in neuromuscular disorders, cardiovascular diseases, as well as in tumors, suggesting a role in pathological processes. Although analyzed in a limited number of patients, there is a considerable body of evidence that MARP proteins could be suitable candidates for prognostic and diagnostic biomarkers.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "Critical Reviews in Clinical Laboratory Sciences",
title = "Muscle ankyrin repeat proteins: their role in striated muscle function in health and disease",
pages = "294-269",
number = "5-6",
volume = "48",
doi = "10.3109/10408363.2011.643857"
}

Kojić, S., Radojković, D.,& Faulkner, G.. (2011). Muscle ankyrin repeat proteins: their role in striated muscle function in health and disease. in Critical Reviews in Clinical Laboratory Sciences
Taylor & Francis Ltd, Abingdon., 48(5-6), 269-294.
https://doi.org/10.3109/10408363.2011.643857

Kojić S, Radojković D, Faulkner G. Muscle ankyrin repeat proteins: their role in striated muscle function in health and disease. in Critical Reviews in Clinical Laboratory Sciences. 2011;48(5-6):269-294.
doi:10.3109/10408363.2011.643857 .

Kojić, Snežana, Radojković, Dragica, Faulkner, Georgine, "Muscle ankyrin repeat proteins: their role in striated muscle function in health and disease" in Critical Reviews in Clinical Laboratory Sciences, 48, no. 5-6 (2011):269-294,
https://doi.org/10.3109/10408363.2011.643857 . .

TY  - JOUR
AU  - Lazić, J.
AU  - Tošić, Nataša
AU  - Dokmanović, Lidija
AU  - Krstovski, N.
AU  - Rodić, P.
AU  - Pavlović, Sonja
AU  - Janić, D.
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/423
AB  - Contemporary protocols ensure high-remission rate and long-term free survival in children with acute lymphoblastic leukemia (ALL), but small percentage of patients is still incurable. Molecular genetic methods helped to establish submicroscopic classification as well as minimal residual disease follow-up, considered to be responsible for relapse. Our study enrolled 70 pediatric patients with de novo ALL, analyzed using reverse transcriptase-polymerase chain reaction for the presence of four major risk-stratifying translocations (BCR/ABL, MLL/AF4, TEL/AML1, and E2A/PBX1). Bone marrow samples were collected at diagnosis, at the end of induction phase, and after intensive chemotherapy with the aim to establish the correlation between chromosomal aberration, clinical features, and treatment response. Presenting the results of this study, we offer another evidence of variable incidence and clinical characteristics of ALL subtypes.
PB  - Humana Press Inc, Totowa
T2  - Medical Oncology
T1  - Clinical features of the most common fusion genes in childhood acute lymphoblastic leukemia
EP  - 453
IS  - 2
SP  - 449
VL  - 27
DO  - 10.1007/s12032-009-9232-x
ER  - 

@article{
author = "Lazić, J. and Tošić, Nataša and Dokmanović, Lidija and Krstovski, N. and Rodić, P. and Pavlović, Sonja and Janić, D.",
year = "2010",
abstract = "Contemporary protocols ensure high-remission rate and long-term free survival in children with acute lymphoblastic leukemia (ALL), but small percentage of patients is still incurable. Molecular genetic methods helped to establish submicroscopic classification as well as minimal residual disease follow-up, considered to be responsible for relapse. Our study enrolled 70 pediatric patients with de novo ALL, analyzed using reverse transcriptase-polymerase chain reaction for the presence of four major risk-stratifying translocations (BCR/ABL, MLL/AF4, TEL/AML1, and E2A/PBX1). Bone marrow samples were collected at diagnosis, at the end of induction phase, and after intensive chemotherapy with the aim to establish the correlation between chromosomal aberration, clinical features, and treatment response. Presenting the results of this study, we offer another evidence of variable incidence and clinical characteristics of ALL subtypes.",
publisher = "Humana Press Inc, Totowa",
journal = "Medical Oncology",
title = "Clinical features of the most common fusion genes in childhood acute lymphoblastic leukemia",
pages = "453-449",
number = "2",
volume = "27",
doi = "10.1007/s12032-009-9232-x"
}

Lazić, J., Tošić, N., Dokmanović, L., Krstovski, N., Rodić, P., Pavlović, S.,& Janić, D.. (2010). Clinical features of the most common fusion genes in childhood acute lymphoblastic leukemia. in Medical Oncology
Humana Press Inc, Totowa., 27(2), 449-453.
https://doi.org/10.1007/s12032-009-9232-x

Lazić J, Tošić N, Dokmanović L, Krstovski N, Rodić P, Pavlović S, Janić D. Clinical features of the most common fusion genes in childhood acute lymphoblastic leukemia. in Medical Oncology. 2010;27(2):449-453.
doi:10.1007/s12032-009-9232-x .

Lazić, J., Tošić, Nataša, Dokmanović, Lidija, Krstovski, N., Rodić, P., Pavlović, Sonja, Janić, D., "Clinical features of the most common fusion genes in childhood acute lymphoblastic leukemia" in Medical Oncology, 27, no. 2 (2010):449-453,
https://doi.org/10.1007/s12032-009-9232-x . .

TY  - JOUR
AU  - Zukić, Branka
AU  - Radmilović Milena
AU  - Stojiljković, Maja
AU  - Tošić, Nataša
AU  - Pourfarzad, Farzin
AU  - Dokmanović, Lidija
AU  - Janić, Dragana
AU  - Čolović, Nataša
AU  - Philipsen, Sjaak
AU  - Patrinos, George P.
AU  - Pavlović, Sonja
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/422
AB  - Aims: Thiopurine S-methyltransferase (TPMT) activity is polymorphic, and a trimodal distribution has been demonstrated in Caucasians (low, intermediate and high methylator groups). The TPMT gene promoter contains a variable number of three GC-rich tandem repeats, namely A, B and C, ranging from three to nine in length in a A(n)B(m),C architecture. Materials & methods: Here, we investigated the influence of number and type of TPMT gene promoter tandem repeats on human TPMT gene transcription in K562 cells transiently transfected with reporter constructs bearing various variable number of tandem repeats (VNTR) and addressed the interaction of transcription factor binding to the VNTRs by electrophoretic mobility shift assays. Results: We found that the distribution patterns of VNTR alleles do not significantly differ among acute lymphoblastic leukemia patients, acute myeloid leukemia patients and normal individuals. We also demonstrated that the A repeat has a negative effect in TPMT gene transcription and that a positive regulatory element, identified immediately upstream to the VNTR region of the TPMT gene promoter, is indispensable for TPMT gene transcription. Our electrophoretic mobility shift assay analysis indicated that the Sp1 and Sp3 transcription factors bind to the VNTR repeats. Conclusion: Overall, our data underline that both the number and type of VNTRs, as well as the upstream regulatory region of the TPMT gene promoter, determine the overall level of TPMT gene transcription. It remains to be seen whether these VNTRs can be employed as pharmacogenetic markers to individualize thiopurine therapy.
PB  - Future Medicine Ltd, London
T2  - Pharmacogenomics
T1  - Functional analysis of the role of the TPMT gene promoter VNTR polymorphism in TPMT gene transcription
EP  - 557
IS  - 4
SP  - 547
VL  - 11
DO  - 10.2217/PGS.10.7
ER  - 

@article{
author = "Zukić, Branka and Radmilović Milena and Stojiljković, Maja and Tošić, Nataša and Pourfarzad, Farzin and Dokmanović, Lidija and Janić, Dragana and Čolović, Nataša and Philipsen, Sjaak and Patrinos, George P. and Pavlović, Sonja",
year = "2010",
abstract = "Aims: Thiopurine S-methyltransferase (TPMT) activity is polymorphic, and a trimodal distribution has been demonstrated in Caucasians (low, intermediate and high methylator groups). The TPMT gene promoter contains a variable number of three GC-rich tandem repeats, namely A, B and C, ranging from three to nine in length in a A(n)B(m),C architecture. Materials & methods: Here, we investigated the influence of number and type of TPMT gene promoter tandem repeats on human TPMT gene transcription in K562 cells transiently transfected with reporter constructs bearing various variable number of tandem repeats (VNTR) and addressed the interaction of transcription factor binding to the VNTRs by electrophoretic mobility shift assays. Results: We found that the distribution patterns of VNTR alleles do not significantly differ among acute lymphoblastic leukemia patients, acute myeloid leukemia patients and normal individuals. We also demonstrated that the A repeat has a negative effect in TPMT gene transcription and that a positive regulatory element, identified immediately upstream to the VNTR region of the TPMT gene promoter, is indispensable for TPMT gene transcription. Our electrophoretic mobility shift assay analysis indicated that the Sp1 and Sp3 transcription factors bind to the VNTR repeats. Conclusion: Overall, our data underline that both the number and type of VNTRs, as well as the upstream regulatory region of the TPMT gene promoter, determine the overall level of TPMT gene transcription. It remains to be seen whether these VNTRs can be employed as pharmacogenetic markers to individualize thiopurine therapy.",
publisher = "Future Medicine Ltd, London",
journal = "Pharmacogenomics",
title = "Functional analysis of the role of the TPMT gene promoter VNTR polymorphism in TPMT gene transcription",
pages = "557-547",
number = "4",
volume = "11",
doi = "10.2217/PGS.10.7"
}

Zukić, B., Radmilović Milena, Stojiljković, M., Tošić, N., Pourfarzad, F., Dokmanović, L., Janić, D., Čolović, N., Philipsen, S., Patrinos, G. P.,& Pavlović, S.. (2010). Functional analysis of the role of the TPMT gene promoter VNTR polymorphism in TPMT gene transcription. in Pharmacogenomics
Future Medicine Ltd, London., 11(4), 547-557.
https://doi.org/10.2217/PGS.10.7

Zukić B, Radmilović Milena, Stojiljković M, Tošić N, Pourfarzad F, Dokmanović L, Janić D, Čolović N, Philipsen S, Patrinos GP, Pavlović S. Functional analysis of the role of the TPMT gene promoter VNTR polymorphism in TPMT gene transcription. in Pharmacogenomics. 2010;11(4):547-557.
doi:10.2217/PGS.10.7 .

Zukić, Branka, Radmilović Milena, Stojiljković, Maja, Tošić, Nataša, Pourfarzad, Farzin, Dokmanović, Lidija, Janić, Dragana, Čolović, Nataša, Philipsen, Sjaak, Patrinos, George P., Pavlović, Sonja, "Functional analysis of the role of the TPMT gene promoter VNTR polymorphism in TPMT gene transcription" in Pharmacogenomics, 11, no. 4 (2010):547-557,
https://doi.org/10.2217/PGS.10.7 . .

TY  - JOUR
AU  - Radmilović Milena
AU  - Zukić, Branka
AU  - Stanković, Biljana
AU  - Karan-Đurašević, Teodora
AU  - Stojiljković, Maja
AU  - Spasovski, Vesna
AU  - Tošić, Nataša
AU  - Dokmanović, Lidija
AU  - Janić, Dragana
AU  - Pavlović, Sonja
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/401
AB  - Thalassemia syndromes constitute a group of genetic disorders, widespread throughout the world. The present study contains data on thalassemia syndromes and their chromosomal environment obtained in Serbia over a period of 10 years. Ten different beta-thalassemia (beta-thal) mutations and two hemoglobin (Hb) variants were detected in 127 members of 68 families. Hb Lepore-Boston-Washington (Lepore-BW) (delta 87Gln-beta-IVS-II-8), a thalassemic Hb variant, was shown to be the most common cause of thalassemia in Serbia. Haplotype analyses of the beta-globin gene clusters of healthy individuals as well as of individuals affected with beta-thal showed that haplotype I was the most frequent haplotype in the Serbian population, followed by haplotypes II and IX. Two novel haplotypes were detected. Haplotype analyses showed the association between certain haplotypes and the most common thalassemic mutations. Results presented in this paper will update the Serbian national mutation database and contribute to a better understanding of genographic history of South European and Balkan populations.
PB  - Taylor & Francis Ltd, Abingdon
T2  - Hemoglobin
T1  - Thalassemia syndromes in Serbia: an update
EP  - 485
IS  - 5
SP  - 477
VL  - 34
DO  - 10.3109/03630269.2010.513637
ER  - 

@article{
author = "Radmilović Milena and Zukić, Branka and Stanković, Biljana and Karan-Đurašević, Teodora and Stojiljković, Maja and Spasovski, Vesna and Tošić, Nataša and Dokmanović, Lidija and Janić, Dragana and Pavlović, Sonja",
year = "2010",
abstract = "Thalassemia syndromes constitute a group of genetic disorders, widespread throughout the world. The present study contains data on thalassemia syndromes and their chromosomal environment obtained in Serbia over a period of 10 years. Ten different beta-thalassemia (beta-thal) mutations and two hemoglobin (Hb) variants were detected in 127 members of 68 families. Hb Lepore-Boston-Washington (Lepore-BW) (delta 87Gln-beta-IVS-II-8), a thalassemic Hb variant, was shown to be the most common cause of thalassemia in Serbia. Haplotype analyses of the beta-globin gene clusters of healthy individuals as well as of individuals affected with beta-thal showed that haplotype I was the most frequent haplotype in the Serbian population, followed by haplotypes II and IX. Two novel haplotypes were detected. Haplotype analyses showed the association between certain haplotypes and the most common thalassemic mutations. Results presented in this paper will update the Serbian national mutation database and contribute to a better understanding of genographic history of South European and Balkan populations.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "Hemoglobin",
title = "Thalassemia syndromes in Serbia: an update",
pages = "485-477",
number = "5",
volume = "34",
doi = "10.3109/03630269.2010.513637"
}

Radmilović Milena, Zukić, B., Stanković, B., Karan-Đurašević, T., Stojiljković, M., Spasovski, V., Tošić, N., Dokmanović, L., Janić, D.,& Pavlović, S.. (2010). Thalassemia syndromes in Serbia: an update. in Hemoglobin
Taylor & Francis Ltd, Abingdon., 34(5), 477-485.
https://doi.org/10.3109/03630269.2010.513637

Radmilović Milena, Zukić B, Stanković B, Karan-Đurašević T, Stojiljković M, Spasovski V, Tošić N, Dokmanović L, Janić D, Pavlović S. Thalassemia syndromes in Serbia: an update. in Hemoglobin. 2010;34(5):477-485.
doi:10.3109/03630269.2010.513637 .

Radmilović Milena, Zukić, Branka, Stanković, Biljana, Karan-Đurašević, Teodora, Stojiljković, Maja, Spasovski, Vesna, Tošić, Nataša, Dokmanović, Lidija, Janić, Dragana, Pavlović, Sonja, "Thalassemia syndromes in Serbia: an update" in Hemoglobin, 34, no. 5 (2010):477-485,
https://doi.org/10.3109/03630269.2010.513637 . .

TY  - JOUR
AU  - Kojić, Snežana
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/456
AB  - Familiju MARP (muscle ankyrin repeat proteins) čine tri strukturno slična proteina: CARP/Ankrd1, Ankrd2/Arpp i DARP/Ankrd23. Sva tri proteina poseduju ankirinske ponovke preko kojih ostvaruju protein-protein interakcije kao i signal za lokalizaciju u jedru. Članovi familije MARP imaju strukturnu i regulatornu funkciju i mogu biti lokalizovani i u jedru i u citoplazmi mišićne ćelije. Učestvuju u signalnoj transdukciji kao molekulski glasnici koji prenose informacije mehaničkog stresa sa sarkomere do jedra, gde učestvuju u regulaciji genske ekspresije. Nivo proteina CARP/Ankrd1 i Ankrd2/Arpp je izmenjen u mišićnim bolestima koje karakteriše atrofija mišića, kao što su Dišenova mišićna distrofija, kongenitalna miopatija i spinalna mišićna atrofija. Mutacije u genu za CARP/Ankrd1 su otkrivene u pacijenata sa dilatiranom i hipertrofičnom kardiomiopatijom. Promene u ekspresiji ovih proteina su takođe uočene u tumorima kao što su rabdomiosarkom, onkocitom bubrega i kancer ovarijuma. U cilju funkcionalne karakterizacije proteina familije MARP, pokazali smo da oba proteina interaguju sa supresorom tumora p53, a geni za CARP/Ankrd1 i Ankrd2/Arpp su pozitivno regulisani ovim transkripcionim faktorom. Rezultati su ukazali na moguću ulogu proteina CARP/Ankrd1 i Ankrd2/Arpp u molekularnim mehanizmima tumorogeneze, čime se otvara novo polje istraživanja ove familije proteina.
AB  - The MARP (muscle ankyrin repeat protein) family comprises three structurally similar proteins: CARP/Ankrd1, Ankrd2/Arpp and DARP/Ankrd23. They share four conserved copies of 33-residue ankyrin repeats and contain a nuclear localization signal, allowing the sorting of MARPs to the nucleus. They are found both in the nucleus and in the cytoplasm of skeletal and cardiac muscle cells, suggesting that MARPs shuttle within the cell enabling them to play a role in signal transduction in striated muscle. Expression of MARPs is altered under different pathological conditions. In skeletal muscle, CARP/Ankrd1 and Ankrd2/Arpp are up-regulated in muscle in patients suffering from Duchene muscular dystrophy, congenital myopathy and spinal muscular atrophy. Mutations in Ankrd1 gene (coding CARP/Ankrd1) were identified in dilated and hypertrophic cardiomyopathies. Altered expression of MARPs is also observed in rhabdomyosarcoma, renal oncocytoma and ovarian cancer. In order to functionally characterize MARP family members CARP/Ankrd1 and Ankrd2/Arpp, we have found that both proteins interact with the tumor suppressor p53 both in vivo and in vitro and that p53 up-regulates their expression. Our results implicate the potential role of MARPs in molecular mechanisms relevant to tumor response and progression.
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze
T1  - MARP protein family: A possible role in molecular mechanisms of tumorigenesis
EP  - 164
IS  - 3
SP  - 157
VL  - 29
DO  - 10.2478/v10011-010-0024-9
ER  - 

@article{
author = "Kojić, Snežana",
year = "2010",
abstract = "Familiju MARP (muscle ankyrin repeat proteins) čine tri strukturno slična proteina: CARP/Ankrd1, Ankrd2/Arpp i DARP/Ankrd23. Sva tri proteina poseduju ankirinske ponovke preko kojih ostvaruju protein-protein interakcije kao i signal za lokalizaciju u jedru. Članovi familije MARP imaju strukturnu i regulatornu funkciju i mogu biti lokalizovani i u jedru i u citoplazmi mišićne ćelije. Učestvuju u signalnoj transdukciji kao molekulski glasnici koji prenose informacije mehaničkog stresa sa sarkomere do jedra, gde učestvuju u regulaciji genske ekspresije. Nivo proteina CARP/Ankrd1 i Ankrd2/Arpp je izmenjen u mišićnim bolestima koje karakteriše atrofija mišića, kao što su Dišenova mišićna distrofija, kongenitalna miopatija i spinalna mišićna atrofija. Mutacije u genu za CARP/Ankrd1 su otkrivene u pacijenata sa dilatiranom i hipertrofičnom kardiomiopatijom. Promene u ekspresiji ovih proteina su takođe uočene u tumorima kao što su rabdomiosarkom, onkocitom bubrega i kancer ovarijuma. U cilju funkcionalne karakterizacije proteina familije MARP, pokazali smo da oba proteina interaguju sa supresorom tumora p53, a geni za CARP/Ankrd1 i Ankrd2/Arpp su pozitivno regulisani ovim transkripcionim faktorom. Rezultati su ukazali na moguću ulogu proteina CARP/Ankrd1 i Ankrd2/Arpp u molekularnim mehanizmima tumorogeneze, čime se otvara novo polje istraživanja ove familije proteina., The MARP (muscle ankyrin repeat protein) family comprises three structurally similar proteins: CARP/Ankrd1, Ankrd2/Arpp and DARP/Ankrd23. They share four conserved copies of 33-residue ankyrin repeats and contain a nuclear localization signal, allowing the sorting of MARPs to the nucleus. They are found both in the nucleus and in the cytoplasm of skeletal and cardiac muscle cells, suggesting that MARPs shuttle within the cell enabling them to play a role in signal transduction in striated muscle. Expression of MARPs is altered under different pathological conditions. In skeletal muscle, CARP/Ankrd1 and Ankrd2/Arpp are up-regulated in muscle in patients suffering from Duchene muscular dystrophy, congenital myopathy and spinal muscular atrophy. Mutations in Ankrd1 gene (coding CARP/Ankrd1) were identified in dilated and hypertrophic cardiomyopathies. Altered expression of MARPs is also observed in rhabdomyosarcoma, renal oncocytoma and ovarian cancer. In order to functionally characterize MARP family members CARP/Ankrd1 and Ankrd2/Arpp, we have found that both proteins interact with the tumor suppressor p53 both in vivo and in vitro and that p53 up-regulates their expression. Our results implicate the potential role of MARPs in molecular mechanisms relevant to tumor response and progression.",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze, MARP protein family: A possible role in molecular mechanisms of tumorigenesis",
pages = "164-157",
number = "3",
volume = "29",
doi = "10.2478/v10011-010-0024-9"
}

Kojić, S.. (2010). Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 29(3), 157-164.
https://doi.org/10.2478/v10011-010-0024-9

Kojić S. Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze. in Journal of Medical Biochemistry. 2010;29(3):157-164.
doi:10.2478/v10011-010-0024-9 .

Kojić, Snežana, "Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze" in Journal of Medical Biochemistry, 29, no. 3 (2010):157-164,
https://doi.org/10.2478/v10011-010-0024-9 . .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Stanković, Marija
AU  - Dinić, Jelena
AU  - Lukić, Snežana
AU  - Anđelić-Jelić, Marina
AU  - Popović, Dragan
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/443
AB  - Jedan od osnovnih izazova u proučavanju patologije bolesti pankreasa predstavlja dalje razjašnjavanje uloge proteaza i antiproteaza, zbog toga što poremećena ravnoteža između njih može dovesti do oštećenja pankreasa. Alfa 1-antitripsin (AAT) je jedan od najvažnijih inhibitora proteolitičkih enzima u serumu, među kojima su i enzimi pankreasa: tripsin, himotripsin i elastaza. Pretpostavlja se da mutacije u AAT genu mogu da utiču na pojavu i razvoj bolesti pankreasa. Prisustvo najčešćih mutacija u AAT genu, označenih kao Z i S, analizirano je u 160 pacijenata sa bolestima pankreasa (50 pacijenata sa kancerom pankreasa, 50 pacijenata sa hroničnim pankreatitisom i 60 pacijenata sa dijabetesom tipa 2) i u 129 zdravih osoba. Prisustvo mutacija detektovano je analizom dužina restrikcionih fragmenata. Jedan pacijent sa kancerom pankreasa je bio heterozigotni nosilac Z mutacije, kao i jedan pacijent sa dijabetesom tipa 2. Jedan pacijent sa hroničnim pankreatitisom je bio heterozigotni nosilac S mutacije. Dve najčešće mutacije u AAT genu su bile statistički značajno učestalije kod pacijenata sa bolestima pankreasa (3 / 160 pacijenata, alelska frekvencija 0,9%) nego u kontrolnoj grupi (1 / 129 osoba, alelska frekvencija 0,4%). Rezultati ove studije, koje ukazuju na moguću povezanost Z i S mutacija sa umerenim povećanjem rizika za razvoj bolesti pankreasa.
AB  - One of the key points in research of pancreatic disease pathology is further elucidation of the role of proteases and antiproteases, since their imbalance can lead to pancreatic injury. Alpha 1-antitrypsin (AAT) is one of the most important serum inhibitors of proteolytic enzymes, including pancreatic enzymes trypsin, chymotrypsin and elastase. It is speculated that mutations in the AAT gene may influence the onset and the development of pancreatic disease. The presence of the most common AAT mutations Z and S was analyzed in 160 patients with pancreatic diseases (50 patients with pancreatic cancer, 50 patients with chronic pancreatitis and 60 patients with type 2 diabetes mellitus) and 129 healthy individuals by PCR-mediated site-directed mutagenesis (PSM) method. One patient with pancreatic cancer was found to be a carrier of Z mutation, as well as one patient with type 2 diabetes mellitus. One patient with chronic pancreatitis was found to be a carrier of S mutation. The common AAT mutations were statistically significantly over-represented in patients with pancreatic diseases (3 of 160 patients, allelic frequency 0.9%) than in the control group (1 of 129 individuals, allelic frequency 0.4%). The results of this study, requiring confirmation, suggest that common AAT mutations Z and S may be associated with a modest increase in susceptibility to the development of pancreatic disease.
PB  - Društvo genetičara Srbije, Beograd
T2  - Genetika-Belgrade
T1  - Učestalost S i Z mutacija u genu za alfa 1-antitripsin kod pacijenata sa bolestima pankreasa
T1  - Prevalence of S and Z alpha 1-antitrypsin mutations in patients with pancreatic diseases in Serbian population
EP  - 385
IS  - 2
SP  - 377
VL  - 42
DO  - 10.2298/GENSR1002377N
ER  - 

@article{
author = "Nikolić, Aleksandra and Divac Rankov, Aleksandra and Stanković, Marija and Dinić, Jelena and Lukić, Snežana and Anđelić-Jelić, Marina and Popović, Dragan and Radojković, Dragica",
year = "2010",
abstract = "Jedan od osnovnih izazova u proučavanju patologije bolesti pankreasa predstavlja dalje razjašnjavanje uloge proteaza i antiproteaza, zbog toga što poremećena ravnoteža između njih može dovesti do oštećenja pankreasa. Alfa 1-antitripsin (AAT) je jedan od najvažnijih inhibitora proteolitičkih enzima u serumu, među kojima su i enzimi pankreasa: tripsin, himotripsin i elastaza. Pretpostavlja se da mutacije u AAT genu mogu da utiču na pojavu i razvoj bolesti pankreasa. Prisustvo najčešćih mutacija u AAT genu, označenih kao Z i S, analizirano je u 160 pacijenata sa bolestima pankreasa (50 pacijenata sa kancerom pankreasa, 50 pacijenata sa hroničnim pankreatitisom i 60 pacijenata sa dijabetesom tipa 2) i u 129 zdravih osoba. Prisustvo mutacija detektovano je analizom dužina restrikcionih fragmenata. Jedan pacijent sa kancerom pankreasa je bio heterozigotni nosilac Z mutacije, kao i jedan pacijent sa dijabetesom tipa 2. Jedan pacijent sa hroničnim pankreatitisom je bio heterozigotni nosilac S mutacije. Dve najčešće mutacije u AAT genu su bile statistički značajno učestalije kod pacijenata sa bolestima pankreasa (3 / 160 pacijenata, alelska frekvencija 0,9%) nego u kontrolnoj grupi (1 / 129 osoba, alelska frekvencija 0,4%). Rezultati ove studije, koje ukazuju na moguću povezanost Z i S mutacija sa umerenim povećanjem rizika za razvoj bolesti pankreasa., One of the key points in research of pancreatic disease pathology is further elucidation of the role of proteases and antiproteases, since their imbalance can lead to pancreatic injury. Alpha 1-antitrypsin (AAT) is one of the most important serum inhibitors of proteolytic enzymes, including pancreatic enzymes trypsin, chymotrypsin and elastase. It is speculated that mutations in the AAT gene may influence the onset and the development of pancreatic disease. The presence of the most common AAT mutations Z and S was analyzed in 160 patients with pancreatic diseases (50 patients with pancreatic cancer, 50 patients with chronic pancreatitis and 60 patients with type 2 diabetes mellitus) and 129 healthy individuals by PCR-mediated site-directed mutagenesis (PSM) method. One patient with pancreatic cancer was found to be a carrier of Z mutation, as well as one patient with type 2 diabetes mellitus. One patient with chronic pancreatitis was found to be a carrier of S mutation. The common AAT mutations were statistically significantly over-represented in patients with pancreatic diseases (3 of 160 patients, allelic frequency 0.9%) than in the control group (1 of 129 individuals, allelic frequency 0.4%). The results of this study, requiring confirmation, suggest that common AAT mutations Z and S may be associated with a modest increase in susceptibility to the development of pancreatic disease.",
publisher = "Društvo genetičara Srbije, Beograd",
journal = "Genetika-Belgrade",
title = "Učestalost S i Z mutacija u genu za alfa 1-antitripsin kod pacijenata sa bolestima pankreasa, Prevalence of S and Z alpha 1-antitrypsin mutations in patients with pancreatic diseases in Serbian population",
pages = "385-377",
number = "2",
volume = "42",
doi = "10.2298/GENSR1002377N"
}

Nikolić, A., Divac Rankov, A., Stanković, M., Dinić, J., Lukić, S., Anđelić-Jelić, M., Popović, D.,& Radojković, D.. (2010). Učestalost S i Z mutacija u genu za alfa 1-antitripsin kod pacijenata sa bolestima pankreasa. in Genetika-Belgrade
Društvo genetičara Srbije, Beograd., 42(2), 377-385.
https://doi.org/10.2298/GENSR1002377N

Nikolić A, Divac Rankov A, Stanković M, Dinić J, Lukić S, Anđelić-Jelić M, Popović D, Radojković D. Učestalost S i Z mutacija u genu za alfa 1-antitripsin kod pacijenata sa bolestima pankreasa. in Genetika-Belgrade. 2010;42(2):377-385.
doi:10.2298/GENSR1002377N .

Nikolić, Aleksandra, Divac Rankov, Aleksandra, Stanković, Marija, Dinić, Jelena, Lukić, Snežana, Anđelić-Jelić, Marina, Popović, Dragan, Radojković, Dragica, "Učestalost S i Z mutacija u genu za alfa 1-antitripsin kod pacijenata sa bolestima pankreasa" in Genetika-Belgrade, 42, no. 2 (2010):377-385,
https://doi.org/10.2298/GENSR1002377N . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Mitić, Gorana
AU  - Miković, Zeljko
AU  - Antonijević, Nebojša
AU  - Đorđević, Valentina
AU  - Miković, Danijela
AU  - Mandić, Vesna
AU  - Rakićević, Ljiljana
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/412
AB  - Factor V Leiden (FVLeiden) and prothrombin G20210A are the most common genetic causes of thrombophilia and established risk factors for different clinical manifestations of venous thromboembolism (VTE). This study investigated whether the clinical manifestation of VTE, the extension of deep vein thrombosis (DVT) and the presence of transient risk factors at the time of the first VTE, differed among patients with mutations (97 with FVLeiden; 33 with prothrombin G20210A) and in 109 patients without thrombophilia. Isolated pulmonary embolism (PE) was less prevalent in patients with FVLeiden (6%) and no thrombophilia (6%) than in those with prothrombin G20210A (15%). No difference was found in the incidence of distal DVT. Regarding the extension of proximal DVT, the lowest incidence for isolated popliteal vein and the highest for iliofemoral vein were observed in patients with prothrombin G20210A. No difference was observed between groups of patients with or without thrombophilia by unprovoked VTE. The pregnancy/puerperium was the most prevalent risk factor in carriers of prothrombin G20210A. Among FVLeiden carriers, the most prevalent risk factor was surgery, and in patients without thrombophilia, it was trauma (P  lt  .05). Thrombosis of the upper limb was more frequent in a group without thrombophilia than in patients with mutations (P  lt  .01). Transverse sinus venous thrombosis was present only in patients with prothrombin G20210A. Carriers of prothrombin G20210A have an increased risk of developing isolated PE and more severe clinical manifestations than those with FVLeiden or without thrombophilia.
PB  - Sage Publications Inc, Thousand Oaks
T2  - Clinical and Applied Thrombosis-Hemostasis
T1  - Type and Location of Venous Thromboembolism in Carriers of Factor V Leiden or Prothrombin G20210A Mutation Versus Patients With No Mutation
EP  - 70
IS  - 1
SP  - 66
VL  - 16
DO  - 10.1177/1076029608320721
ER  - 

@article{
author = "Kovač, Mirjana and Mitić, Gorana and Miković, Zeljko and Antonijević, Nebojša and Đorđević, Valentina and Miković, Danijela and Mandić, Vesna and Rakićević, Ljiljana and Radojković, Dragica",
year = "2010",
abstract = "Factor V Leiden (FVLeiden) and prothrombin G20210A are the most common genetic causes of thrombophilia and established risk factors for different clinical manifestations of venous thromboembolism (VTE). This study investigated whether the clinical manifestation of VTE, the extension of deep vein thrombosis (DVT) and the presence of transient risk factors at the time of the first VTE, differed among patients with mutations (97 with FVLeiden; 33 with prothrombin G20210A) and in 109 patients without thrombophilia. Isolated pulmonary embolism (PE) was less prevalent in patients with FVLeiden (6%) and no thrombophilia (6%) than in those with prothrombin G20210A (15%). No difference was found in the incidence of distal DVT. Regarding the extension of proximal DVT, the lowest incidence for isolated popliteal vein and the highest for iliofemoral vein were observed in patients with prothrombin G20210A. No difference was observed between groups of patients with or without thrombophilia by unprovoked VTE. The pregnancy/puerperium was the most prevalent risk factor in carriers of prothrombin G20210A. Among FVLeiden carriers, the most prevalent risk factor was surgery, and in patients without thrombophilia, it was trauma (P  lt  .05). Thrombosis of the upper limb was more frequent in a group without thrombophilia than in patients with mutations (P  lt  .01). Transverse sinus venous thrombosis was present only in patients with prothrombin G20210A. Carriers of prothrombin G20210A have an increased risk of developing isolated PE and more severe clinical manifestations than those with FVLeiden or without thrombophilia.",
publisher = "Sage Publications Inc, Thousand Oaks",
journal = "Clinical and Applied Thrombosis-Hemostasis",
title = "Type and Location of Venous Thromboembolism in Carriers of Factor V Leiden or Prothrombin G20210A Mutation Versus Patients With No Mutation",
pages = "70-66",
number = "1",
volume = "16",
doi = "10.1177/1076029608320721"
}

Kovač, M., Mitić, G., Miković, Z., Antonijević, N., Đorđević, V., Miković, D., Mandić, V., Rakićević, L.,& Radojković, D.. (2010). Type and Location of Venous Thromboembolism in Carriers of Factor V Leiden or Prothrombin G20210A Mutation Versus Patients With No Mutation. in Clinical and Applied Thrombosis-Hemostasis
Sage Publications Inc, Thousand Oaks., 16(1), 66-70.
https://doi.org/10.1177/1076029608320721

Kovač M, Mitić G, Miković Z, Antonijević N, Đorđević V, Miković D, Mandić V, Rakićević L, Radojković D. Type and Location of Venous Thromboembolism in Carriers of Factor V Leiden or Prothrombin G20210A Mutation Versus Patients With No Mutation. in Clinical and Applied Thrombosis-Hemostasis. 2010;16(1):66-70.
doi:10.1177/1076029608320721 .

Kovač, Mirjana, Mitić, Gorana, Miković, Zeljko, Antonijević, Nebojša, Đorđević, Valentina, Miković, Danijela, Mandić, Vesna, Rakićević, Ljiljana, Radojković, Dragica, "Type and Location of Venous Thromboembolism in Carriers of Factor V Leiden or Prothrombin G20210A Mutation Versus Patients With No Mutation" in Clinical and Applied Thrombosis-Hemostasis, 16, no. 1 (2010):66-70,
https://doi.org/10.1177/1076029608320721 . .

TY  - JOUR
AU  - Pruner, Iva
AU  - Đorđević, Valentina
AU  - Miljić, Predrag
AU  - Kovač, Mirjana
AU  - Antonijević, Nebojša
AU  - Rakićević, Ljiljana
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/441
AB  - Recurrent fetal loss (RFL) is common health problem affecting up to 5% of women of reproductive age. It has been shown that plasma thrombin-activatable fibrinolysis inhibitor (TAFI) concentrations increase during pregnancy and return to baseline levels soon after delivery. The +1040C/T single nucleotide polymorphism in coding region of TAFI gene is associated with TAFI blood levels. The aim of our study was to investigate the relationship between +1040C/T polymorphism in TAFI gene and idiopathic RFL. Study was carried out in a group of 120 women (61 controls and 59 women with idiopathic RFL). The R1040C/T polymorphism was detected by restriction fragment length polymorphism PCR. Increased frequency of +1040T/T genotype was observed in a study group, but without statistically significant difference. Carriers of T/T genotype have increased risk of fetal loss by 1.23-fold, compared with carriers of C/C (95% CI 0.462-3.277; P=0.7) and 1.34-fold compared with carriers of C/T genotype (95% CI 0.501-3.601; P=0.6). C allele is associated with reduced risk of recurrent fetal loss compared with T allele (OR 0.91; 95% CI 0.545-1.533; P=0.7). In conclusion, we observed increased frequency of +1040T/T genotype in a patient group, suggesting that this genotype could be potential risk factor for idiopathic RFL. Further investigation should be carried out in order to establish the role of this polymorphism in the etiology of idiopathic recurrent miscarriages. Blood Coagul Fibrinolysis 21: 679-682
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Blood Coagulation & Fibrinolysis
T1  - +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss
EP  - 682
IS  - 7
SP  - 679
VL  - 21
DO  - 10.1097/MBC.0b013e32833e426d
ER  - 

@article{
author = "Pruner, Iva and Đorđević, Valentina and Miljić, Predrag and Kovač, Mirjana and Antonijević, Nebojša and Rakićević, Ljiljana and Radojković, Dragica",
year = "2010",
abstract = "Recurrent fetal loss (RFL) is common health problem affecting up to 5% of women of reproductive age. It has been shown that plasma thrombin-activatable fibrinolysis inhibitor (TAFI) concentrations increase during pregnancy and return to baseline levels soon after delivery. The +1040C/T single nucleotide polymorphism in coding region of TAFI gene is associated with TAFI blood levels. The aim of our study was to investigate the relationship between +1040C/T polymorphism in TAFI gene and idiopathic RFL. Study was carried out in a group of 120 women (61 controls and 59 women with idiopathic RFL). The R1040C/T polymorphism was detected by restriction fragment length polymorphism PCR. Increased frequency of +1040T/T genotype was observed in a study group, but without statistically significant difference. Carriers of T/T genotype have increased risk of fetal loss by 1.23-fold, compared with carriers of C/C (95% CI 0.462-3.277; P=0.7) and 1.34-fold compared with carriers of C/T genotype (95% CI 0.501-3.601; P=0.6). C allele is associated with reduced risk of recurrent fetal loss compared with T allele (OR 0.91; 95% CI 0.545-1.533; P=0.7). In conclusion, we observed increased frequency of +1040T/T genotype in a patient group, suggesting that this genotype could be potential risk factor for idiopathic RFL. Further investigation should be carried out in order to establish the role of this polymorphism in the etiology of idiopathic recurrent miscarriages. Blood Coagul Fibrinolysis 21: 679-682",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Blood Coagulation & Fibrinolysis",
title = "+1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss",
pages = "682-679",
number = "7",
volume = "21",
doi = "10.1097/MBC.0b013e32833e426d"
}

Pruner, I., Đorđević, V., Miljić, P., Kovač, M., Antonijević, N., Rakićević, L.,& Radojković, D.. (2010). +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss. in Blood Coagulation & Fibrinolysis
Lippincott Williams & Wilkins, Philadelphia., 21(7), 679-682.
https://doi.org/10.1097/MBC.0b013e32833e426d

Pruner I, Đorđević V, Miljić P, Kovač M, Antonijević N, Rakićević L, Radojković D. +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss. in Blood Coagulation & Fibrinolysis. 2010;21(7):679-682.
doi:10.1097/MBC.0b013e32833e426d .

Pruner, Iva, Đorđević, Valentina, Miljić, Predrag, Kovač, Mirjana, Antonijević, Nebojša, Rakićević, Ljiljana, Radojković, Dragica, "+1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss" in Blood Coagulation & Fibrinolysis, 21, no. 7 (2010):679-682,
https://doi.org/10.1097/MBC.0b013e32833e426d . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Miković, Zeljko
AU  - Rakićević, Ljiljana
AU  - Srzentić, Snežana
AU  - Mandić, Vesna
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Elezović, Ivo
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/413
AB  - Objective: D-dimer testing has an important role in the exclusion of acute venous thromboembolism (VTE) in the nonpregnant population. Establishing D-dimers role in the diagnosis of VTE in pregnancy is hampered because of the substantial increase of D-dimer throughout gestational age. Study design: In a prospective study we followed 89 healthy pregnant women to establish the reference range of D-dimer for each trimester. D-dimer testing was also performed in 12 women with clinical suspicion of VTE and their results were compared with the established new reference range of D-dimer, and with the recorded ultrasound findings. Results: In the first trimester, 84% women from reference group had normal D-dimer, in the second 33%, and by the third trimester only 1%, which suggests that D-dimer has no practical diagnostic use in ruling out VTE if the threshold of 230 ng/mL for abnormal is used. All pregnant women with thrombosis who had positive ultrasound findings also had statistically significant elevation of the D-dimer level, considering the established reference range of the corresponding trimester. We found 100% sensitivity of D-dimer test. A women developed thrombosis in the first trimester had 6.7-7.6 time higher level of D-dimer than the mean value in the reference group, and in the third trimester thrombotic women had 2.0-3.8 time higher level of D-dimer, p  lt  0.0001. Conclusion: D-dimer test with the new threshold for: the first of 286, the second of 457 and the third trimester of 644 ng/mL can be useful in diagnosis of pregnancy related VTE.
PB  - Elsevier, Amsterdam
T2  - European Journal of Obstetrics & Gynecology and Reproductive Biology
T1  - The use of D-dimer with new cutoff can be useful in diagnosis of venous thromboembolism in pregnancy
EP  - 30
IS  - 1
SP  - 27
VL  - 148
DO  - 10.1016/j.ejogrb.2009.09.005
ER  - 

@article{
author = "Kovač, Mirjana and Miković, Zeljko and Rakićević, Ljiljana and Srzentić, Snežana and Mandić, Vesna and Đorđević, Valentina and Radojković, Dragica and Elezović, Ivo",
year = "2010",
abstract = "Objective: D-dimer testing has an important role in the exclusion of acute venous thromboembolism (VTE) in the nonpregnant population. Establishing D-dimers role in the diagnosis of VTE in pregnancy is hampered because of the substantial increase of D-dimer throughout gestational age. Study design: In a prospective study we followed 89 healthy pregnant women to establish the reference range of D-dimer for each trimester. D-dimer testing was also performed in 12 women with clinical suspicion of VTE and their results were compared with the established new reference range of D-dimer, and with the recorded ultrasound findings. Results: In the first trimester, 84% women from reference group had normal D-dimer, in the second 33%, and by the third trimester only 1%, which suggests that D-dimer has no practical diagnostic use in ruling out VTE if the threshold of 230 ng/mL for abnormal is used. All pregnant women with thrombosis who had positive ultrasound findings also had statistically significant elevation of the D-dimer level, considering the established reference range of the corresponding trimester. We found 100% sensitivity of D-dimer test. A women developed thrombosis in the first trimester had 6.7-7.6 time higher level of D-dimer than the mean value in the reference group, and in the third trimester thrombotic women had 2.0-3.8 time higher level of D-dimer, p  lt  0.0001. Conclusion: D-dimer test with the new threshold for: the first of 286, the second of 457 and the third trimester of 644 ng/mL can be useful in diagnosis of pregnancy related VTE.",
publisher = "Elsevier, Amsterdam",
journal = "European Journal of Obstetrics & Gynecology and Reproductive Biology",
title = "The use of D-dimer with new cutoff can be useful in diagnosis of venous thromboembolism in pregnancy",
pages = "30-27",
number = "1",
volume = "148",
doi = "10.1016/j.ejogrb.2009.09.005"
}

Kovač, M., Miković, Z., Rakićević, L., Srzentić, S., Mandić, V., Đorđević, V., Radojković, D.,& Elezović, I.. (2010). The use of D-dimer with new cutoff can be useful in diagnosis of venous thromboembolism in pregnancy. in European Journal of Obstetrics & Gynecology and Reproductive Biology
Elsevier, Amsterdam., 148(1), 27-30.
https://doi.org/10.1016/j.ejogrb.2009.09.005

Kovač M, Miković Z, Rakićević L, Srzentić S, Mandić V, Đorđević V, Radojković D, Elezović I. The use of D-dimer with new cutoff can be useful in diagnosis of venous thromboembolism in pregnancy. in European Journal of Obstetrics & Gynecology and Reproductive Biology. 2010;148(1):27-30.
doi:10.1016/j.ejogrb.2009.09.005 .

Kovač, Mirjana, Miković, Zeljko, Rakićević, Ljiljana, Srzentić, Snežana, Mandić, Vesna, Đorđević, Valentina, Radojković, Dragica, Elezović, Ivo, "The use of D-dimer with new cutoff can be useful in diagnosis of venous thromboembolism in pregnancy" in European Journal of Obstetrics & Gynecology and Reproductive Biology, 148, no. 1 (2010):27-30,
https://doi.org/10.1016/j.ejogrb.2009.09.005 . .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Milosević, Katarina
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Grković, Slobodanka
AU  - Nestorović, Branimir
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/466
AB  - This paper reports a novel Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene variant, 1811+1G - gt  T, detected in a 5-year-old girl diagnosed with idiopathic disseminated bronchiectasis and negative sweat chloride test (17 mmol/L). The performed CFTR gene mutation analysis included detection of the F508del mutation, analysis of Tn polymorphism and screening of CFTR exons 3, 10 and 11. The CFTR gene screening has shown the altered band pattern in exon 11. The DNA sequencing of CFTR exon 11 revealed the presence of the novel sequence variation 1811+1G - gt  T in heterozygous state. This sequence variation was not found in any of 100 control alleles, analyzed by polymerase chain reaction - restriction fragment length polymorphism method. The novel sequence variation 1811+1G - gt  T is located at the splicing site at the boundary of exon 11 and intron 11 and might be either a sequence variation or a splicing site defect. lt /.
PB  - Taylor & Francis Inc, Philadelphia
T2  - Fetal and Pediatric Pathology
T1  - Novel cftr gene sequence variation in Serbian patient with idiopathic disseminated bronchiectasis
EP  - 98
IS  - 2
SP  - 95
VL  - 29
DO  - 10.3109/15513811003620815
ER  - 

@article{
author = "Nikolić, Aleksandra and Milosević, Katarina and Divac Rankov, Aleksandra and Ljujić, Mila and Grković, Slobodanka and Nestorović, Branimir",
year = "2010",
abstract = "This paper reports a novel Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene variant, 1811+1G - gt  T, detected in a 5-year-old girl diagnosed with idiopathic disseminated bronchiectasis and negative sweat chloride test (17 mmol/L). The performed CFTR gene mutation analysis included detection of the F508del mutation, analysis of Tn polymorphism and screening of CFTR exons 3, 10 and 11. The CFTR gene screening has shown the altered band pattern in exon 11. The DNA sequencing of CFTR exon 11 revealed the presence of the novel sequence variation 1811+1G - gt  T in heterozygous state. This sequence variation was not found in any of 100 control alleles, analyzed by polymerase chain reaction - restriction fragment length polymorphism method. The novel sequence variation 1811+1G - gt  T is located at the splicing site at the boundary of exon 11 and intron 11 and might be either a sequence variation or a splicing site defect. lt /.",
publisher = "Taylor & Francis Inc, Philadelphia",
journal = "Fetal and Pediatric Pathology",
title = "Novel cftr gene sequence variation in Serbian patient with idiopathic disseminated bronchiectasis",
pages = "98-95",
number = "2",
volume = "29",
doi = "10.3109/15513811003620815"
}

Nikolić, A., Milosević, K., Divac Rankov, A., Ljujić, M., Grković, S.,& Nestorović, B.. (2010). Novel cftr gene sequence variation in Serbian patient with idiopathic disseminated bronchiectasis. in Fetal and Pediatric Pathology
Taylor & Francis Inc, Philadelphia., 29(2), 95-98.
https://doi.org/10.3109/15513811003620815

Nikolić A, Milosević K, Divac Rankov A, Ljujić M, Grković S, Nestorović B. Novel cftr gene sequence variation in Serbian patient with idiopathic disseminated bronchiectasis. in Fetal and Pediatric Pathology. 2010;29(2):95-98.
doi:10.3109/15513811003620815 .

Nikolić, Aleksandra, Milosević, Katarina, Divac Rankov, Aleksandra, Ljujić, Mila, Grković, Slobodanka, Nestorović, Branimir, "Novel cftr gene sequence variation in Serbian patient with idiopathic disseminated bronchiectasis" in Fetal and Pediatric Pathology, 29, no. 2 (2010):95-98,
https://doi.org/10.3109/15513811003620815 . .

TY  - JOUR
AU  - Stojiljković, Maja
AU  - Zukić, Branka
AU  - Tošić, Nataša
AU  - Karan-Đurašević, Teodora
AU  - Spasovski, Vesna
AU  - Nikčević, Gordana
AU  - Pavlović, Sonja
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/435
AB  - We present the first transcriptional regulatory element found in a PAH gene intron. The element is located in the PAH gene intron 8, acts as an enhancer specifically in the hepatoma cell line, and binds GATA-1 transcription factor. Herein the presented data could unlock a new area for the analysis of PAH gene expression and could contribute to refining genotype-phenotype correlation.
PB  - Academic Press Inc Elsevier Science, San Diego
T2  - Molecular Genetics and Metabolism
T1  - Novel transcriptional regulatory element in the phenylalanine hydroxylase gene intron 8
EP  - 83
IS  - 1
SP  - 81
VL  - 101
DO  - 10.1016/j.ymgme.2010.05.014
ER  - 

@article{
author = "Stojiljković, Maja and Zukić, Branka and Tošić, Nataša and Karan-Đurašević, Teodora and Spasovski, Vesna and Nikčević, Gordana and Pavlović, Sonja",
year = "2010",
abstract = "We present the first transcriptional regulatory element found in a PAH gene intron. The element is located in the PAH gene intron 8, acts as an enhancer specifically in the hepatoma cell line, and binds GATA-1 transcription factor. Herein the presented data could unlock a new area for the analysis of PAH gene expression and could contribute to refining genotype-phenotype correlation.",
publisher = "Academic Press Inc Elsevier Science, San Diego",
journal = "Molecular Genetics and Metabolism",
title = "Novel transcriptional regulatory element in the phenylalanine hydroxylase gene intron 8",
pages = "83-81",
number = "1",
volume = "101",
doi = "10.1016/j.ymgme.2010.05.014"
}

Stojiljković, M., Zukić, B., Tošić, N., Karan-Đurašević, T., Spasovski, V., Nikčević, G.,& Pavlović, S.. (2010). Novel transcriptional regulatory element in the phenylalanine hydroxylase gene intron 8. in Molecular Genetics and Metabolism
Academic Press Inc Elsevier Science, San Diego., 101(1), 81-83.
https://doi.org/10.1016/j.ymgme.2010.05.014

Stojiljković M, Zukić B, Tošić N, Karan-Đurašević T, Spasovski V, Nikčević G, Pavlović S. Novel transcriptional regulatory element in the phenylalanine hydroxylase gene intron 8. in Molecular Genetics and Metabolism. 2010;101(1):81-83.
doi:10.1016/j.ymgme.2010.05.014 .

Stojiljković, Maja, Zukić, Branka, Tošić, Nataša, Karan-Đurašević, Teodora, Spasovski, Vesna, Nikčević, Gordana, Pavlović, Sonja, "Novel transcriptional regulatory element in the phenylalanine hydroxylase gene intron 8" in Molecular Genetics and Metabolism, 101, no. 1 (2010):81-83,
https://doi.org/10.1016/j.ymgme.2010.05.014 . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Mitić, G.
AU  - Miković, Z.
AU  - Đorđević, Valentina
AU  - Savić, O.
AU  - Mandić, V.
AU  - Rakićević, Ljiljana
AU  - Antonijević, Nebojša
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/410
AB  - Backgound/Aims: Existing data regarding the prevalence of thrombophilia in women with pregnancy complications are conflicting. Methods: To investigate the relationship between pregnancy-associated complications and the presence of thrombophilia, we studied the records of 453 women with pregnancy-associated complications. In 55 women, intrauterine fetal death ( fetus mortus in utero, FMU) after 20 weeks of gestation was recorded, in 231 two or more consecutive recurrent fetal losses (RFL) were recorded, while 167 had a venous thromboembolism (VTE) during one of their pregnancies. The control group consisted of 128 healthy women, with no previous history of thrombotic events or miscarriages. Results: In the FMU group we found 54.5% of women had thrombophilia, in the RFL group 38%, and in the VTE group 52.7%. The most frequent thrombophilia in the VTE group was the FV Leiden ( OR 17.9, 95% CI 4.2-75.9). The most frequent thrombophilia in the FMU group was the FII G20210A ( OR 7.09, 95% CI 1.8-27.9). Statistical difference between RFL and the control group was observed only for FV Leiden ( OR 6.8, 95% CI 1.6-29.7). Conclusion: Thrombophilia was found to be considerably more common in women with pregnancy-associated complications in comparison with the women with normal pregnancies, most frequently in patients with VTE or FMU.
PB  - Karger, Basel
T2  - Gynecologic and Obstetric Investigation
T1  - Thrombophilia in Women with Pregnancy-Associated Complications: Fetal Loss and Pregnancy-Related Venous Thromboembolism
EP  - 238
IS  - 4
SP  - 233
VL  - 69
DO  - 10.1159/000274012
ER  - 

@article{
author = "Kovač, Mirjana and Mitić, G. and Miković, Z. and Đorđević, Valentina and Savić, O. and Mandić, V. and Rakićević, Ljiljana and Antonijević, Nebojša and Radojković, Dragica",
year = "2010",
abstract = "Backgound/Aims: Existing data regarding the prevalence of thrombophilia in women with pregnancy complications are conflicting. Methods: To investigate the relationship between pregnancy-associated complications and the presence of thrombophilia, we studied the records of 453 women with pregnancy-associated complications. In 55 women, intrauterine fetal death ( fetus mortus in utero, FMU) after 20 weeks of gestation was recorded, in 231 two or more consecutive recurrent fetal losses (RFL) were recorded, while 167 had a venous thromboembolism (VTE) during one of their pregnancies. The control group consisted of 128 healthy women, with no previous history of thrombotic events or miscarriages. Results: In the FMU group we found 54.5% of women had thrombophilia, in the RFL group 38%, and in the VTE group 52.7%. The most frequent thrombophilia in the VTE group was the FV Leiden ( OR 17.9, 95% CI 4.2-75.9). The most frequent thrombophilia in the FMU group was the FII G20210A ( OR 7.09, 95% CI 1.8-27.9). Statistical difference between RFL and the control group was observed only for FV Leiden ( OR 6.8, 95% CI 1.6-29.7). Conclusion: Thrombophilia was found to be considerably more common in women with pregnancy-associated complications in comparison with the women with normal pregnancies, most frequently in patients with VTE or FMU.",
publisher = "Karger, Basel",
journal = "Gynecologic and Obstetric Investigation",
title = "Thrombophilia in Women with Pregnancy-Associated Complications: Fetal Loss and Pregnancy-Related Venous Thromboembolism",
pages = "238-233",
number = "4",
volume = "69",
doi = "10.1159/000274012"
}

Kovač, M., Mitić, G., Miković, Z., Đorđević, V., Savić, O., Mandić, V., Rakićević, L., Antonijević, N.,& Radojković, D.. (2010). Thrombophilia in Women with Pregnancy-Associated Complications: Fetal Loss and Pregnancy-Related Venous Thromboembolism. in Gynecologic and Obstetric Investigation
Karger, Basel., 69(4), 233-238.
https://doi.org/10.1159/000274012

Kovač M, Mitić G, Miković Z, Đorđević V, Savić O, Mandić V, Rakićević L, Antonijević N, Radojković D. Thrombophilia in Women with Pregnancy-Associated Complications: Fetal Loss and Pregnancy-Related Venous Thromboembolism. in Gynecologic and Obstetric Investigation. 2010;69(4):233-238.
doi:10.1159/000274012 .

Kovač, Mirjana, Mitić, G., Miković, Z., Đorđević, Valentina, Savić, O., Mandić, V., Rakićević, Ljiljana, Antonijević, Nebojša, Radojković, Dragica, "Thrombophilia in Women with Pregnancy-Associated Complications: Fetal Loss and Pregnancy-Related Venous Thromboembolism" in Gynecologic and Obstetric Investigation, 69, no. 4 (2010):233-238,
https://doi.org/10.1159/000274012 . .

TY  - JOUR
AU  - Krstovski, Nada
AU  - Tošić, Nataša
AU  - Janić, Dragana
AU  - Dokmanović, Lidija
AU  - Kuzmanović, Milos
AU  - Spasovski, Vesna
AU  - Pavlović, Sonja
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/446
AB  - Mutations in the fms-like tyrosine kinase 3 (FLT3) gene (internal tandem duplication (ITD) and point mutation in the tyrosine kinase domain, FLT3/D835) as well as the nucleophosmin (NPM1) gene are the most common abnormalities in adult acute myeloid leukemia (AML). Their significance in pediatric AML is still unclear. In this study we evaluated the frequency of FLT3 and NPM1 mutations in childhood AML. We also examined clinical features and outcome of these patients. FLT3 and NPM1 mutations were analysed in 42 and 37 childhood AML patients, respectively, using polymerase chain reaction (PCR) and direct sequencing.FLT3 mutations were detected in 4/42 patients (9.5%). The frequencies of FLT3/ITD and FLT3/D835 were the same, 2/42 (4.7%). NMP1 mutations were found in 1/37 patients (2.7%). FLT3 gene mutations were correlated with induction failure. Here we report the results of the study of FLT3 and NPM1 gene mutations in childhood AML patients in Serbia. Low frequencies of these molecular markers point out that these abnormalities are rare in this cohort of patients. Comparative study of data on NPM1 mutations in childhood AML revealed that various NPM1 gene mutation types are associated with childhood AML. Our findings as well as previously reported data, contributes to a hypothesis of different biology and etiology of adult and childhood AML. More extensive studies of NPM1 and FLT3 mutations in childhood AML are needed to determine their biological and clinical importance.
PB  - Humana Press Inc, Totowa
T2  - Medical Oncology
T1  - Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature
EP  - 645
IS  - 3
SP  - 640
VL  - 27
DO  - 10.1007/s12032-009-9261-5
ER  - 

@article{
author = "Krstovski, Nada and Tošić, Nataša and Janić, Dragana and Dokmanović, Lidija and Kuzmanović, Milos and Spasovski, Vesna and Pavlović, Sonja",
year = "2010",
abstract = "Mutations in the fms-like tyrosine kinase 3 (FLT3) gene (internal tandem duplication (ITD) and point mutation in the tyrosine kinase domain, FLT3/D835) as well as the nucleophosmin (NPM1) gene are the most common abnormalities in adult acute myeloid leukemia (AML). Their significance in pediatric AML is still unclear. In this study we evaluated the frequency of FLT3 and NPM1 mutations in childhood AML. We also examined clinical features and outcome of these patients. FLT3 and NPM1 mutations were analysed in 42 and 37 childhood AML patients, respectively, using polymerase chain reaction (PCR) and direct sequencing.FLT3 mutations were detected in 4/42 patients (9.5%). The frequencies of FLT3/ITD and FLT3/D835 were the same, 2/42 (4.7%). NMP1 mutations were found in 1/37 patients (2.7%). FLT3 gene mutations were correlated with induction failure. Here we report the results of the study of FLT3 and NPM1 gene mutations in childhood AML patients in Serbia. Low frequencies of these molecular markers point out that these abnormalities are rare in this cohort of patients. Comparative study of data on NPM1 mutations in childhood AML revealed that various NPM1 gene mutation types are associated with childhood AML. Our findings as well as previously reported data, contributes to a hypothesis of different biology and etiology of adult and childhood AML. More extensive studies of NPM1 and FLT3 mutations in childhood AML are needed to determine their biological and clinical importance.",
publisher = "Humana Press Inc, Totowa",
journal = "Medical Oncology",
title = "Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature",
pages = "645-640",
number = "3",
volume = "27",
doi = "10.1007/s12032-009-9261-5"
}

Krstovski, N., Tošić, N., Janić, D., Dokmanović, L., Kuzmanović, M., Spasovski, V.,& Pavlović, S.. (2010). Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature. in Medical Oncology
Humana Press Inc, Totowa., 27(3), 640-645.
https://doi.org/10.1007/s12032-009-9261-5

Krstovski N, Tošić N, Janić D, Dokmanović L, Kuzmanović M, Spasovski V, Pavlović S. Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature. in Medical Oncology. 2010;27(3):640-645.
doi:10.1007/s12032-009-9261-5 .

Krstovski, Nada, Tošić, Nataša, Janić, Dragana, Dokmanović, Lidija, Kuzmanović, Milos, Spasovski, Vesna, Pavlović, Sonja, "Incidence of FLT3 and nucleophosmin gene mutations in childhood acute myeloid leukemia: Serbian experience and the review of the literature" in Medical Oncology, 27, no. 3 (2010):640-645,
https://doi.org/10.1007/s12032-009-9261-5 . .

TY  - JOUR
AU  - Kojić, Snežana
AU  - Nestorović, Aleksandra
AU  - Rakićević, Ljiljana
AU  - Belgrano, Anna
AU  - Stanković, Marija
AU  - Divac Rankov, Aleksandra
AU  - Faulkner, Georgine
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/445
AB  - The muscle ankyrin repeat protein (MARP) family member Ankrd1/CARP is a part of the titin-mechanosensory signaling complex in the sarcomere and in response to stretch it translocates to the nucleus where it participates in the regulation of cardiac genes as a transcriptional co-repressor. Several studies have focused on its structural role in muscle, but its regulatory role is still poorly understood To gain more insight into the regulatory function of Ankrd1/CARP we searched for transcription factors that could interact and modulate its activity. Using protein array methodology we identified the tumor suppressor protein p53 as an Ankrd1/CARP interacting partner and confirmed their interaction both in vivo and in vitro We demonstrate a novel role for Ankrd1/CARP as a transcriptional co-activator, moderately up regulating p53 activity Furthermore, we show that p53 operates as an upstream effector of Ankrd1/CARP, by up regulating the proximal ANKRD1 promoter Our findings suggest that, besides acting as a transcriptional co-repressor, Ankrd1/CARP could have a stimulatory effect on gene expression in cultured skeletal muscle cells It is probable that Ankrd1 /CARP has a role in the propagation of signals initiated by myogenic regulatory factors (MRFs) during myogenesis
PB  - Elsevier Science Inc, New York
T2  - Archives of Biochemistry and Biophysics
T1  - A novel role for cardiac ankyrin repeat protein Ankrd1/CARP as a co-activator of the p53 tumor suppressor protein
EP  - 67
IS  - 1
SP  - 60
VL  - 502
DO  - 10.1016/j.abb.2010.06.029
ER  - 

@article{
author = "Kojić, Snežana and Nestorović, Aleksandra and Rakićević, Ljiljana and Belgrano, Anna and Stanković, Marija and Divac Rankov, Aleksandra and Faulkner, Georgine",
year = "2010",
abstract = "The muscle ankyrin repeat protein (MARP) family member Ankrd1/CARP is a part of the titin-mechanosensory signaling complex in the sarcomere and in response to stretch it translocates to the nucleus where it participates in the regulation of cardiac genes as a transcriptional co-repressor. Several studies have focused on its structural role in muscle, but its regulatory role is still poorly understood To gain more insight into the regulatory function of Ankrd1/CARP we searched for transcription factors that could interact and modulate its activity. Using protein array methodology we identified the tumor suppressor protein p53 as an Ankrd1/CARP interacting partner and confirmed their interaction both in vivo and in vitro We demonstrate a novel role for Ankrd1/CARP as a transcriptional co-activator, moderately up regulating p53 activity Furthermore, we show that p53 operates as an upstream effector of Ankrd1/CARP, by up regulating the proximal ANKRD1 promoter Our findings suggest that, besides acting as a transcriptional co-repressor, Ankrd1/CARP could have a stimulatory effect on gene expression in cultured skeletal muscle cells It is probable that Ankrd1 /CARP has a role in the propagation of signals initiated by myogenic regulatory factors (MRFs) during myogenesis",
publisher = "Elsevier Science Inc, New York",
journal = "Archives of Biochemistry and Biophysics",
title = "A novel role for cardiac ankyrin repeat protein Ankrd1/CARP as a co-activator of the p53 tumor suppressor protein",
pages = "67-60",
number = "1",
volume = "502",
doi = "10.1016/j.abb.2010.06.029"
}

Kojić, S., Nestorović, A., Rakićević, L., Belgrano, A., Stanković, M., Divac Rankov, A.,& Faulkner, G.. (2010). A novel role for cardiac ankyrin repeat protein Ankrd1/CARP as a co-activator of the p53 tumor suppressor protein. in Archives of Biochemistry and Biophysics
Elsevier Science Inc, New York., 502(1), 60-67.
https://doi.org/10.1016/j.abb.2010.06.029

Kojić S, Nestorović A, Rakićević L, Belgrano A, Stanković M, Divac Rankov A, Faulkner G. A novel role for cardiac ankyrin repeat protein Ankrd1/CARP as a co-activator of the p53 tumor suppressor protein. in Archives of Biochemistry and Biophysics. 2010;502(1):60-67.
doi:10.1016/j.abb.2010.06.029 .

Kojić, Snežana, Nestorović, Aleksandra, Rakićević, Ljiljana, Belgrano, Anna, Stanković, Marija, Divac Rankov, Aleksandra, Faulkner, Georgine, "A novel role for cardiac ankyrin repeat protein Ankrd1/CARP as a co-activator of the p53 tumor suppressor protein" in Archives of Biochemistry and Biophysics, 502, no. 1 (2010):60-67,
https://doi.org/10.1016/j.abb.2010.06.029 . .

TY  - JOUR
AU  - Kušić-Tišma, Jelena
AU  - Tomić, Branko
AU  - Divac Rankov, Aleksandra
AU  - Kojić, Snežana
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/408
AB  - In higher eukaryotes mechanism of DNA replication origin recognition and binding by origin recognition complex (ORC) is still unknown. Origin transfer studies have shown that origin sites are genetically determined, containing functionally interchangeable modules. One of such modules from the human lamin B2 origin of replication has the ability to adopt unorthodox structure partly composed of intramolecular triplex. Sequences involved in triplex formation coincide with ORC binding sites both in vitro and in vivo. To explore potential significance of unorthodox DNA structures in origin recognition by ORC, we tested DNA binding properties of human ORC subunit 4 (HsOrc4) which has independent DNA binding activity in vitro and similar binding characteristics as ORC holocomplex. Our results demonstrated that DNA binding activity of HsOrc4 depends on length and structure of DNA with triplex being the protein's preferred binding target. Such feature could play part in origin selection through directing ORC to DNA sequence prone to adopt unorthodox structure.
PB  - Springer, Dordrecht
T2  - Molecular Biology Reports
T1  - Human initiation protein Orc4 prefers triple stranded DNA
EP  - 2322
IS  - 5
SP  - 2317
VL  - 37
DO  - 10.1007/s11033-009-9735-8
ER  - 

@article{
author = "Kušić-Tišma, Jelena and Tomić, Branko and Divac Rankov, Aleksandra and Kojić, Snežana",
year = "2010",
abstract = "In higher eukaryotes mechanism of DNA replication origin recognition and binding by origin recognition complex (ORC) is still unknown. Origin transfer studies have shown that origin sites are genetically determined, containing functionally interchangeable modules. One of such modules from the human lamin B2 origin of replication has the ability to adopt unorthodox structure partly composed of intramolecular triplex. Sequences involved in triplex formation coincide with ORC binding sites both in vitro and in vivo. To explore potential significance of unorthodox DNA structures in origin recognition by ORC, we tested DNA binding properties of human ORC subunit 4 (HsOrc4) which has independent DNA binding activity in vitro and similar binding characteristics as ORC holocomplex. Our results demonstrated that DNA binding activity of HsOrc4 depends on length and structure of DNA with triplex being the protein's preferred binding target. Such feature could play part in origin selection through directing ORC to DNA sequence prone to adopt unorthodox structure.",
publisher = "Springer, Dordrecht",
journal = "Molecular Biology Reports",
title = "Human initiation protein Orc4 prefers triple stranded DNA",
pages = "2322-2317",
number = "5",
volume = "37",
doi = "10.1007/s11033-009-9735-8"
}

Kušić-Tišma, J., Tomić, B., Divac Rankov, A.,& Kojić, S.. (2010). Human initiation protein Orc4 prefers triple stranded DNA. in Molecular Biology Reports
Springer, Dordrecht., 37(5), 2317-2322.
https://doi.org/10.1007/s11033-009-9735-8

Kušić-Tišma J, Tomić B, Divac Rankov A, Kojić S. Human initiation protein Orc4 prefers triple stranded DNA. in Molecular Biology Reports. 2010;37(5):2317-2322.
doi:10.1007/s11033-009-9735-8 .

Kušić-Tišma, Jelena, Tomić, Branko, Divac Rankov, Aleksandra, Kojić, Snežana, "Human initiation protein Orc4 prefers triple stranded DNA" in Molecular Biology Reports, 37, no. 5 (2010):2317-2322,
https://doi.org/10.1007/s11033-009-9735-8 . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Maslac, Aleksandar R.
AU  - Rakićević, Ljiljana
AU  - Radojković, Dragica 
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/451
AB  - A single nucleotide polymorphism c.-1639G gt A in the promoter region of vitamin K-epoxide reductase (VKORC1) gene has been found to account for most of the variability in response to oral vitamin K antagonist (VKA). Our aim was to study the effect of c.-1639G gt A polymorphism on the acenocoumarol dosage requirements in a group of patients under stable anticoagulation, and to estimate the variability in response to VKA. We conducted a retrospective cohort analysis of 200 stable anticoagulation patients followed from the initiation of VKA. Out of 43 low-dose patients, 40 (93%) carried the A allele. The A allele was less frequent in the group of 30 patients requiring high VKA dose; among these patients 13 (43.3%) carried the A allele in the heterozygous form and none of them carried AA genotype. Patients with GG genotype required 2.6 times higher dose than patients carriers of AA genotype (P lt 0.0001). Carriers of AA genotype were more likely to be overanticoagulated during follow-up after initiation of VKA when compared with carriers of the GA and GG genotypes (P lt 0.0001). Patients with GG genotype spent more time below therapeutic range compared with patients carriers of AA (P=0.0328) and GA genotype (P lt 0.0001). VKORC1 c.-1639G gt A polymorphism significantly influenced VKA dose and represented a good predictor of individuals predisposed to unstable anticoagulation. Pharmacogenetic testing could predict a high risk of overdose among 28.5% of our patients, carriers of AA genotype, before the initiation of anticoagulation. Blood Coagul Fibrinolysis 21:558-563
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Blood Coagulation & Fibrinolysis
T1  - The c.-1639G  gt  A polymorphism of the VKORC1 gene in Serbian population: retrospective study of the variability in response to oral anticoagulant therapy
EP  - 563
IS  - 6
SP  - 558
VL  - 21
DO  - 10.1097/MBC.0b013e32833c2988
ER  - 

@article{
author = "Kovač, Mirjana and Maslac, Aleksandar R. and Rakićević, Ljiljana and Radojković, Dragica ",
year = "2010",
abstract = "A single nucleotide polymorphism c.-1639G gt A in the promoter region of vitamin K-epoxide reductase (VKORC1) gene has been found to account for most of the variability in response to oral vitamin K antagonist (VKA). Our aim was to study the effect of c.-1639G gt A polymorphism on the acenocoumarol dosage requirements in a group of patients under stable anticoagulation, and to estimate the variability in response to VKA. We conducted a retrospective cohort analysis of 200 stable anticoagulation patients followed from the initiation of VKA. Out of 43 low-dose patients, 40 (93%) carried the A allele. The A allele was less frequent in the group of 30 patients requiring high VKA dose; among these patients 13 (43.3%) carried the A allele in the heterozygous form and none of them carried AA genotype. Patients with GG genotype required 2.6 times higher dose than patients carriers of AA genotype (P lt 0.0001). Carriers of AA genotype were more likely to be overanticoagulated during follow-up after initiation of VKA when compared with carriers of the GA and GG genotypes (P lt 0.0001). Patients with GG genotype spent more time below therapeutic range compared with patients carriers of AA (P=0.0328) and GA genotype (P lt 0.0001). VKORC1 c.-1639G gt A polymorphism significantly influenced VKA dose and represented a good predictor of individuals predisposed to unstable anticoagulation. Pharmacogenetic testing could predict a high risk of overdose among 28.5% of our patients, carriers of AA genotype, before the initiation of anticoagulation. Blood Coagul Fibrinolysis 21:558-563",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Blood Coagulation & Fibrinolysis",
title = "The c.-1639G  gt  A polymorphism of the VKORC1 gene in Serbian population: retrospective study of the variability in response to oral anticoagulant therapy",
pages = "563-558",
number = "6",
volume = "21",
doi = "10.1097/MBC.0b013e32833c2988"
}

Kovač, M., Maslac, A. R., Rakićević, L.,& Radojković, D.. (2010). The c.-1639G  gt  A polymorphism of the VKORC1 gene in Serbian population: retrospective study of the variability in response to oral anticoagulant therapy. in Blood Coagulation & Fibrinolysis
Lippincott Williams & Wilkins, Philadelphia., 21(6), 558-563.
https://doi.org/10.1097/MBC.0b013e32833c2988

Kovač M, Maslac AR, Rakićević L, Radojković D. The c.-1639G  gt  A polymorphism of the VKORC1 gene in Serbian population: retrospective study of the variability in response to oral anticoagulant therapy. in Blood Coagulation & Fibrinolysis. 2010;21(6):558-563.
doi:10.1097/MBC.0b013e32833c2988 .

Kovač, Mirjana, Maslac, Aleksandar R., Rakićević, Ljiljana, Radojković, Dragica , "The c.-1639G  gt  A polymorphism of the VKORC1 gene in Serbian population: retrospective study of the variability in response to oral anticoagulant therapy" in Blood Coagulation & Fibrinolysis, 21, no. 6 (2010):558-563,
https://doi.org/10.1097/MBC.0b013e32833c2988 . .

TY  - CONF
AU  - Đorđević, Valentina
AU  - Rakićević, Ljiljana
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/427
AB  - Thrombophilia is a multifactorial disorder, involving both genetic and acquired risk factors that affect the balance between procoagulant and anticoagulant factors and lead to increased tendency to thrombosis. The concept that thrombophilia could be associated with genetic defects was first proposed in 1965 after the discovery of familiar antihrombin III deficiency. Further family studies showed that deficiency of protein C or protein S also increased thrombotic risk. In the coming years the advent in DNA technology, especially the invention of PCR reaction, played an important role in the identification of the exact nature of these deficiencies and opened new possibilities in the genetic research of thrombophilia. The breakthrough came with the discovery of activated protein C resistance and Factor V Leiden mutation. Shortly afterwards a mutation in the 3' untranslated region of Factor II gene (FII G20210A) associated with increased concentration of factor II in plasma, was described. Large epidemiologic studies have conformed that these two common mutations represent significant risk factors for thrombophilia. In the last decade several prothrombotic genetic risk factors have been described, including genes variants associated with increased levels of coagulation factors, defects of natural coagulation inhibitors, defects of the fibrinolytic system and hyperhomocysteinemia. These genetic defects or their combination have been extensively studied in an attempt to elucidate the possible association with increased thrombotic tendency. The large-scale DNA analysis systems are now becoming available, opening a new era in the genetic studies of thrombophilia. New technology will enable many genes to be studied in a single patient bringing us closer to the "personalized" medicine.
PB  - Srpsko lekarsko društvo, Beograd
C3  - Srpski arhiv za celokupno lekarstvo
T1  - An Overview of Genetic Risk Factors in Thrombophilia
EP  - 81
SP  - 79
VL  - 138
DO  - 10.2298/SARH10S1079D
ER  - 

@conference{
author = "Đorđević, Valentina and Rakićević, Ljiljana and Radojković, Dragica",
year = "2010",
abstract = "Thrombophilia is a multifactorial disorder, involving both genetic and acquired risk factors that affect the balance between procoagulant and anticoagulant factors and lead to increased tendency to thrombosis. The concept that thrombophilia could be associated with genetic defects was first proposed in 1965 after the discovery of familiar antihrombin III deficiency. Further family studies showed that deficiency of protein C or protein S also increased thrombotic risk. In the coming years the advent in DNA technology, especially the invention of PCR reaction, played an important role in the identification of the exact nature of these deficiencies and opened new possibilities in the genetic research of thrombophilia. The breakthrough came with the discovery of activated protein C resistance and Factor V Leiden mutation. Shortly afterwards a mutation in the 3' untranslated region of Factor II gene (FII G20210A) associated with increased concentration of factor II in plasma, was described. Large epidemiologic studies have conformed that these two common mutations represent significant risk factors for thrombophilia. In the last decade several prothrombotic genetic risk factors have been described, including genes variants associated with increased levels of coagulation factors, defects of natural coagulation inhibitors, defects of the fibrinolytic system and hyperhomocysteinemia. These genetic defects or their combination have been extensively studied in an attempt to elucidate the possible association with increased thrombotic tendency. The large-scale DNA analysis systems are now becoming available, opening a new era in the genetic studies of thrombophilia. New technology will enable many genes to be studied in a single patient bringing us closer to the "personalized" medicine.",
publisher = "Srpsko lekarsko društvo, Beograd",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "An Overview of Genetic Risk Factors in Thrombophilia",
pages = "81-79",
volume = "138",
doi = "10.2298/SARH10S1079D"
}

Đorđević, V., Rakićević, L.,& Radojković, D.. (2010). An Overview of Genetic Risk Factors in Thrombophilia. in Srpski arhiv za celokupno lekarstvo
Srpsko lekarsko društvo, Beograd., 138, 79-81.
https://doi.org/10.2298/SARH10S1079D

Đorđević V, Rakićević L, Radojković D. An Overview of Genetic Risk Factors in Thrombophilia. in Srpski arhiv za celokupno lekarstvo. 2010;138:79-81.
doi:10.2298/SARH10S1079D .

Đorđević, Valentina, Rakićević, Ljiljana, Radojković, Dragica, "An Overview of Genetic Risk Factors in Thrombophilia" in Srpski arhiv za celokupno lekarstvo, 138 (2010):79-81,
https://doi.org/10.2298/SARH10S1079D . .

TY  - JOUR
AU  - Ljujić, Mila
AU  - Topić, Aleksandra
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Grujić, Milan
AU  - Mitić-Milikić, Marija
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/416
AB  - The alpha-1-antitrypsin (A1AT) gene is highly polymorphic, with more than 100 genetic variants identified of which some can affect A1AT protein concentration and/or function and lead to pulmonary and/or liver disease. This study reports on the characterization of a p.G320R variant found in two patients, one with emphysema and the other with lung cancer. This variant results from a single base-pair substitution in exon 4 of the A1AT gene, and has been characterized as P by isoelectric focusing. Functional evaluation of the A1AT p.G320R variant was through comparing specific trypsin inhibitory activity in two patients with pulmonary disorders, carriers of the p.G320R variant, and 19 healthy individuals, carriers of normal A1AT M variants. Results showed that specific trypsin inhibitory activity was lower in both emphysema (2.45 mU/g) and lung cancer (2.07 mU/g) patients than in carriers of the normal variants (range 2.51-3.71 mU/g). This rare A1AT variant is associated with reduced functional activity of A1AT protein. Considering that it was found in patients with severe pulmonary disorders, this variant could be of clinical significance.
PB  - Soc Brasil Genetica, Ribeirao Pret
T2  - Genetics and Molecular Biology
T1  - Identification of a rare p.G320R alpha-1-antitrypsin variant in emphysema and lung cancer patients
EP  - 8
IS  - 1
SP  - 5
VL  - 33
DO  - 10.1590/S1415-47572009005000100
ER  - 

@article{
author = "Ljujić, Mila and Topić, Aleksandra and Nikolić, Aleksandra and Divac Rankov, Aleksandra and Grujić, Milan and Mitić-Milikić, Marija and Radojković, Dragica",
year = "2010",
abstract = "The alpha-1-antitrypsin (A1AT) gene is highly polymorphic, with more than 100 genetic variants identified of which some can affect A1AT protein concentration and/or function and lead to pulmonary and/or liver disease. This study reports on the characterization of a p.G320R variant found in two patients, one with emphysema and the other with lung cancer. This variant results from a single base-pair substitution in exon 4 of the A1AT gene, and has been characterized as P by isoelectric focusing. Functional evaluation of the A1AT p.G320R variant was through comparing specific trypsin inhibitory activity in two patients with pulmonary disorders, carriers of the p.G320R variant, and 19 healthy individuals, carriers of normal A1AT M variants. Results showed that specific trypsin inhibitory activity was lower in both emphysema (2.45 mU/g) and lung cancer (2.07 mU/g) patients than in carriers of the normal variants (range 2.51-3.71 mU/g). This rare A1AT variant is associated with reduced functional activity of A1AT protein. Considering that it was found in patients with severe pulmonary disorders, this variant could be of clinical significance.",
publisher = "Soc Brasil Genetica, Ribeirao Pret",
journal = "Genetics and Molecular Biology",
title = "Identification of a rare p.G320R alpha-1-antitrypsin variant in emphysema and lung cancer patients",
pages = "8-5",
number = "1",
volume = "33",
doi = "10.1590/S1415-47572009005000100"
}

Ljujić, M., Topić, A., Nikolić, A., Divac Rankov, A., Grujić, M., Mitić-Milikić, M.,& Radojković, D.. (2010). Identification of a rare p.G320R alpha-1-antitrypsin variant in emphysema and lung cancer patients. in Genetics and Molecular Biology
Soc Brasil Genetica, Ribeirao Pret., 33(1), 5-8.
https://doi.org/10.1590/S1415-47572009005000100

Ljujić M, Topić A, Nikolić A, Divac Rankov A, Grujić M, Mitić-Milikić M, Radojković D. Identification of a rare p.G320R alpha-1-antitrypsin variant in emphysema and lung cancer patients. in Genetics and Molecular Biology. 2010;33(1):5-8.
doi:10.1590/S1415-47572009005000100 .

Ljujić, Mila, Topić, Aleksandra, Nikolić, Aleksandra, Divac Rankov, Aleksandra, Grujić, Milan, Mitić-Milikić, Marija, Radojković, Dragica, "Identification of a rare p.G320R alpha-1-antitrypsin variant in emphysema and lung cancer patients" in Genetics and Molecular Biology, 33, no. 1 (2010):5-8,
https://doi.org/10.1590/S1415-47572009005000100 . .

TY  - JOUR
AU  - Đorđević, Valentina
AU  - Nikolić, Aleksandra
AU  - Ljujić, Mila
AU  - Nestorović, A.
AU  - Ristanović, M.
AU  - Tulić, C.
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/464
AB  - The aim of the study was to investigate the association between the GSTM1 and GSTT1 gene deletion and MTHFR C677T mutation and male infertility. The study has encompassed 52 infertile and 56 fertile males. Genotype distributions of GSTM1 and GSTT1 gene deletions and the MTHFR C677T mutation did not differ significantly among the analyzed groups, however, a difference in distribution of certain genotype combinations was observed. The obtained results indicate that carriers of double GSTM1/GSTT1 deletion and the MTHFR 677CC genotype are at higher risk of infertility than carriers of any other combination of genotypes (OR 3.5, 95%CI 0.68-18.30).
PB  - Srpsko biološko društvo, Beograd, i dr.
T2  - Archives of Biological Sciences
T1  - Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility
EP  - 530
IS  - 3
SP  - 525
VL  - 62
DO  - 10.2298/ABS1003525D
ER  - 

@article{
author = "Đorđević, Valentina and Nikolić, Aleksandra and Ljujić, Mila and Nestorović, A. and Ristanović, M. and Tulić, C. and Radojković, Dragica",
year = "2010",
abstract = "The aim of the study was to investigate the association between the GSTM1 and GSTT1 gene deletion and MTHFR C677T mutation and male infertility. The study has encompassed 52 infertile and 56 fertile males. Genotype distributions of GSTM1 and GSTT1 gene deletions and the MTHFR C677T mutation did not differ significantly among the analyzed groups, however, a difference in distribution of certain genotype combinations was observed. The obtained results indicate that carriers of double GSTM1/GSTT1 deletion and the MTHFR 677CC genotype are at higher risk of infertility than carriers of any other combination of genotypes (OR 3.5, 95%CI 0.68-18.30).",
publisher = "Srpsko biološko društvo, Beograd, i dr.",
journal = "Archives of Biological Sciences",
title = "Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility",
pages = "530-525",
number = "3",
volume = "62",
doi = "10.2298/ABS1003525D"
}

Đorđević, V., Nikolić, A., Ljujić, M., Nestorović, A., Ristanović, M., Tulić, C.,& Radojković, D.. (2010). Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility. in Archives of Biological Sciences
Srpsko biološko društvo, Beograd, i dr.., 62(3), 525-530.
https://doi.org/10.2298/ABS1003525D

Đorđević V, Nikolić A, Ljujić M, Nestorović A, Ristanović M, Tulić C, Radojković D. Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility. in Archives of Biological Sciences. 2010;62(3):525-530.
doi:10.2298/ABS1003525D .

Đorđević, Valentina, Nikolić, Aleksandra, Ljujić, Mila, Nestorović, A., Ristanović, M., Tulić, C., Radojković, Dragica, "Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility" in Archives of Biological Sciences, 62, no. 3 (2010):525-530,
https://doi.org/10.2298/ABS1003525D . .