TY  - CONF
AU  - Ljujić, Mila
AU  - Trifunović, Sara
AU  - Ilić, Bojan
AU  - Milovanović, Jelena
AU  - Dinić, Jelena
AU  - Divac Rankov, Aleksandra
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2130
AB  - Introduction: Cigarette smoke exposure is a known risk factor for development of lung diseases and
electronic cigarettes(e-cigarettes) were introduced as a popular and safer alternative to combustible tobacco products. Increasing number of studies are reporting their adverse biological effects both in vivo
and in vitro. Aim of this study was to evaluate the effect of e-cigarettes on mitochondrial function in
lung bronchial epithelial cells.
Methods: Electronic cigarette vapor condensate (ECC) was generated using an e-cigarette device on a
suction trap cooled in a dry ice/ethanol bath.We used unflavoured and flavoured e-cigarette liquids with
and without nicotine. Human bronchial epithelial BEAS2B cells were seeded in 96well plates and treated
with 2% e-cigarette vapour condensate for 24h. Mitochondrial membrane potential was measured using
50nM TMRE (Tetramethyl rhodamine ethyl ester) and cells were visualized on ImageXpress® Pico Automated Cell Imaging System (Molecular Devices, San Jose, CA, USA) with a 10x objective.
Results: We found a significant reduction of TMRE fluorescence in treated cells compared to the control. Imaging of treated cells also revealed changes in cell morphology and the presence of mitochondria in TNT-like structures.
Conclusion: Mitochondrial dysfunction has been associated with various pathological conditions including lung diseases such as asthma, COPD and lung cancer. Due to their relative novelty, the role of
electronic cigarette use in development of chronic lung diseasesisstill relatively unknown. Our findings
contribute to the growing list of studies pointing to their adverse biological effects and imply their involvement in processes contributing to chronic lung diseases.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell
EP  - 139
SP  - 139
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2130
ER  - 

@conference{
author = "Ljujić, Mila and Trifunović, Sara and Ilić, Bojan and Milovanović, Jelena and Dinić, Jelena and Divac Rankov, Aleksandra",
year = "2023",
abstract = "Introduction: Cigarette smoke exposure is a known risk factor for development of lung diseases and
electronic cigarettes(e-cigarettes) were introduced as a popular and safer alternative to combustible tobacco products. Increasing number of studies are reporting their adverse biological effects both in vivo
and in vitro. Aim of this study was to evaluate the effect of e-cigarettes on mitochondrial function in
lung bronchial epithelial cells.
Methods: Electronic cigarette vapor condensate (ECC) was generated using an e-cigarette device on a
suction trap cooled in a dry ice/ethanol bath.We used unflavoured and flavoured e-cigarette liquids with
and without nicotine. Human bronchial epithelial BEAS2B cells were seeded in 96well plates and treated
with 2% e-cigarette vapour condensate for 24h. Mitochondrial membrane potential was measured using
50nM TMRE (Tetramethyl rhodamine ethyl ester) and cells were visualized on ImageXpress® Pico Automated Cell Imaging System (Molecular Devices, San Jose, CA, USA) with a 10x objective.
Results: We found a significant reduction of TMRE fluorescence in treated cells compared to the control. Imaging of treated cells also revealed changes in cell morphology and the presence of mitochondria in TNT-like structures.
Conclusion: Mitochondrial dysfunction has been associated with various pathological conditions including lung diseases such as asthma, COPD and lung cancer. Due to their relative novelty, the role of
electronic cigarette use in development of chronic lung diseasesisstill relatively unknown. Our findings
contribute to the growing list of studies pointing to their adverse biological effects and imply their involvement in processes contributing to chronic lung diseases.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell",
pages = "139-139",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2130"
}

Ljujić, M., Trifunović, S., Ilić, B., Milovanović, J., Dinić, J.,& Divac Rankov, A.. (2023). Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 139-139.
https://hdl.handle.net/21.15107/rcub_imagine_2130

Ljujić M, Trifunović S, Ilić B, Milovanović J, Dinić J, Divac Rankov A. Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:139-139.
https://hdl.handle.net/21.15107/rcub_imagine_2130 .

Ljujić, Mila, Trifunović, Sara, Ilić, Bojan, Milovanović, Jelena, Dinić, Jelena, Divac Rankov, Aleksandra, "Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):139-139,
https://hdl.handle.net/21.15107/rcub_imagine_2130 .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Kostić, Ana
AU  - Ljujić, Mila
AU  - Lupšić, Ema
AU  - Dragoj, Miodrag
AU  - Jovanović, Mirna
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1736
AB  - Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora.
AB  - Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306
T1  - Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306
SP  - 330
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1736
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Kostić, Ana and Ljujić, Mila and Lupšić, Ema and Dragoj, Miodrag and Jovanović, Mirna and Pešić, Milica and Dinić, Jelena",
year = "2022",
abstract = "Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora., Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306, Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306",
pages = "330",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1736"
}

Jovanović Stojanov, S., Kostić, A., Ljujić, M., Lupšić, E., Dragoj, M., Jovanović, M., Pešić, M.,& Dinić, J.. (2022). Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 330.
https://hdl.handle.net/21.15107/rcub_imagine_1736

Jovanović Stojanov S, Kostić A, Ljujić M, Lupšić E, Dragoj M, Jovanović M, Pešić M, Dinić J. Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije. 2022;:330.
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

Jovanović Stojanov, Sofija, Kostić, Ana, Ljujić, Mila, Lupšić, Ema, Dragoj, Miodrag, Jovanović, Mirna, Pešić, Milica, Dinić, Jelena, "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306" in Treći kongres biologa Srbije (2022):330,
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

TY  - JOUR
AU  - Jovanović Stojanov, Sofija
AU  - Kostić, Ana
AU  - Ljujić, Mila
AU  - Lupšić, Ema
AU  - Schenone, Silvia
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1656
AB  - Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibition by bafilomycin A1. Combined treatments of Si306 and pro-Si306 with bafilomycin A1 were synergistic in nature, and the inhibition of autophagy sensitized glioblastoma cells to Src tyrosine kinase inhibitors. Si306 and pro-Si306 more strongly inhibited cell proliferation and triggered necrosis in combination with bafilomycin A1. Our findings suggest that modulation of Si306- and pro-Si306-induced autophagy can be used to enhance the anticancer effects of these Src tyrosine kinase inhibitors and overcome the drug-resistant phenotype in glioblastoma cells.
T2  - Life
T2  - Life
T1  - Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors
IS  - 10
SP  - 1503
VL  - 12
DO  - 10.3390/life12101503
ER  - 

@article{
author = "Jovanović Stojanov, Sofija and Kostić, Ana and Ljujić, Mila and Lupšić, Ema and Schenone, Silvia and Pešić, Milica and Dinić, Jelena",
year = "2022",
abstract = "Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibition by bafilomycin A1. Combined treatments of Si306 and pro-Si306 with bafilomycin A1 were synergistic in nature, and the inhibition of autophagy sensitized glioblastoma cells to Src tyrosine kinase inhibitors. Si306 and pro-Si306 more strongly inhibited cell proliferation and triggered necrosis in combination with bafilomycin A1. Our findings suggest that modulation of Si306- and pro-Si306-induced autophagy can be used to enhance the anticancer effects of these Src tyrosine kinase inhibitors and overcome the drug-resistant phenotype in glioblastoma cells.",
journal = "Life, Life",
title = "Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors",
number = "10",
pages = "1503",
volume = "12",
doi = "10.3390/life12101503"
}

Jovanović Stojanov, S., Kostić, A., Ljujić, M., Lupšić, E., Schenone, S., Pešić, M.,& Dinić, J.. (2022). Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors. in Life, 12(10), 1503.
https://doi.org/10.3390/life12101503

Jovanović Stojanov S, Kostić A, Ljujić M, Lupšić E, Schenone S, Pešić M, Dinić J. Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors. in Life. 2022;12(10):1503.
doi:10.3390/life12101503 .

Jovanović Stojanov, Sofija, Kostić, Ana, Ljujić, Mila, Lupšić, Ema, Schenone, Silvia, Pešić, Milica, Dinić, Jelena, "Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors" in Life, 12, no. 10 (2022):1503,
https://doi.org/10.3390/life12101503 . .

TY  - JOUR
AU  - Jovanović, Mirna
AU  - Stanković, Tijana
AU  - Stojković Burić, Sonja
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Ljujić, Mila
AU  - Pesić, Milica
AU  - Dragoj, Miodrag
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1526
AB  - Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.
PB  - MDPI, Basel
T2  - Life-Basel
T1  - Decreased TSPAN14 Expression Contributes to NSCLC Progression
IS  - 9
VL  - 12
DO  - 10.3390/life12091291
ER  - 

@article{
author = "Jovanović, Mirna and Stanković, Tijana and Stojković Burić, Sonja and Banković, Jasna and Dinić, Jelena and Ljujić, Mila and Pesić, Milica and Dragoj, Miodrag",
year = "2022",
abstract = "Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.",
publisher = "MDPI, Basel",
journal = "Life-Basel",
title = "Decreased TSPAN14 Expression Contributes to NSCLC Progression",
number = "9",
volume = "12",
doi = "10.3390/life12091291"
}

Jovanović, M., Stanković, T., Stojković Burić, S., Banković, J., Dinić, J., Ljujić, M., Pesić, M.,& Dragoj, M.. (2022). Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel
MDPI, Basel., 12(9).
https://doi.org/10.3390/life12091291

Jovanović M, Stanković T, Stojković Burić S, Banković J, Dinić J, Ljujić M, Pesić M, Dragoj M. Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel. 2022;12(9).
doi:10.3390/life12091291 .

Jovanović, Mirna, Stanković, Tijana, Stojković Burić, Sonja, Banković, Jasna, Dinić, Jelena, Ljujić, Mila, Pesić, Milica, Dragoj, Miodrag, "Decreased TSPAN14 Expression Contributes to NSCLC Progression" in Life-Basel, 12, no. 9 (2022),
https://doi.org/10.3390/life12091291 . .

TY  - JOUR
AU  - Alov, Petko
AU  - Al Sharif, Merilin
AU  - Aluani, Denitsa
AU  - Chegaev, Konstantin
AU  - Dinić, Jelena
AU  - Divac Rankov, Aleksandra
AU  - Fernandes, Miguel X.
AU  - Fusi, Fabio
AU  - Garcia-Sosa, Alfonso T.
AU  - Juvonen, Risto
AU  - Kondeva-Burdina, Magdalena
AU  - Padron, Jose M.
AU  - Pajeva, Ilza
AU  - Pencheva, Tania
AU  - Puerta, Adrian
AU  - Raunio, Hannu
AU  - Riganti, Chiara
AU  - Tsakovska, Ivanka
AU  - Tzankova, Virginia
AU  - Yordanov, Yordan
AU  - Saponara, Simona
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1555
AB  - Sdox is a hydrogen sulfide (H2S)-releasing doxorubicin effective in P-glycoprotein-overexpressing/doxorubicin-resistant tumor models and not cytotoxic, as the parental drug, in H9c2 cardiomyocytes. The aim of this study was the assessment of Sdox drug-like features and its absorption, distribution, metabolism, and excretion (ADME)/toxicity properties, by a multi- and transdisciplinary in silico, in vitro, and in vivo approach. Doxorubicin was used as the reference compound. The in silico profiling suggested that Sdox possesses higher lipophilicity and lower solubility compared to doxorubicin, and the off-targets prediction revealed relevant differences between Dox and Sdox towards several cancer targets, suggesting different toxicological profiles. In vitro data showed that Sdox is a substrate with lower affinity for P-glycoprotein, less hepatotoxic, and causes less oxidative damage than doxorubicin. Both anthracyclines inhibited CYP3A4, but not hERG currents. Unlike doxorubicin, the percentage of zebrafish live embryos at 72 hpf was not affected by Sdox treatment. In conclusion, these findings demonstrate that Sdox displays a more favorable drug-like ADME/toxicity profile than doxorubicin, different selectivity towards cancer targets, along with a greater preclinical efficacy in resistant tumors. Therefore, Sdox represents a prototype of innovative anthracyclines, worthy of further investigations in clinical settings.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Pharmacology
T1  - A Comprehensive Evaluation of Sdox, a Promising H2S-Releasing Doxorubicin for the Treatment of Chemoresistant Tumors
VL  - 13
DO  - 10.3389/fphar.2022.831791
ER  - 

@article{
author = "Alov, Petko and Al Sharif, Merilin and Aluani, Denitsa and Chegaev, Konstantin and Dinić, Jelena and Divac Rankov, Aleksandra and Fernandes, Miguel X. and Fusi, Fabio and Garcia-Sosa, Alfonso T. and Juvonen, Risto and Kondeva-Burdina, Magdalena and Padron, Jose M. and Pajeva, Ilza and Pencheva, Tania and Puerta, Adrian and Raunio, Hannu and Riganti, Chiara and Tsakovska, Ivanka and Tzankova, Virginia and Yordanov, Yordan and Saponara, Simona",
year = "2022",
abstract = "Sdox is a hydrogen sulfide (H2S)-releasing doxorubicin effective in P-glycoprotein-overexpressing/doxorubicin-resistant tumor models and not cytotoxic, as the parental drug, in H9c2 cardiomyocytes. The aim of this study was the assessment of Sdox drug-like features and its absorption, distribution, metabolism, and excretion (ADME)/toxicity properties, by a multi- and transdisciplinary in silico, in vitro, and in vivo approach. Doxorubicin was used as the reference compound. The in silico profiling suggested that Sdox possesses higher lipophilicity and lower solubility compared to doxorubicin, and the off-targets prediction revealed relevant differences between Dox and Sdox towards several cancer targets, suggesting different toxicological profiles. In vitro data showed that Sdox is a substrate with lower affinity for P-glycoprotein, less hepatotoxic, and causes less oxidative damage than doxorubicin. Both anthracyclines inhibited CYP3A4, but not hERG currents. Unlike doxorubicin, the percentage of zebrafish live embryos at 72 hpf was not affected by Sdox treatment. In conclusion, these findings demonstrate that Sdox displays a more favorable drug-like ADME/toxicity profile than doxorubicin, different selectivity towards cancer targets, along with a greater preclinical efficacy in resistant tumors. Therefore, Sdox represents a prototype of innovative anthracyclines, worthy of further investigations in clinical settings.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Pharmacology",
title = "A Comprehensive Evaluation of Sdox, a Promising H2S-Releasing Doxorubicin for the Treatment of Chemoresistant Tumors",
volume = "13",
doi = "10.3389/fphar.2022.831791"
}

Alov, P., Al Sharif, M., Aluani, D., Chegaev, K., Dinić, J., Divac Rankov, A., Fernandes, M. X., Fusi, F., Garcia-Sosa, A. T., Juvonen, R., Kondeva-Burdina, M., Padron, J. M., Pajeva, I., Pencheva, T., Puerta, A., Raunio, H., Riganti, C., Tsakovska, I., Tzankova, V., Yordanov, Y.,& Saponara, S.. (2022). A Comprehensive Evaluation of Sdox, a Promising H2S-Releasing Doxorubicin for the Treatment of Chemoresistant Tumors. in Frontiers in Pharmacology
Frontiers Media Sa, Lausanne., 13.
https://doi.org/10.3389/fphar.2022.831791

Alov P, Al Sharif M, Aluani D, Chegaev K, Dinić J, Divac Rankov A, Fernandes MX, Fusi F, Garcia-Sosa AT, Juvonen R, Kondeva-Burdina M, Padron JM, Pajeva I, Pencheva T, Puerta A, Raunio H, Riganti C, Tsakovska I, Tzankova V, Yordanov Y, Saponara S. A Comprehensive Evaluation of Sdox, a Promising H2S-Releasing Doxorubicin for the Treatment of Chemoresistant Tumors. in Frontiers in Pharmacology. 2022;13.
doi:10.3389/fphar.2022.831791 .

Alov, Petko, Al Sharif, Merilin, Aluani, Denitsa, Chegaev, Konstantin, Dinić, Jelena, Divac Rankov, Aleksandra, Fernandes, Miguel X., Fusi, Fabio, Garcia-Sosa, Alfonso T., Juvonen, Risto, Kondeva-Burdina, Magdalena, Padron, Jose M., Pajeva, Ilza, Pencheva, Tania, Puerta, Adrian, Raunio, Hannu, Riganti, Chiara, Tsakovska, Ivanka, Tzankova, Virginia, Yordanov, Yordan, Saponara, Simona, "A Comprehensive Evaluation of Sdox, a Promising H2S-Releasing Doxorubicin for the Treatment of Chemoresistant Tumors" in Frontiers in Pharmacology, 13 (2022),
https://doi.org/10.3389/fphar.2022.831791 . .

TY  - JOUR
AU  - Ugrin, Milena
AU  - Dinić, Jelena
AU  - Jeremić, Sanja
AU  - Dragičević, Sandra
AU  - Banović Đeri, Bojana
AU  - Nikolić, Aleksandra
PY  - 2021
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1478
AB  - Bacterial nanocellulose (BNC) stands out among polymers as a promising biomaterial due to its mechanical strength, hydrophilicity, biocompatibility, biodegradability, low toxicity and renewability. The use of scaffolds based on BNC for 3D cell culture has been previously demonstrated. The study exploited excellent properties of the BNC to develop an efficient and low-cost in vitro cell migration assay. The BNC scaffold was introduced into a cell culture 24 h after the SW480 cells were seeded, and cells were allowed to enter the scaffold within the next 24-48 h. The cells were stained with different fluorophores either before or after the introduction of the scaffold in the culture. Untreated cells were observed to enter the BNC scaffold in significant numbers, form clusters and retain a high viability after 48 h. To validate the assay's usability for drug development, the treatments of SW480 cells were performed using aspirin, an agent known to reduce the migratory potential of this cell line in culture. This study demonstrates the application of BNC as a scaffold for cell migration testing as a low-cost alternative to commercial assays based on the Boyden chamber principle. The assay could be further developed for routine use in cancer research and anticancer drug development.
PB  - MDPI, Basel
T2  - Nanomaterials
T1  - Bacterial Nanocellulose as a Scaffold for In Vitro Cell Migration Assay
IS  - 9
VL  - 11
DO  - 10.3390/nano11092322
ER  - 

@article{
author = "Ugrin, Milena and Dinić, Jelena and Jeremić, Sanja and Dragičević, Sandra and Banović Đeri, Bojana and Nikolić, Aleksandra",
year = "2021",
abstract = "Bacterial nanocellulose (BNC) stands out among polymers as a promising biomaterial due to its mechanical strength, hydrophilicity, biocompatibility, biodegradability, low toxicity and renewability. The use of scaffolds based on BNC for 3D cell culture has been previously demonstrated. The study exploited excellent properties of the BNC to develop an efficient and low-cost in vitro cell migration assay. The BNC scaffold was introduced into a cell culture 24 h after the SW480 cells were seeded, and cells were allowed to enter the scaffold within the next 24-48 h. The cells were stained with different fluorophores either before or after the introduction of the scaffold in the culture. Untreated cells were observed to enter the BNC scaffold in significant numbers, form clusters and retain a high viability after 48 h. To validate the assay's usability for drug development, the treatments of SW480 cells were performed using aspirin, an agent known to reduce the migratory potential of this cell line in culture. This study demonstrates the application of BNC as a scaffold for cell migration testing as a low-cost alternative to commercial assays based on the Boyden chamber principle. The assay could be further developed for routine use in cancer research and anticancer drug development.",
publisher = "MDPI, Basel",
journal = "Nanomaterials",
title = "Bacterial Nanocellulose as a Scaffold for In Vitro Cell Migration Assay",
number = "9",
volume = "11",
doi = "10.3390/nano11092322"
}

Ugrin, M., Dinić, J., Jeremić, S., Dragičević, S., Banović Đeri, B.,& Nikolić, A.. (2021). Bacterial Nanocellulose as a Scaffold for In Vitro Cell Migration Assay. in Nanomaterials
MDPI, Basel., 11(9).
https://doi.org/10.3390/nano11092322

Ugrin M, Dinić J, Jeremić S, Dragičević S, Banović Đeri B, Nikolić A. Bacterial Nanocellulose as a Scaffold for In Vitro Cell Migration Assay. in Nanomaterials. 2021;11(9).
doi:10.3390/nano11092322 .

Ugrin, Milena, Dinić, Jelena, Jeremić, Sanja, Dragičević, Sandra, Banović Đeri, Bojana, Nikolić, Aleksandra, "Bacterial Nanocellulose as a Scaffold for In Vitro Cell Migration Assay" in Nanomaterials, 11, no. 9 (2021),
https://doi.org/10.3390/nano11092322 . .

TY  - JOUR
AU  - Nesović, Marija
AU  - Divac Rankov, Aleksandra
AU  - Podolski-Renić, Ana
AU  - Nikolić, Igor
AU  - Tasić, Goran
AU  - Mancini, Arianna
AU  - Schenone, Silvia
AU  - Pesić, Milica
AU  - Dinić, Jelena
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1315
AB  - Glioblastoma (GBM), as the most aggressive brain tumor, displays a high expression of Src tyrosine kinase, which is involved in the survival, migration, and invasiveness of tumor cells. Thus, Src emerged as a potential target for GBM therapy. The effects of Src inhibitors pyrazolo[3,4-d]pyrimidines, Si306 and its prodrug pro-Si306 were investigated in human GBM cell lines (U87 and U87-TxR) and three primary GBM cell cultures. Primary GBM cells were more resistant to Si306 and pro-Si306 according to the 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. However, the ability of all GBM cells to degrade the extracellular matrix was considerably compromised after Si306 and pro-Si306 applications. Besides reducing the phosphorylation of Src and its downstream signaling pathway components, both compounds decreased the phosphorylated form of focal adhesion kinase (FAK) and epidermal growth factor receptor (EGFR) expression, showing the potential to suppress the aggressiveness of GBM. In vivo, Si306 and pro-Si306 displayed an anti-invasive effect against U87 xenografts in the zebrafish embryo model. Considering that Si306 and pro-Si306 are able to cross the blood-brain barrier and suppress the spread of GBM cells, we anticipate their clinical testing in the near future. Moreover, the prodrug showed similar efficacy to the drug, implying the rationality of its use in clinical settings.
PB  - MDPI, Basel
T2  - Cancers
T1  - Src Inhibitors Pyrazolo[3,4-d]pyrimidines, Si306 and Pro-Si306, Inhibit Focal Adhesion Kinase and Suppress Human Glioblastoma Invasion In Vitro and In Vivo
IS  - 6
VL  - 12
DO  - 10.3390/cancers12061570
ER  - 

@article{
author = "Nesović, Marija and Divac Rankov, Aleksandra and Podolski-Renić, Ana and Nikolić, Igor and Tasić, Goran and Mancini, Arianna and Schenone, Silvia and Pesić, Milica and Dinić, Jelena",
year = "2020",
abstract = "Glioblastoma (GBM), as the most aggressive brain tumor, displays a high expression of Src tyrosine kinase, which is involved in the survival, migration, and invasiveness of tumor cells. Thus, Src emerged as a potential target for GBM therapy. The effects of Src inhibitors pyrazolo[3,4-d]pyrimidines, Si306 and its prodrug pro-Si306 were investigated in human GBM cell lines (U87 and U87-TxR) and three primary GBM cell cultures. Primary GBM cells were more resistant to Si306 and pro-Si306 according to the 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. However, the ability of all GBM cells to degrade the extracellular matrix was considerably compromised after Si306 and pro-Si306 applications. Besides reducing the phosphorylation of Src and its downstream signaling pathway components, both compounds decreased the phosphorylated form of focal adhesion kinase (FAK) and epidermal growth factor receptor (EGFR) expression, showing the potential to suppress the aggressiveness of GBM. In vivo, Si306 and pro-Si306 displayed an anti-invasive effect against U87 xenografts in the zebrafish embryo model. Considering that Si306 and pro-Si306 are able to cross the blood-brain barrier and suppress the spread of GBM cells, we anticipate their clinical testing in the near future. Moreover, the prodrug showed similar efficacy to the drug, implying the rationality of its use in clinical settings.",
publisher = "MDPI, Basel",
journal = "Cancers",
title = "Src Inhibitors Pyrazolo[3,4-d]pyrimidines, Si306 and Pro-Si306, Inhibit Focal Adhesion Kinase and Suppress Human Glioblastoma Invasion In Vitro and In Vivo",
number = "6",
volume = "12",
doi = "10.3390/cancers12061570"
}

Nesović, M., Divac Rankov, A., Podolski-Renić, A., Nikolić, I., Tasić, G., Mancini, A., Schenone, S., Pesić, M.,& Dinić, J.. (2020). Src Inhibitors Pyrazolo[3,4-d]pyrimidines, Si306 and Pro-Si306, Inhibit Focal Adhesion Kinase and Suppress Human Glioblastoma Invasion In Vitro and In Vivo. in Cancers
MDPI, Basel., 12(6).
https://doi.org/10.3390/cancers12061570

Nesović M, Divac Rankov A, Podolski-Renić A, Nikolić I, Tasić G, Mancini A, Schenone S, Pesić M, Dinić J. Src Inhibitors Pyrazolo[3,4-d]pyrimidines, Si306 and Pro-Si306, Inhibit Focal Adhesion Kinase and Suppress Human Glioblastoma Invasion In Vitro and In Vivo. in Cancers. 2020;12(6).
doi:10.3390/cancers12061570 .

Nesović, Marija, Divac Rankov, Aleksandra, Podolski-Renić, Ana, Nikolić, Igor, Tasić, Goran, Mancini, Arianna, Schenone, Silvia, Pesić, Milica, Dinić, Jelena, "Src Inhibitors Pyrazolo[3,4-d]pyrimidines, Si306 and Pro-Si306, Inhibit Focal Adhesion Kinase and Suppress Human Glioblastoma Invasion In Vitro and In Vivo" in Cancers, 12, no. 6 (2020),
https://doi.org/10.3390/cancers12061570 . .

TY  - JOUR
AU  - Babić, Tamara
AU  - Dinić, Jelena
AU  - Stojković Burić, Sonja
AU  - Hadzić, Stefan
AU  - Pesić, Milica
AU  - Radojković, Dragica
AU  - Divac Rankov, Aleksandra
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1132
AB  - Cancer drug resistance and poor selectivity towards cancer cells demand the constant search for new therapeutics. PI3K-Akt-mTOR and RAS-MAPK-ERK signaling pathways are key mechanisms involved in cell survival, proliferation, differentiation, and metabolism and their deregulation in cancer can promote development of therapy resistance. We investigated the effects of targeted inhibitors (wortmannin, GSK690693, AZD2014 and tipifarnib) towards these two pathways on early zebrafish and sea urchin development to assess their toxicity in normal, fast proliferating cells. PI3K inhibitor wortmannin and RAS inhibitor tipifarnib displayed highest toxicity while GSK690693, a pan-Akt kinase inhibitor, exhibited a less significant impact on embryo survival and development. Moreover, inhibition of the upstream part of the PI3K-Akt-mTOR pathway (wortmannin/GSK690693 co-treatment) produced a synergistic effect and impacted zebrafish embryo survival and development at much lower concentrations. Dual mTORC1/mTORC2 inhibitor AZD2014 showed no considerable effects on embryonic cells of zebrafish in concentrations substantially toxic in cancer cells. AZD2014 also caused the least prominent effects on sea urchin embryo development compared to other inhibitors. Significant toxicity of AZD2014 in human cancer cells, its capacity to sensitize resistant cancers, lower antiproliferative activity against human normal cell lines and fast proliferating embryonic cells could make this agent a promising candidate for anticancer therapy.
PB  - Akademiai Kiado Zrt, Budapest
T2  - Acta Biologica Hungarica
T1  - Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models
EP  - 410
IS  - 4
SP  - 395
VL  - 69
DO  - 10.1556/018.69.2018.4.3
ER  - 

@article{
author = "Babić, Tamara and Dinić, Jelena and Stojković Burić, Sonja and Hadzić, Stefan and Pesić, Milica and Radojković, Dragica and Divac Rankov, Aleksandra",
year = "2018",
abstract = "Cancer drug resistance and poor selectivity towards cancer cells demand the constant search for new therapeutics. PI3K-Akt-mTOR and RAS-MAPK-ERK signaling pathways are key mechanisms involved in cell survival, proliferation, differentiation, and metabolism and their deregulation in cancer can promote development of therapy resistance. We investigated the effects of targeted inhibitors (wortmannin, GSK690693, AZD2014 and tipifarnib) towards these two pathways on early zebrafish and sea urchin development to assess their toxicity in normal, fast proliferating cells. PI3K inhibitor wortmannin and RAS inhibitor tipifarnib displayed highest toxicity while GSK690693, a pan-Akt kinase inhibitor, exhibited a less significant impact on embryo survival and development. Moreover, inhibition of the upstream part of the PI3K-Akt-mTOR pathway (wortmannin/GSK690693 co-treatment) produced a synergistic effect and impacted zebrafish embryo survival and development at much lower concentrations. Dual mTORC1/mTORC2 inhibitor AZD2014 showed no considerable effects on embryonic cells of zebrafish in concentrations substantially toxic in cancer cells. AZD2014 also caused the least prominent effects on sea urchin embryo development compared to other inhibitors. Significant toxicity of AZD2014 in human cancer cells, its capacity to sensitize resistant cancers, lower antiproliferative activity against human normal cell lines and fast proliferating embryonic cells could make this agent a promising candidate for anticancer therapy.",
publisher = "Akademiai Kiado Zrt, Budapest",
journal = "Acta Biologica Hungarica",
title = "Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models",
pages = "410-395",
number = "4",
volume = "69",
doi = "10.1556/018.69.2018.4.3"
}

Babić, T., Dinić, J., Stojković Burić, S., Hadzić, S., Pesić, M., Radojković, D.,& Divac Rankov, A.. (2018). Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models. in Acta Biologica Hungarica
Akademiai Kiado Zrt, Budapest., 69(4), 395-410.
https://doi.org/10.1556/018.69.2018.4.3

Babić T, Dinić J, Stojković Burić S, Hadzić S, Pesić M, Radojković D, Divac Rankov A. Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models. in Acta Biologica Hungarica. 2018;69(4):395-410.
doi:10.1556/018.69.2018.4.3 .

Babić, Tamara, Dinić, Jelena, Stojković Burić, Sonja, Hadzić, Stefan, Pesić, Milica, Radojković, Dragica, Divac Rankov, Aleksandra, "Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models" in Acta Biologica Hungarica, 69, no. 4 (2018):395-410,
https://doi.org/10.1556/018.69.2018.4.3 . .

TY  - JOUR
AU  - Podolski-Renić, Ana
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Rios-Luci, Carla
AU  - Fernandes, Miguel X.
AU  - Ortega, Nuria
AU  - Kovačević Grujičić, Nataša
AU  - Martin, Victor S.
AU  - Padron, Jose M.
AU  - Pesić, Milica
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1766
AB  - The efficacy of microtubule targeting agents in cancer treatment has been compromised by the development of drug resistance that may involve both, P-glycoprotein overexpression and the changes in beta-tubulin isoforms' expression. The anti-Topoisomerase II activity of methyl 4-((E)-2-(methoxycarbonyl)vinyloxy)oct-2-ynoate (DTA0100) was recently reported. Herein, we further evaluated this propargylic enol ether derivative and found that it exerts inhibitory effect on tubulin polymerization by binding to colchicine binding site. DTA0100 mitotic arrest properties were investigated in two multi-drug resistant cancer cell lines with P-glycoprotein overexpression (colorectal carcinoma and glioblastoma). The sensitivity of multi-drug resistant cancer cell lines to DTA0100 was not significantly changed in contrast to microtubule targeting agents such as paclitaxel, vinblastine and colchicine. DTA0100 clearly induced microtubule depolymerization, leading to disturbance of cell cycle kinetics and subsequent apoptosis. The fine-tuning in beta-tubulin isoforms expression observed in multi drug resistant cancer cells may influence the efficacy of DTA0100. Importantly, DTA0100 blocked the Pglycoprotein function in both multi-drug resistant cancer cell lines without inducing the increase in Pglycoprotein expression. Therefore, DTA0100 acting as dual inhibitor of Topoisomerase II and microtubule formation could be considered as multi-potent anticancer agent. Besides, it is able to overcome the problem of drug resistance that emerges in the therapeutic approaches with either Topoisomerase II or microtubule targeting agents.
PB  - Elsevier Science Bv, Amsterdam
T2  - European Journal of Pharmaceutical Sciences
T1  - DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells
EP  - 168
SP  - 159
VL  - 105
DO  - 10.1016/j.ejps.2017.05.011
ER  - 

@article{
author = "Podolski-Renić, Ana and Banković, Jasna and Dinić, Jelena and Rios-Luci, Carla and Fernandes, Miguel X. and Ortega, Nuria and Kovačević Grujičić, Nataša and Martin, Victor S. and Padron, Jose M. and Pesić, Milica",
year = "2017",
abstract = "The efficacy of microtubule targeting agents in cancer treatment has been compromised by the development of drug resistance that may involve both, P-glycoprotein overexpression and the changes in beta-tubulin isoforms' expression. The anti-Topoisomerase II activity of methyl 4-((E)-2-(methoxycarbonyl)vinyloxy)oct-2-ynoate (DTA0100) was recently reported. Herein, we further evaluated this propargylic enol ether derivative and found that it exerts inhibitory effect on tubulin polymerization by binding to colchicine binding site. DTA0100 mitotic arrest properties were investigated in two multi-drug resistant cancer cell lines with P-glycoprotein overexpression (colorectal carcinoma and glioblastoma). The sensitivity of multi-drug resistant cancer cell lines to DTA0100 was not significantly changed in contrast to microtubule targeting agents such as paclitaxel, vinblastine and colchicine. DTA0100 clearly induced microtubule depolymerization, leading to disturbance of cell cycle kinetics and subsequent apoptosis. The fine-tuning in beta-tubulin isoforms expression observed in multi drug resistant cancer cells may influence the efficacy of DTA0100. Importantly, DTA0100 blocked the Pglycoprotein function in both multi-drug resistant cancer cell lines without inducing the increase in Pglycoprotein expression. Therefore, DTA0100 acting as dual inhibitor of Topoisomerase II and microtubule formation could be considered as multi-potent anticancer agent. Besides, it is able to overcome the problem of drug resistance that emerges in the therapeutic approaches with either Topoisomerase II or microtubule targeting agents.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "European Journal of Pharmaceutical Sciences",
title = "DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells",
pages = "168-159",
volume = "105",
doi = "10.1016/j.ejps.2017.05.011"
}

Podolski-Renić, A., Banković, J., Dinić, J., Rios-Luci, C., Fernandes, M. X., Ortega, N., Kovačević Grujičić, N., Martin, V. S., Padron, J. M.,& Pesić, M.. (2017). DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells. in European Journal of Pharmaceutical Sciences
Elsevier Science Bv, Amsterdam., 105, 159-168.
https://doi.org/10.1016/j.ejps.2017.05.011

Podolski-Renić A, Banković J, Dinić J, Rios-Luci C, Fernandes MX, Ortega N, Kovačević Grujičić N, Martin VS, Padron JM, Pesić M. DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells. in European Journal of Pharmaceutical Sciences. 2017;105:159-168.
doi:10.1016/j.ejps.2017.05.011 .

Podolski-Renić, Ana, Banković, Jasna, Dinić, Jelena, Rios-Luci, Carla, Fernandes, Miguel X., Ortega, Nuria, Kovačević Grujičić, Nataša, Martin, Victor S., Padron, Jose M., Pesić, Milica, "DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells" in European Journal of Pharmaceutical Sciences, 105 (2017):159-168,
https://doi.org/10.1016/j.ejps.2017.05.011 . .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Petrić, Marija
AU  - Radojković, Dragica
AU  - Pesić, Milica
AU  - Dinić, Jelena
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1758
AB  - Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.
PB  - Springer, New York
T2  - Histochemistry and Cell Biology
T1  - Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells
EP  - 544
IS  - 5
SP  - 529
VL  - 148
DO  - 10.1007/s00418-017-1590-4
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Ljujić, Mila and Petrić, Marija and Radojković, Dragica and Pesić, Milica and Dinić, Jelena",
year = "2017",
abstract = "Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.",
publisher = "Springer, New York",
journal = "Histochemistry and Cell Biology",
title = "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells",
pages = "544-529",
number = "5",
volume = "148",
doi = "10.1007/s00418-017-1590-4"
}

Divac Rankov, A., Ljujić, M., Petrić, M., Radojković, D., Pesić, M.,& Dinić, J.. (2017). Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology
Springer, New York., 148(5), 529-544.
https://doi.org/10.1007/s00418-017-1590-4

Divac Rankov A, Ljujić M, Petrić M, Radojković D, Pesić M, Dinić J. Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology. 2017;148(5):529-544.
doi:10.1007/s00418-017-1590-4 .

Divac Rankov, Aleksandra, Ljujić, Mila, Petrić, Marija, Radojković, Dragica, Pesić, Milica, Dinić, Jelena, "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells" in Histochemistry and Cell Biology, 148, no. 5 (2017):529-544,
https://doi.org/10.1007/s00418-017-1590-4 . .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Petrić, Marija
AU  - Radojković, Dragica
AU  - Pesić, Milica
AU  - Dinić, Jelena
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1004
AB  - Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.
PB  - Springer, New York
T2  - Histochemistry and Cell Biology
T1  - Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells
EP  - 544
IS  - 5
SP  - 529
VL  - 148
DO  - 10.1007/s00418-017-1590-4
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Ljujić, Mila and Petrić, Marija and Radojković, Dragica and Pesić, Milica and Dinić, Jelena",
year = "2017",
abstract = "Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.",
publisher = "Springer, New York",
journal = "Histochemistry and Cell Biology",
title = "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells",
pages = "544-529",
number = "5",
volume = "148",
doi = "10.1007/s00418-017-1590-4"
}

Divac Rankov, A., Ljujić, M., Petrić, M., Radojković, D., Pesić, M.,& Dinić, J.. (2017). Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology
Springer, New York., 148(5), 529-544.
https://doi.org/10.1007/s00418-017-1590-4

Divac Rankov A, Ljujić M, Petrić M, Radojković D, Pesić M, Dinić J. Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology. 2017;148(5):529-544.
doi:10.1007/s00418-017-1590-4 .

Divac Rankov, Aleksandra, Ljujić, Mila, Petrić, Marija, Radojković, Dragica, Pesić, Milica, Dinić, Jelena, "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells" in Histochemistry and Cell Biology, 148, no. 5 (2017):529-544,
https://doi.org/10.1007/s00418-017-1590-4 . .

TY  - JOUR
AU  - Podolski-Renić, Ana
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Rios-Luci, Carla
AU  - Fernandes, Miguel X.
AU  - Ortega, Nuria
AU  - Kovačević Grujičić, Nataša
AU  - Martin, Victor S.
AU  - Padron, Jose M.
AU  - Pesić, Milica
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1079
AB  - The efficacy of microtubule targeting agents in cancer treatment has been compromised by the development of drug resistance that may involve both, P-glycoprotein overexpression and the changes in beta-tubulin isoforms' expression. The anti-Topoisomerase II activity of methyl 4-((E)-2-(methoxycarbonyl)vinyloxy)oct-2-ynoate (DTA0100) was recently reported. Herein, we further evaluated this propargylic enol ether derivative and found that it exerts inhibitory effect on tubulin polymerization by binding to colchicine binding site. DTA0100 mitotic arrest properties were investigated in two multi-drug resistant cancer cell lines with P-glycoprotein overexpression (colorectal carcinoma and glioblastoma). The sensitivity of multi-drug resistant cancer cell lines to DTA0100 was not significantly changed in contrast to microtubule targeting agents such as paclitaxel, vinblastine and colchicine. DTA0100 clearly induced microtubule depolymerization, leading to disturbance of cell cycle kinetics and subsequent apoptosis. The fine-tuning in beta-tubulin isoforms expression observed in multi drug resistant cancer cells may influence the efficacy of DTA0100. Importantly, DTA0100 blocked the Pglycoprotein function in both multi-drug resistant cancer cell lines without inducing the increase in Pglycoprotein expression. Therefore, DTA0100 acting as dual inhibitor of Topoisomerase II and microtubule formation could be considered as multi-potent anticancer agent. Besides, it is able to overcome the problem of drug resistance that emerges in the therapeutic approaches with either Topoisomerase II or microtubule targeting agents.
PB  - Elsevier Science Bv, Amsterdam
T2  - European Journal of Pharmaceutical Sciences
T1  - DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells
EP  - 168
SP  - 159
VL  - 105
DO  - 10.1016/j.ejps.2017.05.011
ER  - 

@article{
author = "Podolski-Renić, Ana and Banković, Jasna and Dinić, Jelena and Rios-Luci, Carla and Fernandes, Miguel X. and Ortega, Nuria and Kovačević Grujičić, Nataša and Martin, Victor S. and Padron, Jose M. and Pesić, Milica",
year = "2017",
abstract = "The efficacy of microtubule targeting agents in cancer treatment has been compromised by the development of drug resistance that may involve both, P-glycoprotein overexpression and the changes in beta-tubulin isoforms' expression. The anti-Topoisomerase II activity of methyl 4-((E)-2-(methoxycarbonyl)vinyloxy)oct-2-ynoate (DTA0100) was recently reported. Herein, we further evaluated this propargylic enol ether derivative and found that it exerts inhibitory effect on tubulin polymerization by binding to colchicine binding site. DTA0100 mitotic arrest properties were investigated in two multi-drug resistant cancer cell lines with P-glycoprotein overexpression (colorectal carcinoma and glioblastoma). The sensitivity of multi-drug resistant cancer cell lines to DTA0100 was not significantly changed in contrast to microtubule targeting agents such as paclitaxel, vinblastine and colchicine. DTA0100 clearly induced microtubule depolymerization, leading to disturbance of cell cycle kinetics and subsequent apoptosis. The fine-tuning in beta-tubulin isoforms expression observed in multi drug resistant cancer cells may influence the efficacy of DTA0100. Importantly, DTA0100 blocked the Pglycoprotein function in both multi-drug resistant cancer cell lines without inducing the increase in Pglycoprotein expression. Therefore, DTA0100 acting as dual inhibitor of Topoisomerase II and microtubule formation could be considered as multi-potent anticancer agent. Besides, it is able to overcome the problem of drug resistance that emerges in the therapeutic approaches with either Topoisomerase II or microtubule targeting agents.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "European Journal of Pharmaceutical Sciences",
title = "DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells",
pages = "168-159",
volume = "105",
doi = "10.1016/j.ejps.2017.05.011"
}

Podolski-Renić, A., Banković, J., Dinić, J., Rios-Luci, C., Fernandes, M. X., Ortega, N., Kovačević Grujičić, N., Martin, V. S., Padron, J. M.,& Pesić, M.. (2017). DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells. in European Journal of Pharmaceutical Sciences
Elsevier Science Bv, Amsterdam., 105, 159-168.
https://doi.org/10.1016/j.ejps.2017.05.011

Podolski-Renić A, Banković J, Dinić J, Rios-Luci C, Fernandes MX, Ortega N, Kovačević Grujičić N, Martin VS, Padron JM, Pesić M. DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells. in European Journal of Pharmaceutical Sciences. 2017;105:159-168.
doi:10.1016/j.ejps.2017.05.011 .

Podolski-Renić, Ana, Banković, Jasna, Dinić, Jelena, Rios-Luci, Carla, Fernandes, Miguel X., Ortega, Nuria, Kovačević Grujičić, Nataša, Martin, Victor S., Padron, Jose M., Pesić, Milica, "DTA0100, dual topoisomerase II and microtubule inhibitor, evades paclitaxel resistance in P-glycoprotein overexpressing cancer cells" in European Journal of Pharmaceutical Sciences, 105 (2017):159-168,
https://doi.org/10.1016/j.ejps.2017.05.011 . .

TY  - CONF
AU  - Kovacević, T.
AU  - Dinić, J.
AU  - Divac Rankov, Aleksandra
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1006
PB  - Wiley, Hoboken
C3  - FEBS Journal
T1  - Effect of GSK690693 and AZD2014, Akt/mTOR pathway inhibitors, on the development of the zebrafish (Danio rerio) embryos
EP  - 349
SP  - 349
VL  - 284
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1006
ER  - 

@conference{
author = "Kovacević, T. and Dinić, J. and Divac Rankov, Aleksandra",
year = "2017",
publisher = "Wiley, Hoboken",
journal = "FEBS Journal",
title = "Effect of GSK690693 and AZD2014, Akt/mTOR pathway inhibitors, on the development of the zebrafish (Danio rerio) embryos",
pages = "349-349",
volume = "284",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1006"
}

Kovacević, T., Dinić, J.,& Divac Rankov, A.. (2017). Effect of GSK690693 and AZD2014, Akt/mTOR pathway inhibitors, on the development of the zebrafish (Danio rerio) embryos. in FEBS Journal
Wiley, Hoboken., 284, 349-349.
https://hdl.handle.net/21.15107/rcub_imagine_1006

Kovacević T, Dinić J, Divac Rankov A. Effect of GSK690693 and AZD2014, Akt/mTOR pathway inhibitors, on the development of the zebrafish (Danio rerio) embryos. in FEBS Journal. 2017;284:349-349.
https://hdl.handle.net/21.15107/rcub_imagine_1006 .

Kovacević, T., Dinić, J., Divac Rankov, Aleksandra, "Effect of GSK690693 and AZD2014, Akt/mTOR pathway inhibitors, on the development of the zebrafish (Danio rerio) embryos" in FEBS Journal, 284 (2017):349-349,
https://hdl.handle.net/21.15107/rcub_imagine_1006 .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Radlović, Nedeljko
AU  - Dinić, Jelena
AU  - Milosević, Katarina
AU  - Radojković, Dragica
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/769
AB  - We present a case of a 19-year old male with uncommon initial clinical cystic fibrosis (CF) presentation and a rare CFTR genotype, homozygote for c.1393-1G gt A mutation (legacy name 1525-1G gt A).
PB  - Elsevier Science Bv, Amsterdam
T2  - Journal of Cystic Fibrosis
T1  - Clinical presentation of mild cystic fibrosis in a Serbian patient homozygous for the CFTR mutation c.1393-1G  gt  A
EP  - 113
IS  - 1
SP  - 111
VL  - 13
DO  - 10.1016/j.jcf.2013.07.001
ER  - 

@article{
author = "Nikolić, Aleksandra and Radlović, Nedeljko and Dinić, Jelena and Milosević, Katarina and Radojković, Dragica",
year = "2014",
abstract = "We present a case of a 19-year old male with uncommon initial clinical cystic fibrosis (CF) presentation and a rare CFTR genotype, homozygote for c.1393-1G gt A mutation (legacy name 1525-1G gt A).",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Journal of Cystic Fibrosis",
title = "Clinical presentation of mild cystic fibrosis in a Serbian patient homozygous for the CFTR mutation c.1393-1G  gt  A",
pages = "113-111",
number = "1",
volume = "13",
doi = "10.1016/j.jcf.2013.07.001"
}

Nikolić, A., Radlović, N., Dinić, J., Milosević, K.,& Radojković, D.. (2014). Clinical presentation of mild cystic fibrosis in a Serbian patient homozygous for the CFTR mutation c.1393-1G  gt  A. in Journal of Cystic Fibrosis
Elsevier Science Bv, Amsterdam., 13(1), 111-113.
https://doi.org/10.1016/j.jcf.2013.07.001

Nikolić A, Radlović N, Dinić J, Milosević K, Radojković D. Clinical presentation of mild cystic fibrosis in a Serbian patient homozygous for the CFTR mutation c.1393-1G  gt  A. in Journal of Cystic Fibrosis. 2014;13(1):111-113.
doi:10.1016/j.jcf.2013.07.001 .

Nikolić, Aleksandra, Radlović, Nedeljko, Dinić, Jelena, Milosević, Katarina, Radojković, Dragica, "Clinical presentation of mild cystic fibrosis in a Serbian patient homozygous for the CFTR mutation c.1393-1G  gt  A" in Journal of Cystic Fibrosis, 13, no. 1 (2014):111-113,
https://doi.org/10.1016/j.jcf.2013.07.001 . .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Dinić, Jelena
AU  - Radojković, Dragica
AU  - Lukić, Snežana
AU  - Popović, Dragan
AU  - Uglješić, Milenko
AU  - Knežević, Srboljub
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/517
AB  - Uvod: Mutacije u CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) genu mogu biti povezane sa različitim tipovima pankreasne patologije i da nose povišen rizik za oboljenja pankreasa. Najčešća mutacija u obolelih od cistične fibroze je F508del, dok je alel 5T povezan sa atipičnim oblicima cistične fibroze. Cilj rada: Cilj ove studije bio je da se utvrdi učestalost F508del mutacije i 5T alela u genu za transmembranski regulator provodljivosti u cističnoj fibrozi (CFTR ili Cystic Fibrosis Transmembrane Conductance Regulator) u grupama pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa, kao i da se istraži da li ove genske varijante predstavljaju faktore rizika za nastanak bolesti pankreasa. Metod rada: Istraživanje je obuhvatilo 50 pacijenata sa hroničnim pankreatitisom i 50 pacijenata sa adenokarcinomom pankreasa, kao i 124 zdrava ispitanika. Utvrđivanje prisustva F508del mutacije i detekcija 5T, 7T i 9T alela politimidinskog trakta vršeni su na DNK izolovanoj iz periferne krvi ispitanika pomoću metode PCR-om posredovane mesto- specifične mutageneze (PSM ili PCR-mediated site-directed mutagenesis). Rezultati: Učestalost F508del mutacije u hroničnom pankreatitisu (3,0%) bila je značajno povišena (p=0,032) u odnosu na učestalost u grupi zdravih ispitanika (0,4%), dok ostale razlike u učestalostima nisu bile statistički značajne. Zaključak: Rezultati ovog istraživanja ukazuju da F508del mutacija u CFTR genu predstavlja faktor rizika za razvoj hroničnog pankreatitisa.
AB  - Introduction: Mutations in the CFTR gene may be associated with various types of pancreatic pathology and result in higher risk of pancreatic disorders. While delta F508 is the most common mutation in cystic fibrosis patients, the allel 5T is associated with atypical forms of cystic fibrosis. Study aim: The aim of this study was to establish the frequencies of F508del mutation and 5T allele in the CFTR gene in patients with chronic pancreatitis and pancreatic cancer, as well as to investigate whether these genetic variants represent risk factors for pancreatic diseases. Study methods: The study has encompassed 50 patients with chronic pancreatitis and 50 patients with pancreatic adenocarcinoma, as well as 124 healthy individuals. The analysis of F508del mutation and alleles 5T, 7T and 9T of the polythymidine tract was performed on DNA extracted from periferal blood by PCR-mediated site-direted mutagenesis (PSM) method. Results: The frequency of F508del mutation in the group of patients with chronic pancreatitis (3.0%) was significantly increased (p=0.032) in comparison to the group of healthy individuals (0.4%), while other analyzed differences were not statistically significant. Conclusion: The results of this study indicate that F508del mutation in the CFTR gene respresents a risk factor for the development of chronic pancreatitis.
PB  - Udruženje hirurga Jugoslavije, Beograd
T2  - Acta chirurgica Iugoslavica
T1  - Zastupljenost F508del mutacije i 5T alela politimidinskog trakta u CFTR genu kod pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa
T1  - CFTR F508del mutation and 5T allele in patients with chronic pancreatitis and pancreatic adenocarcinoma
EP  - 47
IS  - 3
SP  - 43
VL  - 58
DO  - 10.2298/ACI1103043N
ER  - 

@article{
author = "Nikolić, Aleksandra and Dinić, Jelena and Radojković, Dragica and Lukić, Snežana and Popović, Dragan and Uglješić, Milenko and Knežević, Srboljub",
year = "2011",
abstract = "Uvod: Mutacije u CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) genu mogu biti povezane sa različitim tipovima pankreasne patologije i da nose povišen rizik za oboljenja pankreasa. Najčešća mutacija u obolelih od cistične fibroze je F508del, dok je alel 5T povezan sa atipičnim oblicima cistične fibroze. Cilj rada: Cilj ove studije bio je da se utvrdi učestalost F508del mutacije i 5T alela u genu za transmembranski regulator provodljivosti u cističnoj fibrozi (CFTR ili Cystic Fibrosis Transmembrane Conductance Regulator) u grupama pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa, kao i da se istraži da li ove genske varijante predstavljaju faktore rizika za nastanak bolesti pankreasa. Metod rada: Istraživanje je obuhvatilo 50 pacijenata sa hroničnim pankreatitisom i 50 pacijenata sa adenokarcinomom pankreasa, kao i 124 zdrava ispitanika. Utvrđivanje prisustva F508del mutacije i detekcija 5T, 7T i 9T alela politimidinskog trakta vršeni su na DNK izolovanoj iz periferne krvi ispitanika pomoću metode PCR-om posredovane mesto- specifične mutageneze (PSM ili PCR-mediated site-directed mutagenesis). Rezultati: Učestalost F508del mutacije u hroničnom pankreatitisu (3,0%) bila je značajno povišena (p=0,032) u odnosu na učestalost u grupi zdravih ispitanika (0,4%), dok ostale razlike u učestalostima nisu bile statistički značajne. Zaključak: Rezultati ovog istraživanja ukazuju da F508del mutacija u CFTR genu predstavlja faktor rizika za razvoj hroničnog pankreatitisa., Introduction: Mutations in the CFTR gene may be associated with various types of pancreatic pathology and result in higher risk of pancreatic disorders. While delta F508 is the most common mutation in cystic fibrosis patients, the allel 5T is associated with atypical forms of cystic fibrosis. Study aim: The aim of this study was to establish the frequencies of F508del mutation and 5T allele in the CFTR gene in patients with chronic pancreatitis and pancreatic cancer, as well as to investigate whether these genetic variants represent risk factors for pancreatic diseases. Study methods: The study has encompassed 50 patients with chronic pancreatitis and 50 patients with pancreatic adenocarcinoma, as well as 124 healthy individuals. The analysis of F508del mutation and alleles 5T, 7T and 9T of the polythymidine tract was performed on DNA extracted from periferal blood by PCR-mediated site-direted mutagenesis (PSM) method. Results: The frequency of F508del mutation in the group of patients with chronic pancreatitis (3.0%) was significantly increased (p=0.032) in comparison to the group of healthy individuals (0.4%), while other analyzed differences were not statistically significant. Conclusion: The results of this study indicate that F508del mutation in the CFTR gene respresents a risk factor for the development of chronic pancreatitis.",
publisher = "Udruženje hirurga Jugoslavije, Beograd",
journal = "Acta chirurgica Iugoslavica",
title = "Zastupljenost F508del mutacije i 5T alela politimidinskog trakta u CFTR genu kod pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa, CFTR F508del mutation and 5T allele in patients with chronic pancreatitis and pancreatic adenocarcinoma",
pages = "47-43",
number = "3",
volume = "58",
doi = "10.2298/ACI1103043N"
}

Nikolić, A., Dinić, J., Radojković, D., Lukić, S., Popović, D., Uglješić, M.,& Knežević, S.. (2011). Zastupljenost F508del mutacije i 5T alela politimidinskog trakta u CFTR genu kod pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa. in Acta chirurgica Iugoslavica
Udruženje hirurga Jugoslavije, Beograd., 58(3), 43-47.
https://doi.org/10.2298/ACI1103043N

Nikolić A, Dinić J, Radojković D, Lukić S, Popović D, Uglješić M, Knežević S. Zastupljenost F508del mutacije i 5T alela politimidinskog trakta u CFTR genu kod pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa. in Acta chirurgica Iugoslavica. 2011;58(3):43-47.
doi:10.2298/ACI1103043N .

Nikolić, Aleksandra, Dinić, Jelena, Radojković, Dragica, Lukić, Snežana, Popović, Dragan, Uglješić, Milenko, Knežević, Srboljub, "Zastupljenost F508del mutacije i 5T alela politimidinskog trakta u CFTR genu kod pacijenata sa hroničnim pankreatitisom i adenokarcinomom pankreasa" in Acta chirurgica Iugoslavica, 58, no. 3 (2011):43-47,
https://doi.org/10.2298/ACI1103043N . .

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

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

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

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

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

TY  - JOUR
AU  - Dinić, Jelena
AU  - Kušić-Tišma, Jelena
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Ristanović, Momčilo
AU  - Radojković, Dragica
PY  - 2007
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/291
AB  - Uvod/Cilj. Poremećena plodnost muškog partnera je glavni uzrok infertiliteta kod polovine neplodnih parova. Na genetskom nivou infertilitet kod muškaraca mogu uzrokovati hromozomske aberacije ili genske mutacije. U ovoj studiji analizirano je prisustvo i tip mikrodelecija Y hromozoma i mutacija u genu za regulator transmembranske provodljivosti u cističnoj fibrozi (CFTR) kao genetska osnova infertiliteta kod muškaraca u Srbiji. Cilj studije je bio da se analiziraju mutacije u CFTR genu i mikrodelecije Y hromozoma, kao potencijalni uzroci infertiliteta kod muškaraca u Srbiji, kao i da se testira hipoteza da su CFTR mutacije kod infertilnih muškaraca predominantno locirane u nekoliko poslednjih egzona. Metode. Studija je obuhvatila 33 muškarca sa oligo ili azospermijom. Detekcija mikrodelecija Y hromozoma u regionu faktora azospermije (AZF) vršena je pomoću multipleks PCR metode. Pretraživanje CFTR gena vršeno je metodom elektroforeze u gelu sa gradijentom denaturišućeg agensa (DGGE). Rezultati. Delecije Y hromozoma su detektovane kod četiri bolesnika, predominantno u AZFc regionu (četiri od ukupno šest). Mutacije u CFTR genu su detektovane na osam od 66 analizovanih hromozoma infertilnih muškaraca. Najčešće detektovana CFTR mutacija je F508del (šest od osam). Zaključak. Ova studija je potvrdila da mikrodelecije Y hromozoma i mutacije u CFTR genu igraju važnu ulogu u etiologiji infertiliteta kod muškaraca u Srbiji. Genetsko testiranje koje obuhvata detekciju mikrodelecija Y hromozoma i mutacija u CFTR genu uvedeno je u rutinsku dijagnostičku praksu i ponuđeno je parovima koji pristupaju asistiranoj reprodukciji. S obzirom da tip mikrodelecija Y hromozoma i tip mutacija u CFTR genu imaju prognostički značaj, preporuka je da se genotipizacija AZF regiona i CFTR gena ne vrši samo kod bolesnika sa umanjenim kvalitetom sperme pre pristupanja asistiranoj reprodukciji, već i u svrhe preimplantacione i prenatalne dijagnostike kod parova kod kojih je uspešno izvršena in vitro fertilizacija.
AB  - Background/Aim. Impaired fertility of a male partner is the main cause of infertility in up to one half of all infertile couples. At the genetic level, male infertility can be caused by chromosome aberrations or gene mutations. The presence and types of Y chromosome microdeletions and cystic fybrosis transmembrane conductance regulator (CFTR) gene mutations as genetic cause of male infertility was tested in Serbian men. The aim of this study was to analyze CFTR gene mutations and Y chromosome microdelations as potential causes of male infertility in Serbian patients, as well as to test the hypothesis that CFTR mutations in infertile men are predominantly located in the several last exons of the gene. Methods. This study has encompassed 33 men with oligo- or azoospermia. The screening for Y chromosome microdeletions in the azoospermia factor (AZF) region was performed by multiplex PCR analysis. The screening of the CFTR gene was performed by denaturing gradient gel electrophoresis (DGGE) method. Results. Deletions on Y chromosome were detected in four patients, predominantly in AZFc region (four of total six deletions). Mutations in the CFTR gene were detected on eight out of 66 analyzed chromosomes of infertile men. The most common mutation was F508del (six of total eight mutations). Conclusion. This study confirmed that both Y chromosome microdeletions and CFTR gene mutations played important role in etiology of male infertility in Serbian infertile men. Genetic testing for Y chromosome microdeletions and CFTR gene mutations has been introduced in routine diagnostics and offered to couples undergoing assisted reproduction techniques. Considering that both the type of Y chromosome microdeletion and the type of CFTR mutation have a prognostic value, it is recommended that AZF and CFTR genotyping should not only be performed in patients with reduced sperm quality before undergoing assisted reproduction, but also for the purpose of preimplantation and prenatal diagnostics in couples in which in vitro fertilization has been performed successfully.
PB  - Vojnomedicinska akademija - Institut za naučne informacije, Beograd
T2  - Vojnosanitetski pregled
T1  - Analiza mikrodelecija Y hromozoma i mutacija CFTR gena kao genetskih markera infertiliteta kod muškaraca u Srbiji
T1  - Analysis of Y chromosome microdeletions and CFTR gene mutations as genetic markers of infertility in Serbian men
EP  - 256
IS  - 4
SP  - 253
VL  - 64
DO  - 10.2298/VSP0704253D
ER  - 

@article{
author = "Dinić, Jelena and Kušić-Tišma, Jelena and Nikolić, Aleksandra and Divac Rankov, Aleksandra and Ristanović, Momčilo and Radojković, Dragica",
year = "2007",
abstract = "Uvod/Cilj. Poremećena plodnost muškog partnera je glavni uzrok infertiliteta kod polovine neplodnih parova. Na genetskom nivou infertilitet kod muškaraca mogu uzrokovati hromozomske aberacije ili genske mutacije. U ovoj studiji analizirano je prisustvo i tip mikrodelecija Y hromozoma i mutacija u genu za regulator transmembranske provodljivosti u cističnoj fibrozi (CFTR) kao genetska osnova infertiliteta kod muškaraca u Srbiji. Cilj studije je bio da se analiziraju mutacije u CFTR genu i mikrodelecije Y hromozoma, kao potencijalni uzroci infertiliteta kod muškaraca u Srbiji, kao i da se testira hipoteza da su CFTR mutacije kod infertilnih muškaraca predominantno locirane u nekoliko poslednjih egzona. Metode. Studija je obuhvatila 33 muškarca sa oligo ili azospermijom. Detekcija mikrodelecija Y hromozoma u regionu faktora azospermije (AZF) vršena je pomoću multipleks PCR metode. Pretraživanje CFTR gena vršeno je metodom elektroforeze u gelu sa gradijentom denaturišućeg agensa (DGGE). Rezultati. Delecije Y hromozoma su detektovane kod četiri bolesnika, predominantno u AZFc regionu (četiri od ukupno šest). Mutacije u CFTR genu su detektovane na osam od 66 analizovanih hromozoma infertilnih muškaraca. Najčešće detektovana CFTR mutacija je F508del (šest od osam). Zaključak. Ova studija je potvrdila da mikrodelecije Y hromozoma i mutacije u CFTR genu igraju važnu ulogu u etiologiji infertiliteta kod muškaraca u Srbiji. Genetsko testiranje koje obuhvata detekciju mikrodelecija Y hromozoma i mutacija u CFTR genu uvedeno je u rutinsku dijagnostičku praksu i ponuđeno je parovima koji pristupaju asistiranoj reprodukciji. S obzirom da tip mikrodelecija Y hromozoma i tip mutacija u CFTR genu imaju prognostički značaj, preporuka je da se genotipizacija AZF regiona i CFTR gena ne vrši samo kod bolesnika sa umanjenim kvalitetom sperme pre pristupanja asistiranoj reprodukciji, već i u svrhe preimplantacione i prenatalne dijagnostike kod parova kod kojih je uspešno izvršena in vitro fertilizacija., Background/Aim. Impaired fertility of a male partner is the main cause of infertility in up to one half of all infertile couples. At the genetic level, male infertility can be caused by chromosome aberrations or gene mutations. The presence and types of Y chromosome microdeletions and cystic fybrosis transmembrane conductance regulator (CFTR) gene mutations as genetic cause of male infertility was tested in Serbian men. The aim of this study was to analyze CFTR gene mutations and Y chromosome microdelations as potential causes of male infertility in Serbian patients, as well as to test the hypothesis that CFTR mutations in infertile men are predominantly located in the several last exons of the gene. Methods. This study has encompassed 33 men with oligo- or azoospermia. The screening for Y chromosome microdeletions in the azoospermia factor (AZF) region was performed by multiplex PCR analysis. The screening of the CFTR gene was performed by denaturing gradient gel electrophoresis (DGGE) method. Results. Deletions on Y chromosome were detected in four patients, predominantly in AZFc region (four of total six deletions). Mutations in the CFTR gene were detected on eight out of 66 analyzed chromosomes of infertile men. The most common mutation was F508del (six of total eight mutations). Conclusion. This study confirmed that both Y chromosome microdeletions and CFTR gene mutations played important role in etiology of male infertility in Serbian infertile men. Genetic testing for Y chromosome microdeletions and CFTR gene mutations has been introduced in routine diagnostics and offered to couples undergoing assisted reproduction techniques. Considering that both the type of Y chromosome microdeletion and the type of CFTR mutation have a prognostic value, it is recommended that AZF and CFTR genotyping should not only be performed in patients with reduced sperm quality before undergoing assisted reproduction, but also for the purpose of preimplantation and prenatal diagnostics in couples in which in vitro fertilization has been performed successfully.",
publisher = "Vojnomedicinska akademija - Institut za naučne informacije, Beograd",
journal = "Vojnosanitetski pregled",
title = "Analiza mikrodelecija Y hromozoma i mutacija CFTR gena kao genetskih markera infertiliteta kod muškaraca u Srbiji, Analysis of Y chromosome microdeletions and CFTR gene mutations as genetic markers of infertility in Serbian men",
pages = "256-253",
number = "4",
volume = "64",
doi = "10.2298/VSP0704253D"
}

Dinić, J., Kušić-Tišma, J., Nikolić, A., Divac Rankov, A., Ristanović, M.,& Radojković, D.. (2007). Analiza mikrodelecija Y hromozoma i mutacija CFTR gena kao genetskih markera infertiliteta kod muškaraca u Srbiji. in Vojnosanitetski pregled
Vojnomedicinska akademija - Institut za naučne informacije, Beograd., 64(4), 253-256.
https://doi.org/10.2298/VSP0704253D

Dinić J, Kušić-Tišma J, Nikolić A, Divac Rankov A, Ristanović M, Radojković D. Analiza mikrodelecija Y hromozoma i mutacija CFTR gena kao genetskih markera infertiliteta kod muškaraca u Srbiji. in Vojnosanitetski pregled. 2007;64(4):253-256.
doi:10.2298/VSP0704253D .

Dinić, Jelena, Kušić-Tišma, Jelena, Nikolić, Aleksandra, Divac Rankov, Aleksandra, Ristanović, Momčilo, Radojković, Dragica, "Analiza mikrodelecija Y hromozoma i mutacija CFTR gena kao genetskih markera infertiliteta kod muškaraca u Srbiji" in Vojnosanitetski pregled, 64, no. 4 (2007):253-256,
https://doi.org/10.2298/VSP0704253D . .

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

@conference{
author = "Nikolić, Aleksandra and Nisević, I and Dinić, J. and Lukić, S. and Anđelić, M. and Petrović-Stanojević, Nataša and Đorđević, Valentina and Rakićević, Ljiljana and Ugljesić, M. and Radojković, Dragica",
year = "2007",
publisher = "Oxford Univ Press, Oxford",
journal = "Annals of Oncology",
title = "Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer",
pages = "VII65-VII64",
volume = "18",
url = "https://hdl.handle.net/21.15107/rcub_imagine_288"
}

Nikolić, A., Nisević, I., Dinić, J., Lukić, S., Anđelić, M., Petrović-Stanojević, N., Đorđević, V., Rakićević, L., Ugljesić, M.,& Radojković, D.. (2007). Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer. in Annals of Oncology
Oxford Univ Press, Oxford., 18, VII64-VII65.
https://hdl.handle.net/21.15107/rcub_imagine_288

Nikolić A, Nisević I, Dinić J, Lukić S, Anđelić M, Petrović-Stanojević N, Đorđević V, Rakićević L, Ugljesić M, Radojković D. Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer. in Annals of Oncology. 2007;18:VII64-VII65.
https://hdl.handle.net/21.15107/rcub_imagine_288 .

Nikolić, Aleksandra, Nisević, I, Dinić, J., Lukić, S., Anđelić, M., Petrović-Stanojević, Nataša, Đorđević, Valentina, Rakićević, Ljiljana, Ugljesić, M., Radojković, Dragica, "Polymorphism MTHFR C677T in patients with chronic pancreatitis and pancreatic cancer" in Annals of Oncology, 18 (2007):VII64-VII65,
https://hdl.handle.net/21.15107/rcub_imagine_288 .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Stanković, Marija
AU  - Dinić, J.
AU  - Tornić, B.
AU  - Ljujić, Mila
PY  - 2006
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/240
AB  - Three common CFTR polymorphisms, 5T, M470V, and R75Q, have been shown to be relatively frequent in Serbian patients with monosymptomatic CF disorders. Since there is a variation in distribution of common polymorphisms among different populations, it was important to compare their frequencies in patients with the frequencies in healthy population in order to assess the possible role of these polymorphisms in the monosymptomatic CF disorders. Samples obtained from 100 healthy Serbian individuals were analyzed for the presence of CFTR 5T, M470V, and R75Q variants by PSM, RFLP, and DGGE methods, respectively. Allele 5T was present in two individuals, giving the allelic frequency of 1% (2/200 alleles). The frequency obtained for allele M470 was 45% (90/200 alleles), while V470 allele was present with the frequency of 55% (110/200 alleles). Polymorphism R75Q was present in two individuals, with allelic frequency of 1% (2/200 alleles). Our study has shown that the frequencies of two common polymorphisms, 5T and M470V, differ significantly in Serbian population in comparison with other Southern European populations. Since it appears that Serbian population has a specific distribution of studied CFTR gene variants, it would also be interesting to analyze other common variants of this gene in our population. Such data can also be potentially useful as anthropogenic markers in population studies.
PB  - Maik Nauka/Interperiodica/Springer, New York
T2  - Russian Journal of Genetics
T1  - Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population
EP  - 823
IS  - 7
SP  - 821
VL  - 42
DO  - 10.1134/S1022795406070192
ER  - 

@article{
author = "Nikolić, Aleksandra and Divac Rankov, Aleksandra and Stanković, Marija and Dinić, J. and Tornić, B. and Ljujić, Mila",
year = "2006",
abstract = "Three common CFTR polymorphisms, 5T, M470V, and R75Q, have been shown to be relatively frequent in Serbian patients with monosymptomatic CF disorders. Since there is a variation in distribution of common polymorphisms among different populations, it was important to compare their frequencies in patients with the frequencies in healthy population in order to assess the possible role of these polymorphisms in the monosymptomatic CF disorders. Samples obtained from 100 healthy Serbian individuals were analyzed for the presence of CFTR 5T, M470V, and R75Q variants by PSM, RFLP, and DGGE methods, respectively. Allele 5T was present in two individuals, giving the allelic frequency of 1% (2/200 alleles). The frequency obtained for allele M470 was 45% (90/200 alleles), while V470 allele was present with the frequency of 55% (110/200 alleles). Polymorphism R75Q was present in two individuals, with allelic frequency of 1% (2/200 alleles). Our study has shown that the frequencies of two common polymorphisms, 5T and M470V, differ significantly in Serbian population in comparison with other Southern European populations. Since it appears that Serbian population has a specific distribution of studied CFTR gene variants, it would also be interesting to analyze other common variants of this gene in our population. Such data can also be potentially useful as anthropogenic markers in population studies.",
publisher = "Maik Nauka/Interperiodica/Springer, New York",
journal = "Russian Journal of Genetics",
title = "Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population",
pages = "823-821",
number = "7",
volume = "42",
doi = "10.1134/S1022795406070192"
}

Nikolić, A., Divac Rankov, A., Stanković, M., Dinić, J., Tornić, B.,& Ljujić, M.. (2006). Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population. in Russian Journal of Genetics
Maik Nauka/Interperiodica/Springer, New York., 42(7), 821-823.
https://doi.org/10.1134/S1022795406070192

Nikolić A, Divac Rankov A, Stanković M, Dinić J, Tornić B, Ljujić M. Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population. in Russian Journal of Genetics. 2006;42(7):821-823.
doi:10.1134/S1022795406070192 .

Nikolić, Aleksandra, Divac Rankov, Aleksandra, Stanković, Marija, Dinić, J., Tornić, B., Ljujić, Mila, "Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population" in Russian Journal of Genetics, 42, no. 7 (2006):821-823,
https://doi.org/10.1134/S1022795406070192 . .

TY  - JOUR
AU  - Nikolić, Aleksandra
AU  - Divac Rankov, Aleksandra
AU  - Stanković, Marija
AU  - Dinić, J.
AU  - Tomić, Branko
AU  - Ljujić, Mila
PY  - 2006
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/254
AB  - Three common CFTR polymorphisms, 5T, M470V and R75Q, have been shown to be relatively frequent in Serbian patients with monosymptomatic CF disorders. Since there is a variation in distribution of common polymorphisms among different populations, it was important to compare their frequencies in patients with the frequencies in healthy population in order to assess the possible role of these polymorphisms in the monosymptomatic CF disorders. Samples obtained from 100 healthy Serbian individuals were analyzed for the presence of CFTR 5T, M470V and R75Q variants by PSM, RFLP and DGGE methods, respectively. Allele 5T was present in two individuals, giving the allelic frequency of 1% (2/200 alleles). The frequency obtained for allele M470 was 45% (90/200 alleles), while V470 allele was present with the frequency of 55% (110/200 alleles). Polymorphism R75Q was present in two individuals, with allelic frequency of 1% (2/200 alleles). Our study has shown that the frequencies of two common polymorphisms, 5T and M470V, differ significantly in Serbian population in comparison with other South European populations. Since it appears that Serbian population has a specific distribution of studied CFTR gene variants, it would also be interesting to analyze other common variants of this gene in our population. Such data can also be potentially useful as anthropogenetic markers in population studies.
T2  - Genetika
T1  - Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population
EP  - 998
IS  - 7
SP  - 996
VL  - 42
UR  - https://hdl.handle.net/21.15107/rcub_imagine_254
ER  - 

@article{
author = "Nikolić, Aleksandra and Divac Rankov, Aleksandra and Stanković, Marija and Dinić, J. and Tomić, Branko and Ljujić, Mila",
year = "2006",
abstract = "Three common CFTR polymorphisms, 5T, M470V and R75Q, have been shown to be relatively frequent in Serbian patients with monosymptomatic CF disorders. Since there is a variation in distribution of common polymorphisms among different populations, it was important to compare their frequencies in patients with the frequencies in healthy population in order to assess the possible role of these polymorphisms in the monosymptomatic CF disorders. Samples obtained from 100 healthy Serbian individuals were analyzed for the presence of CFTR 5T, M470V and R75Q variants by PSM, RFLP and DGGE methods, respectively. Allele 5T was present in two individuals, giving the allelic frequency of 1% (2/200 alleles). The frequency obtained for allele M470 was 45% (90/200 alleles), while V470 allele was present with the frequency of 55% (110/200 alleles). Polymorphism R75Q was present in two individuals, with allelic frequency of 1% (2/200 alleles). Our study has shown that the frequencies of two common polymorphisms, 5T and M470V, differ significantly in Serbian population in comparison with other South European populations. Since it appears that Serbian population has a specific distribution of studied CFTR gene variants, it would also be interesting to analyze other common variants of this gene in our population. Such data can also be potentially useful as anthropogenetic markers in population studies.",
journal = "Genetika",
title = "Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population",
pages = "998-996",
number = "7",
volume = "42",
url = "https://hdl.handle.net/21.15107/rcub_imagine_254"
}

Nikolić, A., Divac Rankov, A., Stanković, M., Dinić, J., Tomić, B.,& Ljujić, M.. (2006). Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population. in Genetika, 42(7), 996-998.
https://hdl.handle.net/21.15107/rcub_imagine_254

Nikolić A, Divac Rankov A, Stanković M, Dinić J, Tomić B, Ljujić M. Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population. in Genetika. 2006;42(7):996-998.
https://hdl.handle.net/21.15107/rcub_imagine_254 .

Nikolić, Aleksandra, Divac Rankov, Aleksandra, Stanković, Marija, Dinić, J., Tomić, Branko, Ljujić, Mila, "Analysis of common CFTR polymorphisms 5T, M470V and R75Q in healthy Serbian population" in Genetika, 42, no. 7 (2006):996-998,
https://hdl.handle.net/21.15107/rcub_imagine_254 .