TY  - JOUR
AU  - Jovanović, Mirna
AU  - Stanković, Tijana
AU  - Stojković Burić, Sonja
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Ljujić, Mila
AU  - Pešić, Milica
AU  - Dragoj, Miodrag
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5041
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  - Basel : MDPI
T2  - Life
T1  - Decreased TSPAN14 Expression Contributes to NSCLC Progression
IS  - 9
VL  - 12
DO  - 10.3390/life12091291
SP  - 1291
ER  - 

@article{
author = "Jovanović, Mirna and Stanković, Tijana and Stojković Burić, Sonja and Banković, Jasna and Dinić, Jelena and Ljujić, Mila and Pešić, 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 = "Basel : MDPI",
journal = "Life",
title = "Decreased TSPAN14 Expression Contributes to NSCLC Progression",
number = "9",
volume = "12",
doi = "10.3390/life12091291",
pages = "1291"
}

Jovanović, M., Stanković, T., Stojković Burić, S., Banković, J., Dinić, J., Ljujić, M., Pešić, M.,& Dragoj, M.. (2022). Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life
Basel : MDPI., 12(9), 1291.
https://doi.org/10.3390/life12091291

Jovanović M, Stanković T, Stojković Burić S, Banković J, Dinić J, Ljujić M, Pešić M, Dragoj M. Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life. 2022;12(9):1291.
doi:10.3390/life12091291 .

Jovanović, Mirna, Stanković, Tijana, Stojković Burić, Sonja, Banković, Jasna, Dinić, Jelena, Ljujić, Mila, Pešić, Milica, Dragoj, Miodrag, "Decreased TSPAN14 Expression Contributes to NSCLC Progression" in Life, 12, no. 9 (2022):1291,
https://doi.org/10.3390/life12091291 . .

TY  - JOUR
AU  - Stanković, Tijana
AU  - Ranđelović, Teodora
AU  - Dragoj, Miodrag
AU  - Stojković Burić, Sonja
AU  - Fernández, Luis
AU  - Ochoa, Ignacio
AU  - Pérez-García, Victor M.
AU  - Pešić, Milica
PY  - 2021
UR  - https://linkinghub.elsevier.com/retrieve/pii/S136876462100011X
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4242
AB  - The poor response of glioblastoma to current treatment protocols is a consequence of its intrinsic drug resistance. Resistance to chemotherapy is primarily associated with considerable cellular heterogeneity, and plasticity of glioblastoma cells, alterations in gene expression, presence of specific tumor microenvironment conditions and blood-brain barrier. In an attempt to successfully overcome chemoresistance and better understand the biological behavior of glioblastoma, numerous tri-dimensional (3D) biomimetic models were developed in the past decade. These novel advanced models are able to better recapitulate the spatial organization of glioblastoma in a real time, therefore providing more realistic and reliable evidence to the response of glioblastoma to therapy. Moreover, these models enable the fine-tuning of different tumor microenvironment conditions and facilitate studies on the effects of the tumor microenvironment on glioblastoma chemoresistance. This review outlines current knowledge on the essence of glioblastoma chemoresistance and describes the progress achieved by 3D biomimetic models. Moreover, comprehensive literature assessment regarding the influence of 3D culturing and microenvironment mimicking on glioblastoma gene expression and biological behavior is also provided. The contribution of the blood-brain barrier as well as the blood-tumor barrier to glioblastoma chemoresistance is also reviewed from the perspective of 3D biomimetic models. Finally, the role of mathematical models in predicting 3D glioblastoma behavior and drug response is elaborated. In the future, technological innovations along with mathematical simulations should create reliable 3D biomimetic systems for glioblastoma research that should facilitate the identification and possibly application in preclinical drug testing and precision medicine.
PB  - Churchill Livingstone
T2  - Drug Resistance Updates
T1  - In vitro biomimetic models for glioblastoma-a promising tool for drug response studies
VL  - 55
DO  - 10.1016/j.drup.2021.100753
SP  - 100753
ER  - 

@article{
author = "Stanković, Tijana and Ranđelović, Teodora and Dragoj, Miodrag and Stojković Burić, Sonja and Fernández, Luis and Ochoa, Ignacio and Pérez-García, Victor M. and Pešić, Milica",
year = "2021",
abstract = "The poor response of glioblastoma to current treatment protocols is a consequence of its intrinsic drug resistance. Resistance to chemotherapy is primarily associated with considerable cellular heterogeneity, and plasticity of glioblastoma cells, alterations in gene expression, presence of specific tumor microenvironment conditions and blood-brain barrier. In an attempt to successfully overcome chemoresistance and better understand the biological behavior of glioblastoma, numerous tri-dimensional (3D) biomimetic models were developed in the past decade. These novel advanced models are able to better recapitulate the spatial organization of glioblastoma in a real time, therefore providing more realistic and reliable evidence to the response of glioblastoma to therapy. Moreover, these models enable the fine-tuning of different tumor microenvironment conditions and facilitate studies on the effects of the tumor microenvironment on glioblastoma chemoresistance. This review outlines current knowledge on the essence of glioblastoma chemoresistance and describes the progress achieved by 3D biomimetic models. Moreover, comprehensive literature assessment regarding the influence of 3D culturing and microenvironment mimicking on glioblastoma gene expression and biological behavior is also provided. The contribution of the blood-brain barrier as well as the blood-tumor barrier to glioblastoma chemoresistance is also reviewed from the perspective of 3D biomimetic models. Finally, the role of mathematical models in predicting 3D glioblastoma behavior and drug response is elaborated. In the future, technological innovations along with mathematical simulations should create reliable 3D biomimetic systems for glioblastoma research that should facilitate the identification and possibly application in preclinical drug testing and precision medicine.",
publisher = "Churchill Livingstone",
journal = "Drug Resistance Updates",
title = "In vitro biomimetic models for glioblastoma-a promising tool for drug response studies",
volume = "55",
doi = "10.1016/j.drup.2021.100753",
pages = "100753"
}

Stanković, T., Ranđelović, T., Dragoj, M., Stojković Burić, S., Fernández, L., Ochoa, I., Pérez-García, V. M.,& Pešić, M.. (2021). In vitro biomimetic models for glioblastoma-a promising tool for drug response studies. in Drug Resistance Updates
Churchill Livingstone., 55, 100753.
https://doi.org/10.1016/j.drup.2021.100753

Stanković T, Ranđelović T, Dragoj M, Stojković Burić S, Fernández L, Ochoa I, Pérez-García VM, Pešić M. In vitro biomimetic models for glioblastoma-a promising tool for drug response studies. in Drug Resistance Updates. 2021;55:100753.
doi:10.1016/j.drup.2021.100753 .

Stanković, Tijana, Ranđelović, Teodora, Dragoj, Miodrag, Stojković Burić, Sonja, Fernández, Luis, Ochoa, Ignacio, Pérez-García, Victor M., Pešić, Milica, "In vitro biomimetic models for glioblastoma-a promising tool for drug response studies" in Drug Resistance Updates, 55 (2021):100753,
https://doi.org/10.1016/j.drup.2021.100753 . .

TY  - CONF
AU  - Stojković Burić, Sonja
AU  - Podolski-Renić, Ana
AU  - Dinić, Jelena
AU  - Stanković, Tijana
AU  - Jovanović, Mirna
AU  - Hadžić, Stefan
AU  - Ayuso, Jose
AU  - Virumbrales-Muñoz, María
AU  - Fernández, Luis
AU  - Ochoa, Ignacio
AU  - Pérez-García, Victor
AU  - Pešić, Milica
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6043
AB  - Development of chemoresistance and the invasion of cancer cells into surrounding brain tissue are major obstacles to successful glioma treatment. New therapeutic approaches are warranted to improve the survival of glioma patients. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) to increase sensitivity to temozolomide (TMZ) and suppress glioma cells invasion. Therefore, we have developed TMZ resistant RC6 rat glioma cell line with altered antioxidant capacity and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic effect additionally confirmed in a 3D model of microfluidic devices. Co-treatment with TMZ increased
expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential was studied by gelatin degradation and 3D spheroid invasion assays. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, CoQ10 supplementation could be used with standard glioma treatment due to its potential to inhibit cancer cells invasion through modulation of the antioxidant capacity.
PB  - COST Action CA17104
C3  - Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy
T1  - The role of antioxidant, coenzyme Q10, in suppressing invasion of temozolomide resistant rat glioma
SP  - 32
EP  - 32
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6043
ER  - 

@conference{
author = "Stojković Burić, Sonja and Podolski-Renić, Ana and Dinić, Jelena and Stanković, Tijana and Jovanović, Mirna and Hadžić, Stefan and Ayuso, Jose and Virumbrales-Muñoz, María and Fernández, Luis and Ochoa, Ignacio and Pérez-García, Victor and Pešić, Milica",
year = "2019",
abstract = "Development of chemoresistance and the invasion of cancer cells into surrounding brain tissue are major obstacles to successful glioma treatment. New therapeutic approaches are warranted to improve the survival of glioma patients. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) to increase sensitivity to temozolomide (TMZ) and suppress glioma cells invasion. Therefore, we have developed TMZ resistant RC6 rat glioma cell line with altered antioxidant capacity and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic effect additionally confirmed in a 3D model of microfluidic devices. Co-treatment with TMZ increased
expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential was studied by gelatin degradation and 3D spheroid invasion assays. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, CoQ10 supplementation could be used with standard glioma treatment due to its potential to inhibit cancer cells invasion through modulation of the antioxidant capacity.",
publisher = "COST Action CA17104",
journal = "Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy",
title = "The role of antioxidant, coenzyme Q10, in suppressing invasion of temozolomide resistant rat glioma",
pages = "32-32",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6043"
}

Stojković Burić, S., Podolski-Renić, A., Dinić, J., Stanković, T., Jovanović, M., Hadžić, S., Ayuso, J., Virumbrales-Muñoz, M., Fernández, L., Ochoa, I., Pérez-García, V.,& Pešić, M.. (2019). The role of antioxidant, coenzyme Q10, in suppressing invasion of temozolomide resistant rat glioma. in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy
COST Action CA17104., 32-32.
https://hdl.handle.net/21.15107/rcub_ibiss_6043

Stojković Burić S, Podolski-Renić A, Dinić J, Stanković T, Jovanović M, Hadžić S, Ayuso J, Virumbrales-Muñoz M, Fernández L, Ochoa I, Pérez-García V, Pešić M. The role of antioxidant, coenzyme Q10, in suppressing invasion of temozolomide resistant rat glioma. in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy. 2019;:32-32.
https://hdl.handle.net/21.15107/rcub_ibiss_6043 .

Stojković Burić, Sonja, Podolski-Renić, Ana, Dinić, Jelena, Stanković, Tijana, Jovanović, Mirna, Hadžić, Stefan, Ayuso, Jose, Virumbrales-Muñoz, María, Fernández, Luis, Ochoa, Ignacio, Pérez-García, Victor, Pešić, Milica, "The role of antioxidant, coenzyme Q10, in suppressing invasion of temozolomide resistant rat glioma" in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy (2019):32-32,
https://hdl.handle.net/21.15107/rcub_ibiss_6043 .

TY  - JOUR
AU  - Stojković Burić, Sonja
AU  - Podolski-Renić, Ana
AU  - Dinić, Jelena
AU  - Stanković, Tijana
AU  - Jovanović, Mirna
AU  - Hadžić, Stefan
AU  - Ayuso, Jose M.
AU  - Virumbrales-Muñoz, María
AU  - Fernández, Luis J.
AU  - Ochoa, Ignacio
AU  - Pérez-García, Victor M.
AU  - Pešić, Milica
PY  - 2019
UR  - https://www.hindawi.com/journals/omcl/2019/3061607/
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6432727
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3323
AB  - The main reasons for the inefficiency of standard glioblastoma (GBM) therapy are the occurrence of chemoresistance and the invasion of GBM cells into surrounding brain tissues. New therapeutic approaches obstructing these processes may provide substantial survival improvements. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) as a scavenger of reactive oxygen species (ROS) to increase sensitivity to temozolomide (TMZ) and suppress glioma cell invasion. To that end, we used a previously established TMZ-resistant RC6 rat glioma cell line, characterized by increased production of ROS, altered antioxidative capacity, and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic antiproliferative effect. These results were confirmed in a 3D model of microfluidic devices showing that the CoQ10 and TMZ combination is more cytotoxic to RC6 cells than TMZ monotherapy. In addition, cotreatment with TMZ increased expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential of the combined treatment was shown by gelatin degradation, Matrigel invasion, and 3D spheroid invasion assays as well as in animal models. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, our data provide evidences in favor of CoQ10 supplementation to standard GBM treatment due to its potential to inhibit GBM invasion through modulation of the antioxidant capacity.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo.
VL  - 2019
DO  - 10.1155/2019/3061607
SP  - 3061607
ER  - 

@article{
author = "Stojković Burić, Sonja and Podolski-Renić, Ana and Dinić, Jelena and Stanković, Tijana and Jovanović, Mirna and Hadžić, Stefan and Ayuso, Jose M. and Virumbrales-Muñoz, María and Fernández, Luis J. and Ochoa, Ignacio and Pérez-García, Victor M. and Pešić, Milica",
year = "2019",
abstract = "The main reasons for the inefficiency of standard glioblastoma (GBM) therapy are the occurrence of chemoresistance and the invasion of GBM cells into surrounding brain tissues. New therapeutic approaches obstructing these processes may provide substantial survival improvements. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) as a scavenger of reactive oxygen species (ROS) to increase sensitivity to temozolomide (TMZ) and suppress glioma cell invasion. To that end, we used a previously established TMZ-resistant RC6 rat glioma cell line, characterized by increased production of ROS, altered antioxidative capacity, and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic antiproliferative effect. These results were confirmed in a 3D model of microfluidic devices showing that the CoQ10 and TMZ combination is more cytotoxic to RC6 cells than TMZ monotherapy. In addition, cotreatment with TMZ increased expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential of the combined treatment was shown by gelatin degradation, Matrigel invasion, and 3D spheroid invasion assays as well as in animal models. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, our data provide evidences in favor of CoQ10 supplementation to standard GBM treatment due to its potential to inhibit GBM invasion through modulation of the antioxidant capacity.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo.",
volume = "2019",
doi = "10.1155/2019/3061607",
pages = "3061607"
}

Stojković Burić, S., Podolski-Renić, A., Dinić, J., Stanković, T., Jovanović, M., Hadžić, S., Ayuso, J. M., Virumbrales-Muñoz, M., Fernández, L. J., Ochoa, I., Pérez-García, V. M.,& Pešić, M.. (2019). Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo.. in Oxidative Medicine and Cellular Longevity, 2019, 3061607.
https://doi.org/10.1155/2019/3061607

Stojković Burić S, Podolski-Renić A, Dinić J, Stanković T, Jovanović M, Hadžić S, Ayuso JM, Virumbrales-Muñoz M, Fernández LJ, Ochoa I, Pérez-García VM, Pešić M. Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo.. in Oxidative Medicine and Cellular Longevity. 2019;2019:3061607.
doi:10.1155/2019/3061607 .

Stojković Burić, Sonja, Podolski-Renić, Ana, Dinić, Jelena, Stanković, Tijana, Jovanović, Mirna, Hadžić, Stefan, Ayuso, Jose M., Virumbrales-Muñoz, María, Fernández, Luis J., Ochoa, Ignacio, Pérez-García, Victor M., Pešić, Milica, "Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo." in Oxidative Medicine and Cellular Longevity, 2019 (2019):3061607,
https://doi.org/10.1155/2019/3061607 . .

TY  - JOUR
AU  - Fási, Laura
AU  - Di Meo, Florent
AU  - Kuo, Ching-Ying
AU  - Stojković Burić, Sonja
AU  - Martins, Ana
AU  - Kúsz, Norbert
AU  - Béni, Zoltán
AU  - Dékány, Miklós
AU  - Balogh, György Tibor
AU  - Pešić, Milica
AU  - Wang, Hui-Chun
AU  - Trouillas, Patrick
AU  - Hunyadi, Attila
PY  - 2019
UR  - http://pubs.acs.org/doi/10.1021/acs.jmedchem.8b01994
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3278
AB  - Cancer cells generally possess higher levels of reactive oxygen species than normal cells, and this can serve as a possible therapeutic target. In this proof-of-concept study, an antioxidant-inspired drug discovery strategy was evaluated using a hydroxycinnamic acid derivative. The processing of oxidized mixtures of p-coumaric acid methyl ester (pcm) revealed a new antitumor lead, graviquinone. Graviquinone bypassed ABCB1-mediated resistance, induced DNA damage in lung carcinoma cells but exerted DNA protective activity in normal keratinocytes, and modulated DNA damage response in MCF-7 cells. The cytotoxic effect of pcm in MCF-7 cells was potentiated under H2O2-induced oxidative stress, and the formation of graviquinone was confirmed by Fenton's reaction on pcm. In silico DFT calculations suggested graviquinone as a kinetic product of pcm scavenging •OH radicals. Our results demonstrate the pharmacological value of an in situ-formed, oxidative stress-related metabolite of an antioxidant. This might be of particular importance for designing new strategies for antioxidant-based drug discovery.
T2  - Journal of Medicinal Chemistry
T1  - Antioxidant-inspired drug discovery: antitumor metabolite is formed in situ from a hydroxycinnamic acid derivative upon free radical scavenging.
IS  - 3
VL  - 62
DO  - 10.1021/acs.jmedchem.8b01994
SP  - 1657
EP  - 1668
ER  - 

@article{
author = "Fási, Laura and Di Meo, Florent and Kuo, Ching-Ying and Stojković Burić, Sonja and Martins, Ana and Kúsz, Norbert and Béni, Zoltán and Dékány, Miklós and Balogh, György Tibor and Pešić, Milica and Wang, Hui-Chun and Trouillas, Patrick and Hunyadi, Attila",
year = "2019",
abstract = "Cancer cells generally possess higher levels of reactive oxygen species than normal cells, and this can serve as a possible therapeutic target. In this proof-of-concept study, an antioxidant-inspired drug discovery strategy was evaluated using a hydroxycinnamic acid derivative. The processing of oxidized mixtures of p-coumaric acid methyl ester (pcm) revealed a new antitumor lead, graviquinone. Graviquinone bypassed ABCB1-mediated resistance, induced DNA damage in lung carcinoma cells but exerted DNA protective activity in normal keratinocytes, and modulated DNA damage response in MCF-7 cells. The cytotoxic effect of pcm in MCF-7 cells was potentiated under H2O2-induced oxidative stress, and the formation of graviquinone was confirmed by Fenton's reaction on pcm. In silico DFT calculations suggested graviquinone as a kinetic product of pcm scavenging •OH radicals. Our results demonstrate the pharmacological value of an in situ-formed, oxidative stress-related metabolite of an antioxidant. This might be of particular importance for designing new strategies for antioxidant-based drug discovery.",
journal = "Journal of Medicinal Chemistry",
title = "Antioxidant-inspired drug discovery: antitumor metabolite is formed in situ from a hydroxycinnamic acid derivative upon free radical scavenging.",
number = "3",
volume = "62",
doi = "10.1021/acs.jmedchem.8b01994",
pages = "1657-1668"
}

Fási, L., Di Meo, F., Kuo, C., Stojković Burić, S., Martins, A., Kúsz, N., Béni, Z., Dékány, M., Balogh, G. T., Pešić, M., Wang, H., Trouillas, P.,& Hunyadi, A.. (2019). Antioxidant-inspired drug discovery: antitumor metabolite is formed in situ from a hydroxycinnamic acid derivative upon free radical scavenging.. in Journal of Medicinal Chemistry, 62(3), 1657-1668.
https://doi.org/10.1021/acs.jmedchem.8b01994

Fási L, Di Meo F, Kuo C, Stojković Burić S, Martins A, Kúsz N, Béni Z, Dékány M, Balogh GT, Pešić M, Wang H, Trouillas P, Hunyadi A. Antioxidant-inspired drug discovery: antitumor metabolite is formed in situ from a hydroxycinnamic acid derivative upon free radical scavenging.. in Journal of Medicinal Chemistry. 2019;62(3):1657-1668.
doi:10.1021/acs.jmedchem.8b01994 .

Fási, Laura, Di Meo, Florent, Kuo, Ching-Ying, Stojković Burić, Sonja, Martins, Ana, Kúsz, Norbert, Béni, Zoltán, Dékány, Miklós, Balogh, György Tibor, Pešić, Milica, Wang, Hui-Chun, Trouillas, Patrick, Hunyadi, Attila, "Antioxidant-inspired drug discovery: antitumor metabolite is formed in situ from a hydroxycinnamic acid derivative upon free radical scavenging." in Journal of Medicinal Chemistry, 62, no. 3 (2019):1657-1668,
https://doi.org/10.1021/acs.jmedchem.8b01994 . .

TY  - JOUR
AU  - Dragoj, Miodrag
AU  - Banković, Jasna
AU  - Podolski-Renić, Ana
AU  - Stojković Burić, Sonja
AU  - Pešić, Milica
AU  - Tanić, Nikola
AU  - Stanković, Tijana
PY  - 2019
UR  - https://content.sciendo.com/view/journals/jomb/ahead-of-print/article-10.2478-jomb-2018-0022.xml
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3099
AB  - Background: C-Myc is one of the major cellular oncogenes overexpressed in non-small cell lung carcinoma (NSCLC). Its deregulated expression is necessary but not sufficient for malignant transformation. We evaluated expression of MYC gene in NSCLC patients and its association with alterations in the genes previously identified to be related to NSCLC pathogenesis, PHACTR3 and E2F4. Methods: We analyzed MYC gene expression by qRT-PCR in 30 NSCLC patients' samples and paired normal lung tissue. MYC expression was further statistically evaluated in relation to histopathological parameters, PHACTR3 and E2F4 gene alterations and survival. Alterations in aforementioned genes were previously detected and identified based on AP-PCR profiles of paired normal and tumor DNA samples, selection of DNA bands with altered mobility in tumor samples and their characterization by the reamplification, cloning and sequencing. Results: MYC expression was significantly increased in NSCLC samples and its overexpression significantly associated with squamous cell carcinoma subtype. Most importantly, MYC overexpression significantly coincided with mutations in PHACTR3 and E2F4 genes, in group of all patients and in squamous cell carcinoma subtype. Moreover, patients with jointly overexpressed MYC and altered PHACTR3 or E2F4 showed trend of shorter survival. Conclusions: Overall, MYC is frequently overexpressed in NSCLC and it is associated with mutated PHACTR3 gene, as well as mutated E2F4 gene. These joint gene alterations could be considered as potential molecular markers of NSCLC and its specific subtypes.
T2  - Journal of Medical Biochemistry
T1  - Association of Overexpressed MYC Gene with Altered PHACTR3 and E2F4 Genes Contributes to Non-Small Cell Lung Carcinoma Pathogenesis
VL  - 37
DO  - 10.2478/jomb-2018-0022
SP  - 188
EP  - 195
ER  - 

@article{
author = "Dragoj, Miodrag and Banković, Jasna and Podolski-Renić, Ana and Stojković Burić, Sonja and Pešić, Milica and Tanić, Nikola and Stanković, Tijana",
year = "2019",
abstract = "Background: C-Myc is one of the major cellular oncogenes overexpressed in non-small cell lung carcinoma (NSCLC). Its deregulated expression is necessary but not sufficient for malignant transformation. We evaluated expression of MYC gene in NSCLC patients and its association with alterations in the genes previously identified to be related to NSCLC pathogenesis, PHACTR3 and E2F4. Methods: We analyzed MYC gene expression by qRT-PCR in 30 NSCLC patients' samples and paired normal lung tissue. MYC expression was further statistically evaluated in relation to histopathological parameters, PHACTR3 and E2F4 gene alterations and survival. Alterations in aforementioned genes were previously detected and identified based on AP-PCR profiles of paired normal and tumor DNA samples, selection of DNA bands with altered mobility in tumor samples and their characterization by the reamplification, cloning and sequencing. Results: MYC expression was significantly increased in NSCLC samples and its overexpression significantly associated with squamous cell carcinoma subtype. Most importantly, MYC overexpression significantly coincided with mutations in PHACTR3 and E2F4 genes, in group of all patients and in squamous cell carcinoma subtype. Moreover, patients with jointly overexpressed MYC and altered PHACTR3 or E2F4 showed trend of shorter survival. Conclusions: Overall, MYC is frequently overexpressed in NSCLC and it is associated with mutated PHACTR3 gene, as well as mutated E2F4 gene. These joint gene alterations could be considered as potential molecular markers of NSCLC and its specific subtypes.",
journal = "Journal of Medical Biochemistry",
title = "Association of Overexpressed MYC Gene with Altered PHACTR3 and E2F4 Genes Contributes to Non-Small Cell Lung Carcinoma Pathogenesis",
volume = "37",
doi = "10.2478/jomb-2018-0022",
pages = "188-195"
}

Dragoj, M., Banković, J., Podolski-Renić, A., Stojković Burić, S., Pešić, M., Tanić, N.,& Stanković, T.. (2019). Association of Overexpressed MYC Gene with Altered PHACTR3 and E2F4 Genes Contributes to Non-Small Cell Lung Carcinoma Pathogenesis. in Journal of Medical Biochemistry, 37, 188-195.
https://doi.org/10.2478/jomb-2018-0022

Dragoj M, Banković J, Podolski-Renić A, Stojković Burić S, Pešić M, Tanić N, Stanković T. Association of Overexpressed MYC Gene with Altered PHACTR3 and E2F4 Genes Contributes to Non-Small Cell Lung Carcinoma Pathogenesis. in Journal of Medical Biochemistry. 2019;37:188-195.
doi:10.2478/jomb-2018-0022 .

Dragoj, Miodrag, Banković, Jasna, Podolski-Renić, Ana, Stojković Burić, Sonja, Pešić, Milica, Tanić, Nikola, Stanković, Tijana, "Association of Overexpressed MYC Gene with Altered PHACTR3 and E2F4 Genes Contributes to Non-Small Cell Lung Carcinoma Pathogenesis" in Journal of Medical Biochemistry, 37 (2019):188-195,
https://doi.org/10.2478/jomb-2018-0022 . .

TY  - JOUR
AU  - Stanković, Tijana
AU  - Dinić, Jelena
AU  - Podolski-Renić, Ana
AU  - Musso, Loana
AU  - Stojković Burić, Sonja
AU  - Dallavalle, Sabrina
AU  - Pešić, Milica
PY  - 2019
UR  - http://www.eurekaselect.com/162878/article
UR  - https://radar.ibiss.bg.ac.rs/123456789/3875
AB  - Background: Dual-targeting in cancer treatment by a single drug is an unconventional approach in relation to drug combinations. The rationale for the development of dualtargeting agents is to overcome incomplete efficacy and drug resistance frequently present when applying individual targeting agents. Consequently, -a more favorable outcome of cancer treatment is expected with dual-targeting strategies. Methods: We reviewed the literature, concentrating on the association between clinically relevant and/or novel dual inhibitors with the potential to modulate multidrug resistant phenotype of cancer cells, particularly the activity of P-glycoprotein. A balanced analysis of content was performed to emphasize the most important findings and optimize the structure of this review. Results: Two-hundred and forty-five papers were included in the review. The introductory part was interpreted by 9 papers. Tyrosine kinase inhibitors’ role in the inhibition of Pglycoprotein and chemosensitization was illustrated by 87 papers. The contribution of naturalbased compounds in overcoming multidrug resistance was reviewed using 92 papers, while specific dual inhibitors acting against microtubule assembling and/or topoisomerases were described with 55 papers. Eleven papers gave an insight into a novel and less explored approach with hybrid drugs. Their influence on P-glycoprotein and multidrug resistance was also evaluated. Conclusion: These findings bring into focus rational anticancer strategies with dual-targeting agents. Most evaluated synthetic and natural drugs showed a great potential in chemosensitization. Further steps in this direction are needed for the optimization of anticancer treatment.
PB  - Sharjah: Bentham Science Publishers
T2  - Current Medicinal Chemistry
T1  - Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment
IS  - 33
VL  - 26
DO  - 10.2174/0929867325666180607094856
SP  - 6074
EP  - 6106
ER  - 

@article{
author = "Stanković, Tijana and Dinić, Jelena and Podolski-Renić, Ana and Musso, Loana and Stojković Burić, Sonja and Dallavalle, Sabrina and Pešić, Milica",
year = "2019",
abstract = "Background: Dual-targeting in cancer treatment by a single drug is an unconventional approach in relation to drug combinations. The rationale for the development of dualtargeting agents is to overcome incomplete efficacy and drug resistance frequently present when applying individual targeting agents. Consequently, -a more favorable outcome of cancer treatment is expected with dual-targeting strategies. Methods: We reviewed the literature, concentrating on the association between clinically relevant and/or novel dual inhibitors with the potential to modulate multidrug resistant phenotype of cancer cells, particularly the activity of P-glycoprotein. A balanced analysis of content was performed to emphasize the most important findings and optimize the structure of this review. Results: Two-hundred and forty-five papers were included in the review. The introductory part was interpreted by 9 papers. Tyrosine kinase inhibitors’ role in the inhibition of Pglycoprotein and chemosensitization was illustrated by 87 papers. The contribution of naturalbased compounds in overcoming multidrug resistance was reviewed using 92 papers, while specific dual inhibitors acting against microtubule assembling and/or topoisomerases were described with 55 papers. Eleven papers gave an insight into a novel and less explored approach with hybrid drugs. Their influence on P-glycoprotein and multidrug resistance was also evaluated. Conclusion: These findings bring into focus rational anticancer strategies with dual-targeting agents. Most evaluated synthetic and natural drugs showed a great potential in chemosensitization. Further steps in this direction are needed for the optimization of anticancer treatment.",
publisher = "Sharjah: Bentham Science Publishers",
journal = "Current Medicinal Chemistry",
title = "Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment",
number = "33",
volume = "26",
doi = "10.2174/0929867325666180607094856",
pages = "6074-6106"
}

Stanković, T., Dinić, J., Podolski-Renić, A., Musso, L., Stojković Burić, S., Dallavalle, S.,& Pešić, M.. (2019). Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment. in Current Medicinal Chemistry
Sharjah: Bentham Science Publishers., 26(33), 6074-6106.
https://doi.org/10.2174/0929867325666180607094856

Stanković T, Dinić J, Podolski-Renić A, Musso L, Stojković Burić S, Dallavalle S, Pešić M. Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment. in Current Medicinal Chemistry. 2019;26(33):6074-6106.
doi:10.2174/0929867325666180607094856 .

Stanković, Tijana, Dinić, Jelena, Podolski-Renić, Ana, Musso, Loana, Stojković Burić, Sonja, Dallavalle, Sabrina, Pešić, Milica, "Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment" in Current Medicinal Chemistry, 26, no. 33 (2019):6074-6106,
https://doi.org/10.2174/0929867325666180607094856 . .

TY  - JOUR
AU  - Stanković, Tijana
AU  - Dinić, Jelena
AU  - Podolski-Renić, Ana
AU  - Musso, Loana
AU  - Stojković Burić, Sonja
AU  - Dallavalle, Sabrina
AU  - Pešić, Milica
PY  - 2019
UR  - http://www.eurekaselect.com/162878/article
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3567
AB  - BACKGROUND Dual-targeting in cancer treatment by a single drug is an unconventional approach in relation to drug combinations. The rationale for the development of dualtargeting agents is to overcome incomplete efficacy and drug resistance frequently present when applying individual targeting agents. Consequently, -a more favorable outcome of cancer treatment is expected with dual-targeting strategies. METHODS We reviewed the literature, concentrating on the association between clinically relevant and/or novel dual inhibitors with the potential to modulate multidrug resistant phenotype of cancer cells, particularly the activity of P-glycoprotein. A balanced analysis of content was performed to emphasize the most important findings and optimize the structure of this review. RESULTS Two-hundred and forty-five papers were included in the review. The introductory part was interpreted by 9 papers. Tyrosine kinase inhibitors' role in the inhibition of Pglycoprotein and chemosensitization was illustrated by 87 papers. The contribution of naturalbased compounds in overcoming multidrug resistance was reviewed using 92 papers, while specific dual inhibitors acting against microtubule assembling and/or topoisomerases were described with 55 papers. Eleven papers gave an insight into a novel and less explored approach with hybrid drugs. Their influence on P-glycoprotein and multidrug resistance was also evaluated. CONCLUSION These findings bring into focus rational anticancer strategies with dual-targeting agents. Most evaluated synthetic and natural drugs showed a great potential in chemosensitization. Further steps in this direction are needed for the optimization of anticancer treatment.
T2  - Current Medicinal Chemistry
T1  - Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment.
IS  - 33
VL  - 26
DO  - 10.2174/0929867325666180607094856
SP  - 6074
EP  - 6106
ER  - 

@article{
author = "Stanković, Tijana and Dinić, Jelena and Podolski-Renić, Ana and Musso, Loana and Stojković Burić, Sonja and Dallavalle, Sabrina and Pešić, Milica",
year = "2019",
abstract = "BACKGROUND Dual-targeting in cancer treatment by a single drug is an unconventional approach in relation to drug combinations. The rationale for the development of dualtargeting agents is to overcome incomplete efficacy and drug resistance frequently present when applying individual targeting agents. Consequently, -a more favorable outcome of cancer treatment is expected with dual-targeting strategies. METHODS We reviewed the literature, concentrating on the association between clinically relevant and/or novel dual inhibitors with the potential to modulate multidrug resistant phenotype of cancer cells, particularly the activity of P-glycoprotein. A balanced analysis of content was performed to emphasize the most important findings and optimize the structure of this review. RESULTS Two-hundred and forty-five papers were included in the review. The introductory part was interpreted by 9 papers. Tyrosine kinase inhibitors' role in the inhibition of Pglycoprotein and chemosensitization was illustrated by 87 papers. The contribution of naturalbased compounds in overcoming multidrug resistance was reviewed using 92 papers, while specific dual inhibitors acting against microtubule assembling and/or topoisomerases were described with 55 papers. Eleven papers gave an insight into a novel and less explored approach with hybrid drugs. Their influence on P-glycoprotein and multidrug resistance was also evaluated. CONCLUSION These findings bring into focus rational anticancer strategies with dual-targeting agents. Most evaluated synthetic and natural drugs showed a great potential in chemosensitization. Further steps in this direction are needed for the optimization of anticancer treatment.",
journal = "Current Medicinal Chemistry",
title = "Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment.",
number = "33",
volume = "26",
doi = "10.2174/0929867325666180607094856",
pages = "6074-6106"
}

Stanković, T., Dinić, J., Podolski-Renić, A., Musso, L., Stojković Burić, S., Dallavalle, S.,& Pešić, M.. (2019). Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment.. in Current Medicinal Chemistry, 26(33), 6074-6106.
https://doi.org/10.2174/0929867325666180607094856

Stanković T, Dinić J, Podolski-Renić A, Musso L, Stojković Burić S, Dallavalle S, Pešić M. Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment.. in Current Medicinal Chemistry. 2019;26(33):6074-6106.
doi:10.2174/0929867325666180607094856 .

Stanković, Tijana, Dinić, Jelena, Podolski-Renić, Ana, Musso, Loana, Stojković Burić, Sonja, Dallavalle, Sabrina, Pešić, Milica, "Dual Inhibitors as a New Challenge for Cancer Multidrug Resistance Treatment." in Current Medicinal Chemistry, 26, no. 33 (2019):6074-6106,
https://doi.org/10.2174/0929867325666180607094856 . .

TY  - CONF
AU  - Nešović, Marija
AU  - Garcia, Catarina
AU  - Stanković, Tijana
AU  - Dinić, Jelena
AU  - Podolski-Renić, Ana
AU  - Stojković Burić, Sonja
AU  - Dragoj, Miodrag
AU  - Jovanović, Mirna
AU  - Rijo, Patricia
AU  - Pešić, Milica
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6433
AB  - Natural compound-based green chemistry has been the focus of current nanobiotechnology
research to improve efficacy and safety of medicines through targeted drug delivery. The Lamiaceae family, widely used in traditional medicine, is a well-known source of natural compounds with
anticancer properties. A wide spectrum of bioactive diterpenes have been isolated from the genus Plectranthus, including 6,7-dehydroroyleanone (DHR), a abietane found in the essential oil of P.
madagascariensis. The biological activity of DHR was investigated in P-glycoprotein-overexpressing multidrug resistant (MDR) non-small cell lung cancer cell line (NCI-H460/R), its sensitive counterpart (NCI-H460) and normal human embryonic bronchial epithelial cells (MRC-5). DHR showed
significant growth inhibition and slight selectivity against cancer cell lines when compared to
normal cells. The results also confirmed that DHR is not a substrate for P-glycoprotein as it does
not interfere with its activity. This diterpene was incorporated into Hybrid nanoparticles in order
to increase treatment efficacy and delivery selectivity. Anticancer properties of this nanosystem
were compared to the activity of DHR alone. Additionally, to address the problem of multidrug
resistance, this nanosystem was tested against cancer cells with MDR phenotype. Coupling of
DHR with Hybrid nanoparticles additionally improved the cytotoxicity of DHR, decreasing the IC50
value 8-fold in NCI-H460 cells and 5-fold in NCI-H460/R cells. These findings imply that combining
natural products, such as DHR, with nanoparticles could be considered as a promising anticancer
strategy with potential to overcome drug resistance.
PB  - Belgrade: Serbian Plant Physiology Society; Institute for Biological Research "Siniša Stanković"; Faculty of Biology
C3  - Book of abstracts. 3rd International Conference on Plant Biology (22nd SPPS Meeting); 2018 Jun 9-12; Belgrade, Serbia
T1  - Anticancer properties of the abietane diterpene 6,7-dehydroroyleanone from Plectranthus madagascariensis
SP  - 150
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6433
ER  - 

@conference{
author = "Nešović, Marija and Garcia, Catarina and Stanković, Tijana and Dinić, Jelena and Podolski-Renić, Ana and Stojković Burić, Sonja and Dragoj, Miodrag and Jovanović, Mirna and Rijo, Patricia and Pešić, Milica",
year = "2018",
abstract = "Natural compound-based green chemistry has been the focus of current nanobiotechnology
research to improve efficacy and safety of medicines through targeted drug delivery. The Lamiaceae family, widely used in traditional medicine, is a well-known source of natural compounds with
anticancer properties. A wide spectrum of bioactive diterpenes have been isolated from the genus Plectranthus, including 6,7-dehydroroyleanone (DHR), a abietane found in the essential oil of P.
madagascariensis. The biological activity of DHR was investigated in P-glycoprotein-overexpressing multidrug resistant (MDR) non-small cell lung cancer cell line (NCI-H460/R), its sensitive counterpart (NCI-H460) and normal human embryonic bronchial epithelial cells (MRC-5). DHR showed
significant growth inhibition and slight selectivity against cancer cell lines when compared to
normal cells. The results also confirmed that DHR is not a substrate for P-glycoprotein as it does
not interfere with its activity. This diterpene was incorporated into Hybrid nanoparticles in order
to increase treatment efficacy and delivery selectivity. Anticancer properties of this nanosystem
were compared to the activity of DHR alone. Additionally, to address the problem of multidrug
resistance, this nanosystem was tested against cancer cells with MDR phenotype. Coupling of
DHR with Hybrid nanoparticles additionally improved the cytotoxicity of DHR, decreasing the IC50
value 8-fold in NCI-H460 cells and 5-fold in NCI-H460/R cells. These findings imply that combining
natural products, such as DHR, with nanoparticles could be considered as a promising anticancer
strategy with potential to overcome drug resistance.",
publisher = "Belgrade: Serbian Plant Physiology Society; Institute for Biological Research "Siniša Stanković"; Faculty of Biology",
journal = "Book of abstracts. 3rd International Conference on Plant Biology (22nd SPPS Meeting); 2018 Jun 9-12; Belgrade, Serbia",
title = "Anticancer properties of the abietane diterpene 6,7-dehydroroyleanone from Plectranthus madagascariensis",
pages = "150",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6433"
}

Nešović, M., Garcia, C., Stanković, T., Dinić, J., Podolski-Renić, A., Stojković Burić, S., Dragoj, M., Jovanović, M., Rijo, P.,& Pešić, M.. (2018). Anticancer properties of the abietane diterpene 6,7-dehydroroyleanone from Plectranthus madagascariensis. in Book of abstracts. 3rd International Conference on Plant Biology (22nd SPPS Meeting); 2018 Jun 9-12; Belgrade, Serbia
Belgrade: Serbian Plant Physiology Society; Institute for Biological Research "Siniša Stanković"; Faculty of Biology., 150.
https://hdl.handle.net/21.15107/rcub_ibiss_6433

Nešović M, Garcia C, Stanković T, Dinić J, Podolski-Renić A, Stojković Burić S, Dragoj M, Jovanović M, Rijo P, Pešić M. Anticancer properties of the abietane diterpene 6,7-dehydroroyleanone from Plectranthus madagascariensis. in Book of abstracts. 3rd International Conference on Plant Biology (22nd SPPS Meeting); 2018 Jun 9-12; Belgrade, Serbia. 2018;:150.
https://hdl.handle.net/21.15107/rcub_ibiss_6433 .

Nešović, Marija, Garcia, Catarina, Stanković, Tijana, Dinić, Jelena, Podolski-Renić, Ana, Stojković Burić, Sonja, Dragoj, Miodrag, Jovanović, Mirna, Rijo, Patricia, Pešić, Milica, "Anticancer properties of the abietane diterpene 6,7-dehydroroyleanone from Plectranthus madagascariensis" in Book of abstracts. 3rd International Conference on Plant Biology (22nd SPPS Meeting); 2018 Jun 9-12; Belgrade, Serbia (2018):150,
https://hdl.handle.net/21.15107/rcub_ibiss_6433 .

TY  - JOUR
AU  - Babić, Tamara
AU  - Dinić, Jelena
AU  - Stojković Burić, Sonja
AU  - Hadzic, Stefan
AU  - Pešić, Milica
AU  - Radojković, Dragica
AU  - Divac Rankov, Aleksandra
PY  - 2018
UR  - https://akjournals.com/view/journals/018/69/4/article-p395.xml
UR  - https://radar.ibiss.bg.ac.rs/123456789/3881
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  - Budapest : Akadémiai Kiadó
T2  - Acta Biologica Hungarica
T1  - Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models
IS  - 4
VL  - 69
DO  - 10.1556/018.69.2018.4.3
SP  - 395
EP  - 410
ER  - 

@article{
author = "Babić, Tamara and Dinić, Jelena and Stojković Burić, Sonja and Hadzic, Stefan and Pešić, 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 = "Budapest : Akadémiai Kiadó",
journal = "Acta Biologica Hungarica",
title = "Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models",
number = "4",
volume = "69",
doi = "10.1556/018.69.2018.4.3",
pages = "395-410"
}

Babić, T., Dinić, J., Stojković Burić, S., Hadzic, S., Pešić, 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
Budapest : Akadémiai Kiadó., 69(4), 395-410.
https://doi.org/10.1556/018.69.2018.4.3

Babić T, Dinić J, Stojković Burić S, Hadzic S, Pešić 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, Hadzic, Stefan, Pešić, 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  - Babić, Tamara
AU  - Dinić, Jelena
AU  - Stojković Burić, Sonja
AU  - Hadžić, Stefan
AU  - Pešić, Milica
AU  - Radojković, Dragica
AU  - Divac Rankov, Aleksandra
PY  - 2018
UR  - https://www.akademiai.com/doi/10.1556/018.69.2018.4.3
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3231
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.
T2  - Acta Biologica Hungarica
T1  - Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models.
IS  - 4
VL  - 69
DO  - 10.1556/018.69.2018.4.3
SP  - 395
EP  - 410
ER  - 

@article{
author = "Babić, Tamara and Dinić, Jelena and Stojković Burić, Sonja and Hadžić, Stefan and Pešić, 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.",
journal = "Acta Biologica Hungarica",
title = "Comparative toxicity evaluation of targeted anticancer therapeutics in embryonic zebrafish and sea urchin models.",
number = "4",
volume = "69",
doi = "10.1556/018.69.2018.4.3",
pages = "395-410"
}

Babić, T., Dinić, J., Stojković Burić, S., Hadžić, S., Pešić, 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, 69(4), 395-410.
https://doi.org/10.1556/018.69.2018.4.3

Babić T, Dinić J, Stojković Burić S, Hadžić S, Pešić 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, Hadžić, Stefan, Pešić, 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  - THES
AU  - Stojković Burić, Sonja
PY  - 2017
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=4997
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025151666
UR  - http://nardus.mpn.gov.rs/123456789/8252
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2798
AB  - Uspešnost terapije glioblastoma, najĉešćeg i najagresivnijeg malignog tumora centralnog nervnog sistema, je osujećena usled visokog stepena invazivnosti, kao i pojave rezistencije na hemioterapiju. Cilj ove doktorske disertacije je bio da se uspostavi i okarakteriše rezistentni gliomski model koji bi imao primenu u ispitivanju novih terapeutskih strategija u leĉenju ove teške bolesti. Kao poĉetni materijal korišćena je pacovska C6 ćelijska linija glioma, fenotipski sliĉna humanim glioblastomima. Za uspostavljanje rezistencije korišćen je prvi odobreni antigliomski lek 1,3-bis(2-hloroetil)-1-nitrozoureom (BCNU, karmustin), alkilirajući agens koji se koristi u terapiji primarnih i rekurentnih glioblastoma. Kontinuirana primena BCNU je dovela do razvoja rezistencije C6 ćelija ne samo na ovaj hemioterapeutik, već i na druge DNK oštećujuće agense, cisplatin (CPt) i temozolomid (TMZ). Novouspostavljena rezistentna ćelijska linija je oznaĉena kao RC6. Ispitivanje mehanizama rezistencije je obuhvatilo analizu promena na nivou apoptotske mašinerije i oštećenja DNK lanaca, kao i analizu promena u antioksidativnom kapacitetu izmeĊu C6 i RC6 ćelija. Rezistentna RC6 linija pokazuje smanjenu osetljivost na indukciju ćelijske smrti koja je praćena smanjenjem ekspresije antiapoptotskog faktora Bcl-2, proapoptotskog faktora Bad i efektorske kaspaze 3 na nivou iRNK i proteina. TakoĊe je pokazano smanjenje ekspresije iRNK antiapoptoskog Bcl-Xl i proapoptotskog Bax-a. Razvoj rezistencije je doveo i do znaĉajnog povećanja produkcije reaktivnih kiseoniĉnih vrsta (ROS) i smanjenja odnosa koncentracije oksidovanog i redukovanog glutationa. Zapaţeno je povećanje ekspresije iRNK komponenti antioksidativnog sistema (MnSOD, iNOS, GPx i MRP1) i smanjenje ekspresije iRNK za HIF-1α kod RC6 ćelija u odnosu na C6 ćelije.RC6 ćelije pokazuju povećanu osetljivost na delovanje doksorubicina (DOX). UtvrĊeno je da RC6 ćelije akumuliraju više DOX-a od C6 ćelija ĉemu doprinosi znaĉajno smanjenje ekspresije iRNK za ABCB1 membranski transporter, kao i smanjenje unutarćelijskog pH.Pored toga, RC6 ćelije proliferišu znatno sporije u odnosu na C6 ćelije što je karakteristiĉno za rezistentne ćelije, ali i za ćelije sa većim invazivnim sposobnostima. Rezultati potvrĊuju da invazivnosti RC6 ćelija doprinosi povišena ekspresija iRNK za metaloproteinazu MMP9...
AB  - The most common and aggressive malignant tumor of the central nervous system is glioblastoma which successful treatment is compromised due to its high invasiveness, and resistance to chemotherapy. This study aimed to establish and characterize resistant glioma model for testing new therapeutic strategies for treatment of this serious disease. Rat C6 glioma cell line, which is phenotypically similar to human glioblastoma, was chosen as starting material. The first approved antiglioma drug, 1,3-bis (2-chloroethyl) -1-nitrosourea (BCNU, carmustine), an alkylating agent for treatment of primary and recurrent glioblastoma was used for establishing the resistant phenotype. Continuous treatment with BCNU led to the development of resistance not only to this chemotherapeutic, but also to other DNA damaging agents, cisplatin (CPt) and temozolomide (TMZ). The newly established drug resistant cell line was labeled as RC6. Resistance mechanisms analysis adressed the changes in apoptotic machinery and DNA damage, as well as the changes in antioxidant capacity between C6 and RC6 cells. Resistant RC6 line showed reduced sensitivity to cell death induction which was accompanied by a significant decrease in mRNA and protein expression of antiapoptotic factor Bcl-2, proapoptotic factor Bad and effector caspase 3. The mRNA expression of antiapoptotic factor Bcl-Xl and proapoptotic factor Bax was also decreased. The development of resistance was accompanied by significantly increased reactive oxygen species (ROS) production and decreased oxidized to reduced glutathione ratio. mRNA expression of antioxidant system components (MnSOD, iNOS, GPx and MRP1) was significantly increased in RC6 compared to C6 cells, while HIF-1α mRNA expression was decreased.RC6 cells exibited increased sensitivity to doxorubicin (DOX). It was determined that RC6 cells accumulated more DOX than C6 cells as a result of decreased mRNA expression of ABCB1 membrane transporter, as well as lower intracellular pH.In addition, RC6 cells proliferated significantly slower compared to C6 cells which is characteristic for drug resistant cells and cells with greater invasive capacity. The results confirmed that increased mRNA expression of metalloprotease MMP9 contributed to RC6 cells invasiveness...
PB  - University of Belgrade, Faculty of Biology
T2  - University of Belgrade, Faculty of Biology
T1  - Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo
T1  - Rat C6 glioma model as a tool for discovering new therapeutic strategies: characterization of the resistant phenotype in vitro and in vivo
UR  - https://hdl.handle.net/21.15107/rcub_nardus_8252
ER  - 

@phdthesis{
author = "Stojković Burić, Sonja",
year = "2017",
abstract = "Uspešnost terapije glioblastoma, najĉešćeg i najagresivnijeg malignog tumora centralnog nervnog sistema, je osujećena usled visokog stepena invazivnosti, kao i pojave rezistencije na hemioterapiju. Cilj ove doktorske disertacije je bio da se uspostavi i okarakteriše rezistentni gliomski model koji bi imao primenu u ispitivanju novih terapeutskih strategija u leĉenju ove teške bolesti. Kao poĉetni materijal korišćena je pacovska C6 ćelijska linija glioma, fenotipski sliĉna humanim glioblastomima. Za uspostavljanje rezistencije korišćen je prvi odobreni antigliomski lek 1,3-bis(2-hloroetil)-1-nitrozoureom (BCNU, karmustin), alkilirajući agens koji se koristi u terapiji primarnih i rekurentnih glioblastoma. Kontinuirana primena BCNU je dovela do razvoja rezistencije C6 ćelija ne samo na ovaj hemioterapeutik, već i na druge DNK oštećujuće agense, cisplatin (CPt) i temozolomid (TMZ). Novouspostavljena rezistentna ćelijska linija je oznaĉena kao RC6. Ispitivanje mehanizama rezistencije je obuhvatilo analizu promena na nivou apoptotske mašinerije i oštećenja DNK lanaca, kao i analizu promena u antioksidativnom kapacitetu izmeĊu C6 i RC6 ćelija. Rezistentna RC6 linija pokazuje smanjenu osetljivost na indukciju ćelijske smrti koja je praćena smanjenjem ekspresije antiapoptotskog faktora Bcl-2, proapoptotskog faktora Bad i efektorske kaspaze 3 na nivou iRNK i proteina. TakoĊe je pokazano smanjenje ekspresije iRNK antiapoptoskog Bcl-Xl i proapoptotskog Bax-a. Razvoj rezistencije je doveo i do znaĉajnog povećanja produkcije reaktivnih kiseoniĉnih vrsta (ROS) i smanjenja odnosa koncentracije oksidovanog i redukovanog glutationa. Zapaţeno je povećanje ekspresije iRNK komponenti antioksidativnog sistema (MnSOD, iNOS, GPx i MRP1) i smanjenje ekspresije iRNK za HIF-1α kod RC6 ćelija u odnosu na C6 ćelije.RC6 ćelije pokazuju povećanu osetljivost na delovanje doksorubicina (DOX). UtvrĊeno je da RC6 ćelije akumuliraju više DOX-a od C6 ćelija ĉemu doprinosi znaĉajno smanjenje ekspresije iRNK za ABCB1 membranski transporter, kao i smanjenje unutarćelijskog pH.Pored toga, RC6 ćelije proliferišu znatno sporije u odnosu na C6 ćelije što je karakteristiĉno za rezistentne ćelije, ali i za ćelije sa većim invazivnim sposobnostima. Rezultati potvrĊuju da invazivnosti RC6 ćelija doprinosi povišena ekspresija iRNK za metaloproteinazu MMP9..., The most common and aggressive malignant tumor of the central nervous system is glioblastoma which successful treatment is compromised due to its high invasiveness, and resistance to chemotherapy. This study aimed to establish and characterize resistant glioma model for testing new therapeutic strategies for treatment of this serious disease. Rat C6 glioma cell line, which is phenotypically similar to human glioblastoma, was chosen as starting material. The first approved antiglioma drug, 1,3-bis (2-chloroethyl) -1-nitrosourea (BCNU, carmustine), an alkylating agent for treatment of primary and recurrent glioblastoma was used for establishing the resistant phenotype. Continuous treatment with BCNU led to the development of resistance not only to this chemotherapeutic, but also to other DNA damaging agents, cisplatin (CPt) and temozolomide (TMZ). The newly established drug resistant cell line was labeled as RC6. Resistance mechanisms analysis adressed the changes in apoptotic machinery and DNA damage, as well as the changes in antioxidant capacity between C6 and RC6 cells. Resistant RC6 line showed reduced sensitivity to cell death induction which was accompanied by a significant decrease in mRNA and protein expression of antiapoptotic factor Bcl-2, proapoptotic factor Bad and effector caspase 3. The mRNA expression of antiapoptotic factor Bcl-Xl and proapoptotic factor Bax was also decreased. The development of resistance was accompanied by significantly increased reactive oxygen species (ROS) production and decreased oxidized to reduced glutathione ratio. mRNA expression of antioxidant system components (MnSOD, iNOS, GPx and MRP1) was significantly increased in RC6 compared to C6 cells, while HIF-1α mRNA expression was decreased.RC6 cells exibited increased sensitivity to doxorubicin (DOX). It was determined that RC6 cells accumulated more DOX than C6 cells as a result of decreased mRNA expression of ABCB1 membrane transporter, as well as lower intracellular pH.In addition, RC6 cells proliferated significantly slower compared to C6 cells which is characteristic for drug resistant cells and cells with greater invasive capacity. The results confirmed that increased mRNA expression of metalloprotease MMP9 contributed to RC6 cells invasiveness...",
publisher = "University of Belgrade, Faculty of Biology",
journal = "University of Belgrade, Faculty of Biology",
title = "Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo, Rat C6 glioma model as a tool for discovering new therapeutic strategies: characterization of the resistant phenotype in vitro and in vivo",
url = "https://hdl.handle.net/21.15107/rcub_nardus_8252"
}

Stojković Burić, S.. (2017). Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo. in University of Belgrade, Faculty of Biology
University of Belgrade, Faculty of Biology..
https://hdl.handle.net/21.15107/rcub_nardus_8252

Stojković Burić S. Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo. in University of Belgrade, Faculty of Biology. 2017;.
https://hdl.handle.net/21.15107/rcub_nardus_8252 .

Stojković Burić, Sonja, "Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo" in University of Belgrade, Faculty of Biology (2017),
https://hdl.handle.net/21.15107/rcub_nardus_8252 .

TY  - JOUR
AU  - Stojković Burić, Sonja
AU  - Podolski-Renić, Ana
AU  - Dinić, Jelena
AU  - Pavković, Željko
AU  - Ayuso, Jose M.
AU  - Fernández, Luis J.
AU  - Ochoa, Ignacio
AU  - Pérez-Martínez, Víctor Manuel
AU  - Pešić, Vesna
AU  - Pešić, Milica
PY  - 2016
UR  - https://radar.ibiss.bg.ac.rs/123456789/3872
AB  - Chemoresistance and invasion properties are severe limitations to efficient glioma therapy. Therefore, development of glioma in vivo models that more accurately resemble the situation observed in patients emerges. Previously, we established RC6 rat glioma cell line resistant to DNA damaging agents including antiglioma approved therapies such as 3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ). Herein, we evaluated the invasiveness of RC6 cells in vitro and in a new orthotopic animal model. For comparison, we used C6 cells from which RC6 cells originated. Differences in cell growth properties were assessed by real-time cell analyzer. Cells’ invasive potential in vitro was studied in fluorescently labeled gelatin and by formation of multicellular spheroids in hydrogel. For animal studies, fluorescently labeled cells were inoculated into adult male Wistar rat brains. Consecutive coronal and sagittal brain sections were analyzed 10 and 25 days post-inoculation, while rats’ behavior was recorded during three days in the open field test starting from 25th day post-inoculation. We demonstrated that development of chemoresistance induced invasive phenotype of RC6 cells with significant behavioral impediments implying usefulness of orthotopic RC6 glioma allograft in preclinical studies for the examination of new approaches to counteract both chemoresistance and invasion of glioma cells.
PB  - Basel : MDPI
T2  - Molecules
T1  - Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model
IS  - 7
VL  - 21
DO  - 10.3390/molecules21070843
SP  - 843
ER  - 

@article{
author = "Stojković Burić, Sonja and Podolski-Renić, Ana and Dinić, Jelena and Pavković, Željko and Ayuso, Jose M. and Fernández, Luis J. and Ochoa, Ignacio and Pérez-Martínez, Víctor Manuel and Pešić, Vesna and Pešić, Milica",
year = "2016",
abstract = "Chemoresistance and invasion properties are severe limitations to efficient glioma therapy. Therefore, development of glioma in vivo models that more accurately resemble the situation observed in patients emerges. Previously, we established RC6 rat glioma cell line resistant to DNA damaging agents including antiglioma approved therapies such as 3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ). Herein, we evaluated the invasiveness of RC6 cells in vitro and in a new orthotopic animal model. For comparison, we used C6 cells from which RC6 cells originated. Differences in cell growth properties were assessed by real-time cell analyzer. Cells’ invasive potential in vitro was studied in fluorescently labeled gelatin and by formation of multicellular spheroids in hydrogel. For animal studies, fluorescently labeled cells were inoculated into adult male Wistar rat brains. Consecutive coronal and sagittal brain sections were analyzed 10 and 25 days post-inoculation, while rats’ behavior was recorded during three days in the open field test starting from 25th day post-inoculation. We demonstrated that development of chemoresistance induced invasive phenotype of RC6 cells with significant behavioral impediments implying usefulness of orthotopic RC6 glioma allograft in preclinical studies for the examination of new approaches to counteract both chemoresistance and invasion of glioma cells.",
publisher = "Basel : MDPI",
journal = "Molecules",
title = "Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model",
number = "7",
volume = "21",
doi = "10.3390/molecules21070843",
pages = "843"
}

Stojković Burić, S., Podolski-Renić, A., Dinić, J., Pavković, Ž., Ayuso, J. M., Fernández, L. J., Ochoa, I., Pérez-Martínez, V. M., Pešić, V.,& Pešić, M.. (2016). Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model. in Molecules
Basel : MDPI., 21(7), 843.
https://doi.org/10.3390/molecules21070843

Stojković Burić S, Podolski-Renić A, Dinić J, Pavković Ž, Ayuso JM, Fernández LJ, Ochoa I, Pérez-Martínez VM, Pešić V, Pešić M. Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model. in Molecules. 2016;21(7):843.
doi:10.3390/molecules21070843 .

Stojković Burić, Sonja, Podolski-Renić, Ana, Dinić, Jelena, Pavković, Željko, Ayuso, Jose M., Fernández, Luis J., Ochoa, Ignacio, Pérez-Martínez, Víctor Manuel, Pešić, Vesna, Pešić, Milica, "Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model" in Molecules, 21, no. 7 (2016):843,
https://doi.org/10.3390/molecules21070843 . .

TY  - JOUR
AU  - Stojković Burić, Sonja
AU  - Podolski-Renić, Ana
AU  - Dinić, Jelena
AU  - Stanković, Tijana
AU  - Banković, Jasna Z.
AU  - Hadzic, Stefan
AU  - Paunovic, Verica
AU  - Isakovic, Aleksandra
AU  - Tanić, Nikola
AU  - Pešić, Milica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4046
AB  - Chemoresistance is a severe limitation to glioblastoma (GBM) therapy and there is a strong need to understand the underlying mechanisms that determine its response to different chemotherapeutics. Therefore, we induced resistance in C6 rat glioma cell line, which considerably resembles the characteristics of human GBM. The resistant phenotype was developed by 3-bis (2-chloroethyl)-1-nitrosourea (BCNU), one of the most commonly used therapeutic drug in the course of GBM treatment. After confirmation of the cross-resistance to cisplatin (CPt) and temozolomide (TMZ) in newly established RC6 cell line, we examined cell death induction and DNA damage by these drugs. Resistance to apoptosis and deficiency in forming DNA double-strand breaks was followed by significant decrease in the mRNA expression of pro-apoptotic and anti-apoptotic genes. The development of drug resistance was associated with significant increase in reactive oxygen species (ROS) and decrease in oxidized to reduced gluthatione ratio in RC6 cell line indicating a reduced level of oxidative stress. The mRNA expression levels of manganese superoxid dismutase (MnSOD), inducible nitric oxide synthase (iNOS) and gluthatione peroxidase (GPx) were increased while hypoxia-inducible factor 1-alpha (HIF-1 alpha) was decreased in RC6 compared to C6 cells. This was in line with obtained changes in ROS content and increased antioxidative capacity of RC6 cells. Importantly, RC6 cells demonstrated collateral sensitivity to doxorubicin (DOX). The analysis of this phenomenon revealed increased accumulation of DOX in RC6 cells due to their adaptation to high ROS content and acidification of cytoplasm. In conclusion, newly established RC6 rat glioma cell line could be used as a starting material for the development of allogenic animal model and preclinical evaluation of new antiglioma agents. Collateral sensitivity to DOX obtained after BCNU treatment may prompt new studies aimed to find efficient delivery of DOX to the glioma site in brain.
PB  - Elsevier Inc.
T2  - Experimental Cell Research
T1  - Development of resistance to antiglioma agents in rat C6 cells caused collateral sensitivity to doxorubicin
IS  - 2
VL  - 335
DO  - 10.1016/j.yexcr.2015.05.018
SP  - 248
EP  - 257
ER  - 

@article{
author = "Stojković Burić, Sonja and Podolski-Renić, Ana and Dinić, Jelena and Stanković, Tijana and Banković, Jasna Z. and Hadzic, Stefan and Paunovic, Verica and Isakovic, Aleksandra and Tanić, Nikola and Pešić, Milica",
year = "2015",
abstract = "Chemoresistance is a severe limitation to glioblastoma (GBM) therapy and there is a strong need to understand the underlying mechanisms that determine its response to different chemotherapeutics. Therefore, we induced resistance in C6 rat glioma cell line, which considerably resembles the characteristics of human GBM. The resistant phenotype was developed by 3-bis (2-chloroethyl)-1-nitrosourea (BCNU), one of the most commonly used therapeutic drug in the course of GBM treatment. After confirmation of the cross-resistance to cisplatin (CPt) and temozolomide (TMZ) in newly established RC6 cell line, we examined cell death induction and DNA damage by these drugs. Resistance to apoptosis and deficiency in forming DNA double-strand breaks was followed by significant decrease in the mRNA expression of pro-apoptotic and anti-apoptotic genes. The development of drug resistance was associated with significant increase in reactive oxygen species (ROS) and decrease in oxidized to reduced gluthatione ratio in RC6 cell line indicating a reduced level of oxidative stress. The mRNA expression levels of manganese superoxid dismutase (MnSOD), inducible nitric oxide synthase (iNOS) and gluthatione peroxidase (GPx) were increased while hypoxia-inducible factor 1-alpha (HIF-1 alpha) was decreased in RC6 compared to C6 cells. This was in line with obtained changes in ROS content and increased antioxidative capacity of RC6 cells. Importantly, RC6 cells demonstrated collateral sensitivity to doxorubicin (DOX). The analysis of this phenomenon revealed increased accumulation of DOX in RC6 cells due to their adaptation to high ROS content and acidification of cytoplasm. In conclusion, newly established RC6 rat glioma cell line could be used as a starting material for the development of allogenic animal model and preclinical evaluation of new antiglioma agents. Collateral sensitivity to DOX obtained after BCNU treatment may prompt new studies aimed to find efficient delivery of DOX to the glioma site in brain.",
publisher = "Elsevier Inc.",
journal = "Experimental Cell Research",
title = "Development of resistance to antiglioma agents in rat C6 cells caused collateral sensitivity to doxorubicin",
number = "2",
volume = "335",
doi = "10.1016/j.yexcr.2015.05.018",
pages = "248-257"
}

Stojković Burić, S., Podolski-Renić, A., Dinić, J., Stanković, T., Banković, J. Z., Hadzic, S., Paunovic, V., Isakovic, A., Tanić, N.,& Pešić, M.. (2015). Development of resistance to antiglioma agents in rat C6 cells caused collateral sensitivity to doxorubicin. in Experimental Cell Research
Elsevier Inc.., 335(2), 248-257.
https://doi.org/10.1016/j.yexcr.2015.05.018

Stojković Burić S, Podolski-Renić A, Dinić J, Stanković T, Banković JZ, Hadzic S, Paunovic V, Isakovic A, Tanić N, Pešić M. Development of resistance to antiglioma agents in rat C6 cells caused collateral sensitivity to doxorubicin. in Experimental Cell Research. 2015;335(2):248-257.
doi:10.1016/j.yexcr.2015.05.018 .

Stojković Burić, Sonja, Podolski-Renić, Ana, Dinić, Jelena, Stanković, Tijana, Banković, Jasna Z., Hadzic, Stefan, Paunovic, Verica, Isakovic, Aleksandra, Tanić, Nikola, Pešić, Milica, "Development of resistance to antiglioma agents in rat C6 cells caused collateral sensitivity to doxorubicin" in Experimental Cell Research, 335, no. 2 (2015):248-257,
https://doi.org/10.1016/j.yexcr.2015.05.018 . .

TY  - JOUR
AU  - Stojković Burić, Sonja
AU  - Podolski-Renić, Ana
AU  - Dinić, Jelena
AU  - Stankovic, Tijana
AU  - Banković, Jasna Z.
AU  - Hadzic, Stefan
AU  - Paunovic, Verica
AU  - Isakovic, Aleksandra
AU  - Tanić, Nikola
AU  - Pešić, Milica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1926
AB  - Chemoresistance is a severe limitation to glioblastoma (GBM) therapy and
   there is a strong need to understand the underlying mechanisms that
   determine its response to different chemotherapeutics. Therefore, we
   induced resistance in C6 rat glioma cell line, which considerably
   resembles the characteristics of human GBM. The resistant phenotype was
   developed by 3-bis (2-chloroethyl)-1-nitrosourea (BCNU), one of the most
   commonly used therapeutic drug in the course of GBM treatment. After
   confirmation of the cross-resistance to cisplatin (CPt) and temozolomide
   (TMZ) in newly established RC6 cell line, we examined cell death
   induction and DNA damage by these drugs. Resistance to apoptosis and
   deficiency in forming DNA double-strand breaks was followed by
   significant decrease in the mRNA expression of pro-apoptotic and
   anti-apoptotic genes. The development of drug resistance was associated
   with significant increase in reactive oxygen species (ROS) and decrease
   in oxidized to reduced gluthatione ratio in RC6 cell line indicating a
   reduced level of oxidative stress. The mRNA expression levels of
   manganese superoxid dismutase (MnSOD), inducible nitric oxide synthase
   (iNOS) and gluthatione peroxidase (GPx) were increased while
   hypoxia-inducible factor 1-alpha (HIF-1 alpha) was decreased in RC6
   compared to C6 cells. This was in line with obtained changes in ROS
   content and increased antioxidative capacity of RC6 cells. Importantly,
   RC6 cells demonstrated collateral sensitivity to doxorubicin (DOX). The
   analysis of this phenomenon revealed increased accumulation of DOX in
   RC6 cells due to their adaptation to high ROS content and acidification
   of cytoplasm. In conclusion, newly established RC6 rat glioma cell line
   could be used as a starting material for the development of allogenic
   animal model and preclinical evaluation of new antiglioma agents.
   Collateral sensitivity to DOX obtained after BCNU treatment may prompt
   new studies aimed to find efficient delivery of DOX to the glioma site
   in brain. (C) 2015 Elsevier Inc. All rights reserved.
T2  - Experimental Cell Research
T1  - Development of resistance to antiglioma agents in rat C6 cells caused
 collateral sensitivity to doxorubicin
IS  - 2
VL  - 335
DO  - 10.1016/j.yexcr.2015.05.018
SP  - 248
EP  - 257
ER  - 

@article{
author = "Stojković Burić, Sonja and Podolski-Renić, Ana and Dinić, Jelena and Stankovic, Tijana and Banković, Jasna Z. and Hadzic, Stefan and Paunovic, Verica and Isakovic, Aleksandra and Tanić, Nikola and Pešić, Milica",
year = "2015",
abstract = "Chemoresistance is a severe limitation to glioblastoma (GBM) therapy and
   there is a strong need to understand the underlying mechanisms that
   determine its response to different chemotherapeutics. Therefore, we
   induced resistance in C6 rat glioma cell line, which considerably
   resembles the characteristics of human GBM. The resistant phenotype was
   developed by 3-bis (2-chloroethyl)-1-nitrosourea (BCNU), one of the most
   commonly used therapeutic drug in the course of GBM treatment. After
   confirmation of the cross-resistance to cisplatin (CPt) and temozolomide
   (TMZ) in newly established RC6 cell line, we examined cell death
   induction and DNA damage by these drugs. Resistance to apoptosis and
   deficiency in forming DNA double-strand breaks was followed by
   significant decrease in the mRNA expression of pro-apoptotic and
   anti-apoptotic genes. The development of drug resistance was associated
   with significant increase in reactive oxygen species (ROS) and decrease
   in oxidized to reduced gluthatione ratio in RC6 cell line indicating a
   reduced level of oxidative stress. The mRNA expression levels of
   manganese superoxid dismutase (MnSOD), inducible nitric oxide synthase
   (iNOS) and gluthatione peroxidase (GPx) were increased while
   hypoxia-inducible factor 1-alpha (HIF-1 alpha) was decreased in RC6
   compared to C6 cells. This was in line with obtained changes in ROS
   content and increased antioxidative capacity of RC6 cells. Importantly,
   RC6 cells demonstrated collateral sensitivity to doxorubicin (DOX). The
   analysis of this phenomenon revealed increased accumulation of DOX in
   RC6 cells due to their adaptation to high ROS content and acidification
   of cytoplasm. In conclusion, newly established RC6 rat glioma cell line
   could be used as a starting material for the development of allogenic
   animal model and preclinical evaluation of new antiglioma agents.
   Collateral sensitivity to DOX obtained after BCNU treatment may prompt
   new studies aimed to find efficient delivery of DOX to the glioma site
   in brain. (C) 2015 Elsevier Inc. All rights reserved.",
journal = "Experimental Cell Research",
title = "Development of resistance to antiglioma agents in rat C6 cells caused
 collateral sensitivity to doxorubicin",
number = "2",
volume = "335",
doi = "10.1016/j.yexcr.2015.05.018",
pages = "248-257"
}

Stojković Burić, S., Podolski-Renić, A., Dinić, J., Stankovic, T., Banković, J. Z., Hadzic, S., Paunovic, V., Isakovic, A., Tanić, N.,& Pešić, M.. (2015). Development of resistance to antiglioma agents in rat C6 cells caused
 collateral sensitivity to doxorubicin. in Experimental Cell Research, 335(2), 248-257.
https://doi.org/10.1016/j.yexcr.2015.05.018

Stojković Burić S, Podolski-Renić A, Dinić J, Stankovic T, Banković JZ, Hadzic S, Paunovic V, Isakovic A, Tanić N, Pešić M. Development of resistance to antiglioma agents in rat C6 cells caused
 collateral sensitivity to doxorubicin. in Experimental Cell Research. 2015;335(2):248-257.
doi:10.1016/j.yexcr.2015.05.018 .

Stojković Burić, Sonja, Podolski-Renić, Ana, Dinić, Jelena, Stankovic, Tijana, Banković, Jasna Z., Hadzic, Stefan, Paunovic, Verica, Isakovic, Aleksandra, Tanić, Nikola, Pešić, Milica, "Development of resistance to antiglioma agents in rat C6 cells caused
 collateral sensitivity to doxorubicin" in Experimental Cell Research, 335, no. 2 (2015):248-257,
https://doi.org/10.1016/j.yexcr.2015.05.018 . .

TY  - JOUR
AU  - Stojsic, Jelena
AU  - Stankovic, Tijana
AU  - Stojković Burić, Sonja
AU  - Milinkovic, Vedrana
AU  - Dinić, Jelena
AU  - Milosevic, Zorica
AU  - Milovanovic, Zorka
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2005
AB  - Lung cancer is the most common cause of neoplasia-related death
   worldwide. Accounting for approximately 80\% of all lung carcinomas, the
   non-small cell lung carcinoma (NSCLC) is the most common clinical form
   with its two predominant histological types, adenocarcinoma (ADC) and
   squamous cell carcinoma (SCC). Although surgical resection is the most
   favorable treatment for patients with NSCLC, relapse is still high, so
   neoadjuvant chemotherapy (NAC) is an accepted treatment modality. In
   this study we examined whether some of the key molecules associated with
   the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways could have
   predictive and prognostic value for the NAC application. To that end we
   examined the expression status of PTEN, pAKT, pERK and loss of
   heterozygosity (LOH) of PTEN in two groups of NSCLC patients, those who
   received and those who did not receive NAG LOH PTEN and low pERK
   expression is shown to be correlated with the longest survival of
   patients with SCC and ADC, respectively, who received NAC. These results
   point that the application of NAC is beneficial in the NSCLC patients
   with specific molecular alterations which could further help to improve
   constant search for the druggable molecular targets used in personalized
   therapy. (C) 2014 Elsevier Inc. All rights reserved.
T2  - Experimental and Molecular Pathology
T1  - Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma
IS  - 1
VL  - 98
DO  - 10.1016/j.yexmp.2014.11.010
SP  - 27
EP  - 32
ER  - 

@article{
author = "Stojsic, Jelena and Stankovic, Tijana and Stojković Burić, Sonja and Milinkovic, Vedrana and Dinić, Jelena and Milosevic, Zorica and Milovanovic, Zorka and Tanić, Nikola and Banković, Jasna Z.",
year = "2015",
abstract = "Lung cancer is the most common cause of neoplasia-related death
   worldwide. Accounting for approximately 80\% of all lung carcinomas, the
   non-small cell lung carcinoma (NSCLC) is the most common clinical form
   with its two predominant histological types, adenocarcinoma (ADC) and
   squamous cell carcinoma (SCC). Although surgical resection is the most
   favorable treatment for patients with NSCLC, relapse is still high, so
   neoadjuvant chemotherapy (NAC) is an accepted treatment modality. In
   this study we examined whether some of the key molecules associated with
   the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways could have
   predictive and prognostic value for the NAC application. To that end we
   examined the expression status of PTEN, pAKT, pERK and loss of
   heterozygosity (LOH) of PTEN in two groups of NSCLC patients, those who
   received and those who did not receive NAG LOH PTEN and low pERK
   expression is shown to be correlated with the longest survival of
   patients with SCC and ADC, respectively, who received NAC. These results
   point that the application of NAC is beneficial in the NSCLC patients
   with specific molecular alterations which could further help to improve
   constant search for the druggable molecular targets used in personalized
   therapy. (C) 2014 Elsevier Inc. All rights reserved.",
journal = "Experimental and Molecular Pathology",
title = "Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma",
number = "1",
volume = "98",
doi = "10.1016/j.yexmp.2014.11.010",
pages = "27-32"
}

Stojsic, J., Stankovic, T., Stojković Burić, S., Milinkovic, V., Dinić, J., Milosevic, Z., Milovanovic, Z., Tanić, N.,& Banković, J. Z.. (2015). Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma. in Experimental and Molecular Pathology, 98(1), 27-32.
https://doi.org/10.1016/j.yexmp.2014.11.010

Stojsic J, Stankovic T, Stojković Burić S, Milinkovic V, Dinić J, Milosevic Z, Milovanovic Z, Tanić N, Banković JZ. Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma. in Experimental and Molecular Pathology. 2015;98(1):27-32.
doi:10.1016/j.yexmp.2014.11.010 .

Stojsic, Jelena, Stankovic, Tijana, Stojković Burić, Sonja, Milinkovic, Vedrana, Dinić, Jelena, Milosevic, Zorica, Milovanovic, Zorka, Tanić, Nikola, Banković, Jasna Z., "Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma" in Experimental and Molecular Pathology, 98, no. 1 (2015):27-32,
https://doi.org/10.1016/j.yexmp.2014.11.010 . .

TY  - JOUR
AU  - Pešić, Milica
AU  - Podolski-Renić, Ana
AU  - Stojković Burić, Sonja
AU  - Matovic, Branko
AU  - Zmejkoski, Danica
AU  - Kojic, Vesna
AU  - Bogdanovic, Gordana
AU  - Pavicevic, Aleksandra
AU  - Mojovic, Milos
AU  - Savic, Aleksandar
AU  - Milenkovic, Ivana
AU  - Kalauzi, Aleksandar
AU  - Radotic, Ksenija
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1957
AB  - Data on medical applications of cerium oxide nanoparticles CeO2 (CONP)
   are promising, yet information regarding their action in cells is
   incomplete and there are conflicting reports about in vitro toxicity.
   Herein, we have studied cytotoxic effect of CONP in several cancer and
   normal cell lines and their potential to change intracellular redox
   status. The IC50 was achieved only in two of eight tested cell lines,
   melanoma 518A2 and colorectal adenocarcinoma HT-29. Self-propagating
   room temperature method was applied to produce CONP with an average
   crystalline size of 4 nm. The results confirmed presence of Ce3+ and O2-
   vacancies. The induction of cell death by CONP and the production of
   reactive oxygen species (ROS) were analyzed by flow-cytometry. Free
   radicals related antioxidant capacity of the cells was studied by the
   reduction of stable free radical TEMPONE using electron spin resonance
   spectroscopy. CONP showed low or moderate cytotoxicity in cancer cell
   lines: adenocarcinoma DLD1 and multi-drug resistant DLD1-TxR, non-small
   cell lung carcinoma NCI-H460 and multi-drug resistant NCI-H460/R, while
   normal cell lines (keratinocytes HaCaT, lung fetal fibroblasts MRC-5)
   were insensitive. The most sensitive were 518A2 melanoma and HT-29
   colorectal adenocarcinoma cell lines, with the IC50 values being between
   100 and 200 mu M. Decreased rate of TEMPONE reduction and increased
   production of certain ROS species (peroxynitrite and hydrogen peroxide
   anion) indicates that free radical metabolism, thus redox status was
   changed, and antioxidant capacity damaged in the CONP treated 518A2 and
   HT-29 cells. In conclusion, changes in intracellular redox status
   induced by CONP are partly attributed to the prooxidant activity of the
   nanoparticles. Further, ROS induced cell damages might eventually lead
   to the cell death. However, low inhibitory potential of CONP in the
   other human cell lines tested indicates that CONP may be safe for human
   usage in industry and medicine. (C) 2015 Elsevier Ireland Ltd. All
   rights reserved.
T2  - Chemico-Biological Interactions
T1  - Anti-cancer effects of cerium oxide nanoparticles and its intracellular
 redox activity
VL  - 232
DO  - 10.1016/j.cbi.2015.03.013
SP  - 85
EP  - 93
ER  - 

@article{
author = "Pešić, Milica and Podolski-Renić, Ana and Stojković Burić, Sonja and Matovic, Branko and Zmejkoski, Danica and Kojic, Vesna and Bogdanovic, Gordana and Pavicevic, Aleksandra and Mojovic, Milos and Savic, Aleksandar and Milenkovic, Ivana and Kalauzi, Aleksandar and Radotic, Ksenija",
year = "2015",
abstract = "Data on medical applications of cerium oxide nanoparticles CeO2 (CONP)
   are promising, yet information regarding their action in cells is
   incomplete and there are conflicting reports about in vitro toxicity.
   Herein, we have studied cytotoxic effect of CONP in several cancer and
   normal cell lines and their potential to change intracellular redox
   status. The IC50 was achieved only in two of eight tested cell lines,
   melanoma 518A2 and colorectal adenocarcinoma HT-29. Self-propagating
   room temperature method was applied to produce CONP with an average
   crystalline size of 4 nm. The results confirmed presence of Ce3+ and O2-
   vacancies. The induction of cell death by CONP and the production of
   reactive oxygen species (ROS) were analyzed by flow-cytometry. Free
   radicals related antioxidant capacity of the cells was studied by the
   reduction of stable free radical TEMPONE using electron spin resonance
   spectroscopy. CONP showed low or moderate cytotoxicity in cancer cell
   lines: adenocarcinoma DLD1 and multi-drug resistant DLD1-TxR, non-small
   cell lung carcinoma NCI-H460 and multi-drug resistant NCI-H460/R, while
   normal cell lines (keratinocytes HaCaT, lung fetal fibroblasts MRC-5)
   were insensitive. The most sensitive were 518A2 melanoma and HT-29
   colorectal adenocarcinoma cell lines, with the IC50 values being between
   100 and 200 mu M. Decreased rate of TEMPONE reduction and increased
   production of certain ROS species (peroxynitrite and hydrogen peroxide
   anion) indicates that free radical metabolism, thus redox status was
   changed, and antioxidant capacity damaged in the CONP treated 518A2 and
   HT-29 cells. In conclusion, changes in intracellular redox status
   induced by CONP are partly attributed to the prooxidant activity of the
   nanoparticles. Further, ROS induced cell damages might eventually lead
   to the cell death. However, low inhibitory potential of CONP in the
   other human cell lines tested indicates that CONP may be safe for human
   usage in industry and medicine. (C) 2015 Elsevier Ireland Ltd. All
   rights reserved.",
journal = "Chemico-Biological Interactions",
title = "Anti-cancer effects of cerium oxide nanoparticles and its intracellular
 redox activity",
volume = "232",
doi = "10.1016/j.cbi.2015.03.013",
pages = "85-93"
}

Pešić, M., Podolski-Renić, A., Stojković Burić, S., Matovic, B., Zmejkoski, D., Kojic, V., Bogdanovic, G., Pavicevic, A., Mojovic, M., Savic, A., Milenkovic, I., Kalauzi, A.,& Radotic, K.. (2015). Anti-cancer effects of cerium oxide nanoparticles and its intracellular
 redox activity. in Chemico-Biological Interactions, 232, 85-93.
https://doi.org/10.1016/j.cbi.2015.03.013

Pešić M, Podolski-Renić A, Stojković Burić S, Matovic B, Zmejkoski D, Kojic V, Bogdanovic G, Pavicevic A, Mojovic M, Savic A, Milenkovic I, Kalauzi A, Radotic K. Anti-cancer effects of cerium oxide nanoparticles and its intracellular
 redox activity. in Chemico-Biological Interactions. 2015;232:85-93.
doi:10.1016/j.cbi.2015.03.013 .

Pešić, Milica, Podolski-Renić, Ana, Stojković Burić, Sonja, Matovic, Branko, Zmejkoski, Danica, Kojic, Vesna, Bogdanovic, Gordana, Pavicevic, Aleksandra, Mojovic, Milos, Savic, Aleksandar, Milenkovic, Ivana, Kalauzi, Aleksandar, Radotic, Ksenija, "Anti-cancer effects of cerium oxide nanoparticles and its intracellular
 redox activity" in Chemico-Biological Interactions, 232 (2015):85-93,
https://doi.org/10.1016/j.cbi.2015.03.013 . .

TY  - JOUR
AU  - Milosevic, Zorica
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
AU  - Stankovic, Tijana
AU  - Buta, Marko
AU  - Lavrnic, Dragana
AU  - Milovanovic, Zorka
AU  - Pupic, Gordana
AU  - Stojković Burić, Sonja
AU  - Milinkovic, Vedrana
AU  - Ito, Yasuhiro
AU  - Džodić, Radan R.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2290
AB  - Multiple cancers represent 2.42\% of all human cancers and are mainly
   double or triple cancers. Many possible causes of multiple malignancies
   have been reported such as genetic alterations, exposure to anti-cancer
   chemotherapy, radiotherapy, immunosuppressive therapy and reduced
   immunologic response. We report a female patient with multiple sclerosis
   and quadruple cancers of different embryological origin. Patient was
   diagnosed with stage III (T3, N1a, MO) medullary thyroid carcinoma
   (MTC), multicentric micropapillary thyroid carcinoma, scapular and
   lumbar melanomas (Clark II, Breslow II), and lobular invasive breast
   carcinoma (T1a, NO, MO). All tumors present in our patient except
   micropapillary thyroid carcinomas were investigated for gene alterations
   known to have a key role in cancer promotion and progression. Tumor
   samples were screened for the p16 alterations (loss of heterozygosity
   and homozygous deletions), loss of heterozygosity of PTEN, p53
   alterations (mutational status and loss of heterozygosity) and
   mutational status of RET, HRAS and KRAS. Each type of tumor investigated
   had specific pattern of analyzed genetic alterations. The most prominent
   genetic changes were mutual alterations in PTEN and p53 tumor
   suppressors present in breast cancer and two melanomas. These
   co-alterations could be crucial for promoting development of multiple
   malignancies. Moreover the insertion in 4th codon of HRAS gene was
   common for all tumor types investigated. It represents frameshift
   mutation introducing stop codon at position 5 which prevents synthesis
   of a full-length protein. Since the inactivated RAS enhances sensitivity
   to tamoxifen and radiotherapy this genetic alteration could be
   considered as a good prognostic factor for this patient.
T2  - International Journal of Clinical and Experimental Pathology
T1  - Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy
IS  - 4
VL  - 7
SP  - 1826
EP  - 1833
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_2290
ER  - 

@article{
author = "Milosevic, Zorica and Tanić, Nikola and Banković, Jasna Z. and Stankovic, Tijana and Buta, Marko and Lavrnic, Dragana and Milovanovic, Zorka and Pupic, Gordana and Stojković Burić, Sonja and Milinkovic, Vedrana and Ito, Yasuhiro and Džodić, Radan R.",
year = "2014",
abstract = "Multiple cancers represent 2.42\% of all human cancers and are mainly
   double or triple cancers. Many possible causes of multiple malignancies
   have been reported such as genetic alterations, exposure to anti-cancer
   chemotherapy, radiotherapy, immunosuppressive therapy and reduced
   immunologic response. We report a female patient with multiple sclerosis
   and quadruple cancers of different embryological origin. Patient was
   diagnosed with stage III (T3, N1a, MO) medullary thyroid carcinoma
   (MTC), multicentric micropapillary thyroid carcinoma, scapular and
   lumbar melanomas (Clark II, Breslow II), and lobular invasive breast
   carcinoma (T1a, NO, MO). All tumors present in our patient except
   micropapillary thyroid carcinomas were investigated for gene alterations
   known to have a key role in cancer promotion and progression. Tumor
   samples were screened for the p16 alterations (loss of heterozygosity
   and homozygous deletions), loss of heterozygosity of PTEN, p53
   alterations (mutational status and loss of heterozygosity) and
   mutational status of RET, HRAS and KRAS. Each type of tumor investigated
   had specific pattern of analyzed genetic alterations. The most prominent
   genetic changes were mutual alterations in PTEN and p53 tumor
   suppressors present in breast cancer and two melanomas. These
   co-alterations could be crucial for promoting development of multiple
   malignancies. Moreover the insertion in 4th codon of HRAS gene was
   common for all tumor types investigated. It represents frameshift
   mutation introducing stop codon at position 5 which prevents synthesis
   of a full-length protein. Since the inactivated RAS enhances sensitivity
   to tamoxifen and radiotherapy this genetic alteration could be
   considered as a good prognostic factor for this patient.",
journal = "International Journal of Clinical and Experimental Pathology",
title = "Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy",
number = "4",
volume = "7",
pages = "1826-1833",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_2290"
}

Milosevic, Z., Tanić, N., Banković, J. Z., Stankovic, T., Buta, M., Lavrnic, D., Milovanovic, Z., Pupic, G., Stojković Burić, S., Milinkovic, V., Ito, Y.,& Džodić, R. R.. (2014). Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy. in International Journal of Clinical and Experimental Pathology, 7(4), 1826-1833.
https://hdl.handle.net/21.15107/rcub_ibiss_2290

Milosevic Z, Tanić N, Banković JZ, Stankovic T, Buta M, Lavrnic D, Milovanovic Z, Pupic G, Stojković Burić S, Milinkovic V, Ito Y, Džodić RR. Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy. in International Journal of Clinical and Experimental Pathology. 2014;7(4):1826-1833.
https://hdl.handle.net/21.15107/rcub_ibiss_2290 .

Milosevic, Zorica, Tanić, Nikola, Banković, Jasna Z., Stankovic, Tijana, Buta, Marko, Lavrnic, Dragana, Milovanovic, Zorka, Pupic, Gordana, Stojković Burić, Sonja, Milinkovic, Vedrana, Ito, Yasuhiro, Džodić, Radan R., "Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy" in International Journal of Clinical and Experimental Pathology, 7, no. 4 (2014):1826-1833,
https://hdl.handle.net/21.15107/rcub_ibiss_2290 .