TY  - JOUR
AU  - Podolski-Renić, Ana
AU  - Milošević, Zorica
AU  - Dinić, Jelena
AU  - Stanković, Tijana
AU  - Banković, Jasna Z.
AU  - Pešić, Milica
PY  - 2016
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4051
AB  - Cancer-initiating cells referred to as cancer stem cells (CSCs) retain the essential property of self-renewal and protection. The protective mechanisms enable tumour regrowth even after the application of chemotherapy that was believed to be successful. Among the protective mechanisms of CSCs, the overexpression of ATP binding cassette (ABC) membrane transporters is highly important. ABC transporters involved in the development of cancer multidrug resistance (MDR) such as P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are considered as particular features of CSCs. They provide a shield for CSCs and protect them from the adverse effects of chemotherapeutics. Hence, combating MDR would be one of the strategies for the elimination of CSCs. In order to investigate this phenomenon many model systems comprising MDR cancer cells have been established. Some of them were developed by a selection process through exposure to various anticancer drugs, others by transfection of genes for ABC transporters, while some were obtained by sorting the side population considered to possess stemness and resistant phenotypes. Herein we review the potential of cancer MDR models for studying CSCs because gaining a better insight into the mechanisms of CSC resistance to chemotherapy may lead to the discovery of new therapeutic targets and the development of better anticancer strategies.
PB  - The Royal Society of Chemistry
T2  - MedChemComm
T1  - Mutual regulation and targeting of multidrug resistance and cancer stem phenotype
IS  - 12
VL  - 7
DO  - 10.1039/C6MD00391E
SP  - 2265
EP  - 2281
ER  - 

@article{
author = "Podolski-Renić, Ana and Milošević, Zorica and Dinić, Jelena and Stanković, Tijana and Banković, Jasna Z. and Pešić, Milica",
year = "2016",
abstract = "Cancer-initiating cells referred to as cancer stem cells (CSCs) retain the essential property of self-renewal and protection. The protective mechanisms enable tumour regrowth even after the application of chemotherapy that was believed to be successful. Among the protective mechanisms of CSCs, the overexpression of ATP binding cassette (ABC) membrane transporters is highly important. ABC transporters involved in the development of cancer multidrug resistance (MDR) such as P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are considered as particular features of CSCs. They provide a shield for CSCs and protect them from the adverse effects of chemotherapeutics. Hence, combating MDR would be one of the strategies for the elimination of CSCs. In order to investigate this phenomenon many model systems comprising MDR cancer cells have been established. Some of them were developed by a selection process through exposure to various anticancer drugs, others by transfection of genes for ABC transporters, while some were obtained by sorting the side population considered to possess stemness and resistant phenotypes. Herein we review the potential of cancer MDR models for studying CSCs because gaining a better insight into the mechanisms of CSC resistance to chemotherapy may lead to the discovery of new therapeutic targets and the development of better anticancer strategies.",
publisher = "The Royal Society of Chemistry",
journal = "MedChemComm",
title = "Mutual regulation and targeting of multidrug resistance and cancer stem phenotype",
number = "12",
volume = "7",
doi = "10.1039/C6MD00391E",
pages = "2265-2281"
}

Podolski-Renić, A., Milošević, Z., Dinić, J., Stanković, T., Banković, J. Z.,& Pešić, M.. (2016). Mutual regulation and targeting of multidrug resistance and cancer stem phenotype. in MedChemComm
The Royal Society of Chemistry., 7(12), 2265-2281.
https://doi.org/10.1039/C6MD00391E

Podolski-Renić A, Milošević Z, Dinić J, Stanković T, Banković JZ, Pešić M. Mutual regulation and targeting of multidrug resistance and cancer stem phenotype. in MedChemComm. 2016;7(12):2265-2281.
doi:10.1039/C6MD00391E .

Podolski-Renić, Ana, Milošević, Zorica, Dinić, Jelena, Stanković, Tijana, Banković, Jasna Z., Pešić, Milica, "Mutual regulation and targeting of multidrug resistance and cancer stem phenotype" in MedChemComm, 7, no. 12 (2016):2265-2281,
https://doi.org/10.1039/C6MD00391E . .

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  - Dinić, Jelena
AU  - Podolski-Renić, Ana
AU  - Stankovic, Tijana
AU  - Banković, Jasna Z.
AU  - Pešić, Milica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2041
AB  - Resistance to chemotherapeautic drugs is one of the main obstacles to
   effective cancer treatment. Multidrug resistance (MDR) is defined as
   resistance to structurally and/or functionally unrelated drugs, and has
   been extensively investigated for the last three decades. There are two
   types of MDR: intrinsic and acquired. Tumor microenvironment selection
   pressure leads to the development of intrinsic MDR, while acquired
   resistance is a consequence of the administered chemotherapy. A central
   issue in chemotherapy failure is the existence of heterogeneous
   populations of cancer cells within one patient and patient-to-patient
   variability within each type of cancer.
   Numerous genes and pathways contribute to the development of MDR in
   cancer. Point mutations, gene amplification or other genetic or
   epigenetic changes all affect biological functions and may lead to the
   occurrence of MDR phenotype. Similar to the characteristics of
   cancerogenesis, the main features of MDR include abnormal tumor
   vasculature, regions of hypoxia, aerobic glycolysis, and a lower
   susceptibility to apoptosis. In order to achieve a lethal effect on
   cancer cells, drugs need to reach their intracellular target molecules.
   The overexpression of the efflux transporter P-glycoprotein (P-gp) in
   MDR cancer cells leads to decreased uptake of the drug and intracellular
   drug accumulation, minimising drug-target interactions.
   New agents being or inspired by natural products that sucessfully target
   these mechanisms are the main subject of this review. Two key approaches
   in combating MDR in cancer are discussed (i) finding agents that
   preserve citotoxicity toward MDR cancer cells; (ii) developing compounds
   that restore the cytotoxic activity of classic anticancer drugs.
T2  - Current Pharmaceutical Design
T1  - New Approaches With Natural Product Drugs for Overcoming Multidrug
 Resistance in Cancer
IS  - 38
VL  - 21
DO  - 10.2174/1381612821666151002113546
SP  - 5589
EP  - 5604
ER  - 

@article{
author = "Dinić, Jelena and Podolski-Renić, Ana and Stankovic, Tijana and Banković, Jasna Z. and Pešić, Milica",
year = "2015",
abstract = "Resistance to chemotherapeautic drugs is one of the main obstacles to
   effective cancer treatment. Multidrug resistance (MDR) is defined as
   resistance to structurally and/or functionally unrelated drugs, and has
   been extensively investigated for the last three decades. There are two
   types of MDR: intrinsic and acquired. Tumor microenvironment selection
   pressure leads to the development of intrinsic MDR, while acquired
   resistance is a consequence of the administered chemotherapy. A central
   issue in chemotherapy failure is the existence of heterogeneous
   populations of cancer cells within one patient and patient-to-patient
   variability within each type of cancer.
   Numerous genes and pathways contribute to the development of MDR in
   cancer. Point mutations, gene amplification or other genetic or
   epigenetic changes all affect biological functions and may lead to the
   occurrence of MDR phenotype. Similar to the characteristics of
   cancerogenesis, the main features of MDR include abnormal tumor
   vasculature, regions of hypoxia, aerobic glycolysis, and a lower
   susceptibility to apoptosis. In order to achieve a lethal effect on
   cancer cells, drugs need to reach their intracellular target molecules.
   The overexpression of the efflux transporter P-glycoprotein (P-gp) in
   MDR cancer cells leads to decreased uptake of the drug and intracellular
   drug accumulation, minimising drug-target interactions.
   New agents being or inspired by natural products that sucessfully target
   these mechanisms are the main subject of this review. Two key approaches
   in combating MDR in cancer are discussed (i) finding agents that
   preserve citotoxicity toward MDR cancer cells; (ii) developing compounds
   that restore the cytotoxic activity of classic anticancer drugs.",
journal = "Current Pharmaceutical Design",
title = "New Approaches With Natural Product Drugs for Overcoming Multidrug
 Resistance in Cancer",
number = "38",
volume = "21",
doi = "10.2174/1381612821666151002113546",
pages = "5589-5604"
}

Dinić, J., Podolski-Renić, A., Stankovic, T., Banković, J. Z.,& Pešić, M.. (2015). New Approaches With Natural Product Drugs for Overcoming Multidrug
 Resistance in Cancer. in Current Pharmaceutical Design, 21(38), 5589-5604.
https://doi.org/10.2174/1381612821666151002113546

Dinić J, Podolski-Renić A, Stankovic T, Banković JZ, Pešić M. New Approaches With Natural Product Drugs for Overcoming Multidrug
 Resistance in Cancer. in Current Pharmaceutical Design. 2015;21(38):5589-5604.
doi:10.2174/1381612821666151002113546 .

Dinić, Jelena, Podolski-Renić, Ana, Stankovic, Tijana, Banković, Jasna Z., Pešić, Milica, "New Approaches With Natural Product Drugs for Overcoming Multidrug
 Resistance in Cancer" in Current Pharmaceutical Design, 21, no. 38 (2015):5589-5604,
https://doi.org/10.2174/1381612821666151002113546 . .

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 .

TY  - JOUR
AU  - Liu, Qing
AU  - Manzano, David
AU  - Tanić, Nikola
AU  - Pešić, Milica
AU  - Banković, Jasna Z.
AU  - Pateraki, Irini
AU  - Ricard, Lea
AU  - Ferrer, Albert
AU  - de Vos, Ric
AU  - van de Krol, Sander
AU  - Bouwmeester, Harro
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2218
AB  - Parthenolide, the main bioactive compound of the medicinal plant
   feverfew (Tanacetum parthenium), is a promising anti-cancer drug.
   However, the biosynthetic pathway of parthenolide has not been
   elucidated yet. Here we report on the isolation and characterization of
   all the genes from feverfew that are required for the biosynthesis of
   parthenolide, using a combination of 454 sequencing of a feverfew
   glandular trichome cDNA library, co-expression analysis and
   metabolomics. When parthenolide biosynthesis was reconstituted by
   transient co-expression of all pathway genes in Nicotiana benthamiana,
   up to 1.4 mu g g(-1) parthenolide was produced, mostly present as
   cysteine and glutathione conjugates. These relatively polar conjugates
   were highly active against colon cancer cells, with only slightly lower
   activity than free parthenolide. In addition to these biosynthetic
   genes, another gene encoding a costunolide and parthenolide 3
   beta-hydroxylase was identified opening up further options to improve
   the water solubility of parthenolide and therefore its potential as a
   drug. (C) 2014 International Metabolic Engineering Society. Published by
   Elsevier Inc. All rights reserved.
T2  - Metabolic Engineering
T1  - Elucidation and in planta reconstitution of the parthenolide
 biosynthetic pathway
VL  - 23
DO  - 10.1016/j.ymben.2014.03.005
SP  - 145
EP  - 153
ER  - 

@article{
author = "Liu, Qing and Manzano, David and Tanić, Nikola and Pešić, Milica and Banković, Jasna Z. and Pateraki, Irini and Ricard, Lea and Ferrer, Albert and de Vos, Ric and van de Krol, Sander and Bouwmeester, Harro",
year = "2014",
abstract = "Parthenolide, the main bioactive compound of the medicinal plant
   feverfew (Tanacetum parthenium), is a promising anti-cancer drug.
   However, the biosynthetic pathway of parthenolide has not been
   elucidated yet. Here we report on the isolation and characterization of
   all the genes from feverfew that are required for the biosynthesis of
   parthenolide, using a combination of 454 sequencing of a feverfew
   glandular trichome cDNA library, co-expression analysis and
   metabolomics. When parthenolide biosynthesis was reconstituted by
   transient co-expression of all pathway genes in Nicotiana benthamiana,
   up to 1.4 mu g g(-1) parthenolide was produced, mostly present as
   cysteine and glutathione conjugates. These relatively polar conjugates
   were highly active against colon cancer cells, with only slightly lower
   activity than free parthenolide. In addition to these biosynthetic
   genes, another gene encoding a costunolide and parthenolide 3
   beta-hydroxylase was identified opening up further options to improve
   the water solubility of parthenolide and therefore its potential as a
   drug. (C) 2014 International Metabolic Engineering Society. Published by
   Elsevier Inc. All rights reserved.",
journal = "Metabolic Engineering",
title = "Elucidation and in planta reconstitution of the parthenolide
 biosynthetic pathway",
volume = "23",
doi = "10.1016/j.ymben.2014.03.005",
pages = "145-153"
}

Liu, Q., Manzano, D., Tanić, N., Pešić, M., Banković, J. Z., Pateraki, I., Ricard, L., Ferrer, A., de Vos, R., van de Krol, S.,& Bouwmeester, H.. (2014). Elucidation and in planta reconstitution of the parthenolide
 biosynthetic pathway. in Metabolic Engineering, 23, 145-153.
https://doi.org/10.1016/j.ymben.2014.03.005

Liu Q, Manzano D, Tanić N, Pešić M, Banković JZ, Pateraki I, Ricard L, Ferrer A, de Vos R, van de Krol S, Bouwmeester H. Elucidation and in planta reconstitution of the parthenolide
 biosynthetic pathway. in Metabolic Engineering. 2014;23:145-153.
doi:10.1016/j.ymben.2014.03.005 .

Liu, Qing, Manzano, David, Tanić, Nikola, Pešić, Milica, Banković, Jasna Z., Pateraki, Irini, Ricard, Lea, Ferrer, Albert, de Vos, Ric, van de Krol, Sander, Bouwmeester, Harro, "Elucidation and in planta reconstitution of the parthenolide
 biosynthetic pathway" in Metabolic Engineering, 23 (2014):145-153,
https://doi.org/10.1016/j.ymben.2014.03.005 . .

TY  - JOUR
AU  - Milosevic, Zorica
AU  - Pešić, Milica
AU  - Stankovic, Tijana
AU  - Dinić, Jelena
AU  - Milovanovic, Zorka
AU  - Stojsic, Jelena
AU  - Džodić, Radan R.
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2133
AB  - Anaplastic thyroid carcinoma (ATC) is a rare, but aggressive and
   chemoresistant tumor with dismal prognosis. Most ATCs harbor mutations
   that activate RAS/MAPK/ERK and PI3K/AKT/mTOR pathways. Therefore, we
   investigated and correlated the expression of phosphatase and tensin
   homolog, pERK, and pAKT proteins as well as mutations of BRAF, RAS, and
   p53 genes in samples of patients with ATC. Furthermore, we evaluated the
   potential of inhibition of these pathways on chemosensitization of ATC
   using 2 thyroid carcinoma cell lines (FRO and SW1736). Our results
   revealed a negative correlation between the activity of RAS-MAPK-ERK and
   PI3K-AKT-mTOR pathways in samples of patients. To be specific, the
   PI3K-AKT-mTOR pathway was suppressed in patients with activated NRAS or
   high pERK expression. In vitro results suggest that the inhibition of
   either RAS-MAPK-ERK or PI3K-AKT-mTOR components may confer sensitivity
   of thyroid cancer cells to classic chemotherapeutics. This may form a
   basis for the development of novel genetic-based therapeutic approach
   for this cancer type.
T2  - Translational Research
T1  - Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma
IS  - 5
VL  - 164
DO  - 10.1016/j.trsl.2014.06.005
SP  - 411
EP  - 423
ER  - 

@article{
author = "Milosevic, Zorica and Pešić, Milica and Stankovic, Tijana and Dinić, Jelena and Milovanovic, Zorka and Stojsic, Jelena and Džodić, Radan R. and Tanić, Nikola and Banković, Jasna Z.",
year = "2014",
abstract = "Anaplastic thyroid carcinoma (ATC) is a rare, but aggressive and
   chemoresistant tumor with dismal prognosis. Most ATCs harbor mutations
   that activate RAS/MAPK/ERK and PI3K/AKT/mTOR pathways. Therefore, we
   investigated and correlated the expression of phosphatase and tensin
   homolog, pERK, and pAKT proteins as well as mutations of BRAF, RAS, and
   p53 genes in samples of patients with ATC. Furthermore, we evaluated the
   potential of inhibition of these pathways on chemosensitization of ATC
   using 2 thyroid carcinoma cell lines (FRO and SW1736). Our results
   revealed a negative correlation between the activity of RAS-MAPK-ERK and
   PI3K-AKT-mTOR pathways in samples of patients. To be specific, the
   PI3K-AKT-mTOR pathway was suppressed in patients with activated NRAS or
   high pERK expression. In vitro results suggest that the inhibition of
   either RAS-MAPK-ERK or PI3K-AKT-mTOR components may confer sensitivity
   of thyroid cancer cells to classic chemotherapeutics. This may form a
   basis for the development of novel genetic-based therapeutic approach
   for this cancer type.",
journal = "Translational Research",
title = "Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma",
number = "5",
volume = "164",
doi = "10.1016/j.trsl.2014.06.005",
pages = "411-423"
}

Milosevic, Z., Pešić, M., Stankovic, T., Dinić, J., Milovanovic, Z., Stojsic, J., Džodić, R. R., Tanić, N.,& Banković, J. Z.. (2014). Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma. in Translational Research, 164(5), 411-423.
https://doi.org/10.1016/j.trsl.2014.06.005

Milosevic Z, Pešić M, Stankovic T, Dinić J, Milovanovic Z, Stojsic J, Džodić RR, Tanić N, Banković JZ. Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma. in Translational Research. 2014;164(5):411-423.
doi:10.1016/j.trsl.2014.06.005 .

Milosevic, Zorica, Pešić, Milica, Stankovic, Tijana, Dinić, Jelena, Milovanovic, Zorka, Stojsic, Jelena, Džodić, Radan R., Tanić, Nikola, Banković, Jasna Z., "Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma" in Translational Research, 164, no. 5 (2014):411-423,
https://doi.org/10.1016/j.trsl.2014.06.005 . .

TY  - JOUR
AU  - Banković, Jasna Z.
AU  - Joerg, Andrae
AU  - Todorović, Nataša
AU  - Podolski-Renić, Ana
AU  - Milošević, Zorica Z.
AU  - Miljković, Đorđe
AU  - Krause, Jannike
AU  - Ruždijić, Sabera
AU  - Tanić, Nikola
AU  - Pešić, Milica
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1018
AB  - Most chemotherapeutics harm normal cells causing severe side effects and induce the development of resistance in cancer cells. Antimicrobial peptides (AMPs), recognized as anticancer agents, may overcome these limitations. The most studied mechanism underlying multidrug resistance (MDR) is the over-expression of cell membrane transporter P-glycoprotein (P-gp), which extrudes a variety of hydrophobic drugs. Additionally, P-gp contributes to cell membrane composition and increases the net negative charge on cell surface. We postulated that NK-lysin derived cationic peptide NK-2 might discriminate and preferentially eliminate P-gp over-expressing cancer cells. To test this hypothesis, we employed MDR non-small cell lung carcinoma (NCI-H460/R) and colorectal carcinoma (DLD1-TxR) cell lines with high P-gp expression. MDR cancer cells that survived NK-2 treatment had decreased P-gp expression and were more susceptible to doxorubicin. We found that NK-2 more readily eliminated P-gp high-expressing cells. Acting in 'carpet-like' manner NK-2 co-localized with P-gp on the MDR cancer cell membrane. The inhibition of P-gp reduced the NK-2 effect in MDR cancer cells and, vice versa, NK-2 decreased P-gp transport activity. In conclusion, NK-2 could modulate MDR in unique way, eliminating the P-gp high-expressing cells from heterogeneous cancers and making them more vulnerable to classical drug treatment. (C) 2012 Elsevier Inc. All rights reserved.
PB  - Elsevier
T2  - Experimental Cell Research
T1  - The elimination of P-glycoprotein over-expressing cancer cells by antimicrobial cationic peptide NK-2: The unique way of multi-drug resistance modulation
IS  - 7
VL  - 319
DO  - 10.1016/j.yexcr.2012.12.017
SP  - 1013
EP  - 1027
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1018
ER  - 

@article{
author = "Banković, Jasna Z. and Joerg, Andrae and Todorović, Nataša and Podolski-Renić, Ana and Milošević, Zorica Z. and Miljković, Đorđe and Krause, Jannike and Ruždijić, Sabera and Tanić, Nikola and Pešić, Milica",
year = "2013",
abstract = "Most chemotherapeutics harm normal cells causing severe side effects and induce the development of resistance in cancer cells. Antimicrobial peptides (AMPs), recognized as anticancer agents, may overcome these limitations. The most studied mechanism underlying multidrug resistance (MDR) is the over-expression of cell membrane transporter P-glycoprotein (P-gp), which extrudes a variety of hydrophobic drugs. Additionally, P-gp contributes to cell membrane composition and increases the net negative charge on cell surface. We postulated that NK-lysin derived cationic peptide NK-2 might discriminate and preferentially eliminate P-gp over-expressing cancer cells. To test this hypothesis, we employed MDR non-small cell lung carcinoma (NCI-H460/R) and colorectal carcinoma (DLD1-TxR) cell lines with high P-gp expression. MDR cancer cells that survived NK-2 treatment had decreased P-gp expression and were more susceptible to doxorubicin. We found that NK-2 more readily eliminated P-gp high-expressing cells. Acting in 'carpet-like' manner NK-2 co-localized with P-gp on the MDR cancer cell membrane. The inhibition of P-gp reduced the NK-2 effect in MDR cancer cells and, vice versa, NK-2 decreased P-gp transport activity. In conclusion, NK-2 could modulate MDR in unique way, eliminating the P-gp high-expressing cells from heterogeneous cancers and making them more vulnerable to classical drug treatment. (C) 2012 Elsevier Inc. All rights reserved.",
publisher = "Elsevier",
journal = "Experimental Cell Research",
title = "The elimination of P-glycoprotein over-expressing cancer cells by antimicrobial cationic peptide NK-2: The unique way of multi-drug resistance modulation",
number = "7",
volume = "319",
doi = "10.1016/j.yexcr.2012.12.017",
pages = "1013-1027",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1018"
}

Banković, J. Z., Joerg, A., Todorović, N., Podolski-Renić, A., Milošević, Z. Z., Miljković, Đ., Krause, J., Ruždijić, S., Tanić, N.,& Pešić, M.. (2013). The elimination of P-glycoprotein over-expressing cancer cells by antimicrobial cationic peptide NK-2: The unique way of multi-drug resistance modulation. in Experimental Cell Research
Elsevier., 319(7), 1013-1027.
https://doi.org/10.1016/j.yexcr.2012.12.017
https://hdl.handle.net/21.15107/rcub_ibiss_1018

Banković JZ, Joerg A, Todorović N, Podolski-Renić A, Milošević ZZ, Miljković Đ, Krause J, Ruždijić S, Tanić N, Pešić M. The elimination of P-glycoprotein over-expressing cancer cells by antimicrobial cationic peptide NK-2: The unique way of multi-drug resistance modulation. in Experimental Cell Research. 2013;319(7):1013-1027.
doi:10.1016/j.yexcr.2012.12.017
https://hdl.handle.net/21.15107/rcub_ibiss_1018 .

Banković, Jasna Z., Joerg, Andrae, Todorović, Nataša, Podolski-Renić, Ana, Milošević, Zorica Z., Miljković, Đorđe, Krause, Jannike, Ruždijić, Sabera, Tanić, Nikola, Pešić, Milica, "The elimination of P-glycoprotein over-expressing cancer cells by antimicrobial cationic peptide NK-2: The unique way of multi-drug resistance modulation" in Experimental Cell Research, 319, no. 7 (2013):1013-1027,
https://doi.org/10.1016/j.yexcr.2012.12.017 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1018 .

TY  - JOUR
AU  - Fischedick, Justin T
AU  - Pešić, Milica
AU  - Podolski-Renić, Ana
AU  - Banković, Jasna Z.
AU  - de Vos, Ric CH
AU  - Perić, Marija
AU  - Todorović, Slađana
AU  - Tanić, Nikola T
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1016
AB  - Five new sesquiterpene lactones (1-5) were isolated from Inula britannica collected in the wild from Serbia along with five known compounds (6-10). Sesquiterpene lactones were isolated using centrifugal partition chromatography followed by combination of flash chromatography and semi-preparative HPLC. Isolated compounds were screened for cytotoxic activity on four different human cancer cell lines and their multi-drug resistant counterparts, as well as on normal human keratinocytes. Sesquiterpene lactones showed similar cytotoxic activity toward drug sensitive and drug resistant cancer cell lines. (C) 2013 Phytochemical Society of Europe. Published by Elsevier B. V. All rights reserved.
T2  - Phytochemistry Letters
T1  - Cytotoxic activity of sesquiterpene lactones from Inula britannica on human cancer cell lines
IS  - 2
VL  - 6
SP  - 1
EP  - 252
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1016
ER  - 

@article{
author = "Fischedick, Justin T and Pešić, Milica and Podolski-Renić, Ana and Banković, Jasna Z. and de Vos, Ric CH and Perić, Marija and Todorović, Slađana and Tanić, Nikola T",
year = "2013",
abstract = "Five new sesquiterpene lactones (1-5) were isolated from Inula britannica collected in the wild from Serbia along with five known compounds (6-10). Sesquiterpene lactones were isolated using centrifugal partition chromatography followed by combination of flash chromatography and semi-preparative HPLC. Isolated compounds were screened for cytotoxic activity on four different human cancer cell lines and their multi-drug resistant counterparts, as well as on normal human keratinocytes. Sesquiterpene lactones showed similar cytotoxic activity toward drug sensitive and drug resistant cancer cell lines. (C) 2013 Phytochemical Society of Europe. Published by Elsevier B. V. All rights reserved.",
journal = "Phytochemistry Letters",
title = "Cytotoxic activity of sesquiterpene lactones from Inula britannica on human cancer cell lines",
number = "2",
volume = "6",
pages = "1-252",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1016"
}

Fischedick, J. T., Pešić, M., Podolski-Renić, A., Banković, J. Z., de Vos, R. C., Perić, M., Todorović, S.,& Tanić, N. T.. (2013). Cytotoxic activity of sesquiterpene lactones from Inula britannica on human cancer cell lines. in Phytochemistry Letters, 6(2), 1-252.
https://hdl.handle.net/21.15107/rcub_ibiss_1016

Fischedick JT, Pešić M, Podolski-Renić A, Banković JZ, de Vos RC, Perić M, Todorović S, Tanić NT. Cytotoxic activity of sesquiterpene lactones from Inula britannica on human cancer cell lines. in Phytochemistry Letters. 2013;6(2):1-252.
https://hdl.handle.net/21.15107/rcub_ibiss_1016 .

Fischedick, Justin T, Pešić, Milica, Podolski-Renić, Ana, Banković, Jasna Z., de Vos, Ric CH, Perić, Marija, Todorović, Slađana, Tanić, Nikola T, "Cytotoxic activity of sesquiterpene lactones from Inula britannica on human cancer cell lines" in Phytochemistry Letters, 6, no. 2 (2013):1-252,
https://hdl.handle.net/21.15107/rcub_ibiss_1016 .

TY  - JOUR
AU  - Milinković, Vedrana P.
AU  - Banković, Jasna Z.
AU  - Rakić, Miodrag L
AU  - Stanković, Tijana
AU  - Skender-Gazibara, Milica K
AU  - Ruždijić, Sabera
AU  - Tanić, Nikola T
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/938
AB  - Glioblastoma is the most frequent and malignant human brain tumor. High level of genomic instability detected in glioma cells implies that numerous genetic alterations accumulate during glioma pathogenesis. We investigated alterations in AP-PCR DNA profiles of 30 glioma patients, and detected specific changes in 11 genes not previously associated with this disease: LHFPL3, SGCG, HTR4, ITGB1, CPS1, PROS1, GP2, KCNG2, PDE4D, KIR3DL3, and INPP5A. Further correlations revealed that 8 genes might play important role in pathogenesis of glial tumors, while changes in GP2, KCNG2 and KIR3DL3 should be considered as passenger mutations, consequence of high level of genomic instability. Identified genes have a significant role in signal transduction or cell adhesion, which are important processes for cancer development and progression. According to our results, LHFPL3 might be characteristic of primary glioblastoma, SGCG, HTR4, ITGB1, CPS1, PROS1 and INPP5A were detected predominantly in anaplastic astrocytoma, suggesting their role in progression of secondary glioblastoma, while alterations of PDE4D seem to have important role in development of both glioblastoma subtypes. Some of the identified genes showed significant association with p53, p16, and EGFR, but there was no significant correlation between loss of PTEN and any of identified genes. In conclusion our study revealed genetic alterations that were not previously associated with glioma pathogenesis and could be potentially used as molecular markers of different glioblastoma subtypes.
T2  - Plos One
T1  - Identification of Novel Genetic Alterations in Samples of Malignant Glioma Patients
IS  - 12
VL  - 8
SP  - 977
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_938
ER  - 

@article{
author = "Milinković, Vedrana P. and Banković, Jasna Z. and Rakić, Miodrag L and Stanković, Tijana and Skender-Gazibara, Milica K and Ruždijić, Sabera and Tanić, Nikola T",
year = "2013",
abstract = "Glioblastoma is the most frequent and malignant human brain tumor. High level of genomic instability detected in glioma cells implies that numerous genetic alterations accumulate during glioma pathogenesis. We investigated alterations in AP-PCR DNA profiles of 30 glioma patients, and detected specific changes in 11 genes not previously associated with this disease: LHFPL3, SGCG, HTR4, ITGB1, CPS1, PROS1, GP2, KCNG2, PDE4D, KIR3DL3, and INPP5A. Further correlations revealed that 8 genes might play important role in pathogenesis of glial tumors, while changes in GP2, KCNG2 and KIR3DL3 should be considered as passenger mutations, consequence of high level of genomic instability. Identified genes have a significant role in signal transduction or cell adhesion, which are important processes for cancer development and progression. According to our results, LHFPL3 might be characteristic of primary glioblastoma, SGCG, HTR4, ITGB1, CPS1, PROS1 and INPP5A were detected predominantly in anaplastic astrocytoma, suggesting their role in progression of secondary glioblastoma, while alterations of PDE4D seem to have important role in development of both glioblastoma subtypes. Some of the identified genes showed significant association with p53, p16, and EGFR, but there was no significant correlation between loss of PTEN and any of identified genes. In conclusion our study revealed genetic alterations that were not previously associated with glioma pathogenesis and could be potentially used as molecular markers of different glioblastoma subtypes.",
journal = "Plos One",
title = "Identification of Novel Genetic Alterations in Samples of Malignant Glioma Patients",
number = "12",
volume = "8",
pages = "977-na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_938"
}

Milinković, V. P., Banković, J. Z., Rakić, M. L., Stanković, T., Skender-Gazibara, M. K., Ruždijić, S.,& Tanić, N. T.. (2013). Identification of Novel Genetic Alterations in Samples of Malignant Glioma Patients. in Plos One, 8(12), 977-na.
https://hdl.handle.net/21.15107/rcub_ibiss_938

Milinković VP, Banković JZ, Rakić ML, Stanković T, Skender-Gazibara MK, Ruždijić S, Tanić NT. Identification of Novel Genetic Alterations in Samples of Malignant Glioma Patients. in Plos One. 2013;8(12):977-na.
https://hdl.handle.net/21.15107/rcub_ibiss_938 .

Milinković, Vedrana P., Banković, Jasna Z., Rakić, Miodrag L, Stanković, Tijana, Skender-Gazibara, Milica K, Ruždijić, Sabera, Tanić, Nikola T, "Identification of Novel Genetic Alterations in Samples of Malignant Glioma Patients" in Plos One, 8, no. 12 (2013):977-na,
https://hdl.handle.net/21.15107/rcub_ibiss_938 .

TY  - CONF
AU  - Stojsić, Jelena
AU  - Milinković, Vedrana P.
AU  - Stojković, Sonja
AU  - Dinić, Jelena
AU  - Tanić, Nikola T
AU  - Banković, Jasna Z.
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/975
C3  - European Respiratory Journal
T1  - Loss of heterozygosity of PTEN in patients with non-small cell lung cancer treated and not treated with neoadjuvant chemotherapy
IS  - null
VL  - 42
SP  - 143
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_975
ER  - 

@conference{
author = "Stojsić, Jelena and Milinković, Vedrana P. and Stojković, Sonja and Dinić, Jelena and Tanić, Nikola T and Banković, Jasna Z.",
year = "2013",
journal = "European Respiratory Journal",
title = "Loss of heterozygosity of PTEN in patients with non-small cell lung cancer treated and not treated with neoadjuvant chemotherapy",
number = "null",
volume = "42",
pages = "143-na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_975"
}

Stojsić, J., Milinković, V. P., Stojković, S., Dinić, J., Tanić, N. T.,& Banković, J. Z.. (2013). Loss of heterozygosity of PTEN in patients with non-small cell lung cancer treated and not treated with neoadjuvant chemotherapy. in European Respiratory Journal, 42(null), 143-na.
https://hdl.handle.net/21.15107/rcub_ibiss_975

Stojsić J, Milinković VP, Stojković S, Dinić J, Tanić NT, Banković JZ. Loss of heterozygosity of PTEN in patients with non-small cell lung cancer treated and not treated with neoadjuvant chemotherapy. in European Respiratory Journal. 2013;42(null):143-na.
https://hdl.handle.net/21.15107/rcub_ibiss_975 .

Stojsić, Jelena, Milinković, Vedrana P., Stojković, Sonja, Dinić, Jelena, Tanić, Nikola T, Banković, Jasna Z., "Loss of heterozygosity of PTEN in patients with non-small cell lung cancer treated and not treated with neoadjuvant chemotherapy" in European Respiratory Journal, 42, no. null (2013):143-na,
https://hdl.handle.net/21.15107/rcub_ibiss_975 .

TY  - CONF
AU  - Ruždijić, Sabera
AU  - Banković, Jasna Z.
AU  - Podolski-Renić, Ana
AU  - Pešić, Milica
AU  - Milošević, Zorica Z.
AU  - Tanić, Nikola T
AU  - Andra, J
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1161
C3  - European Journal of Cancer
T1  - NK-lysin Derived Peptide (NK-2) Sensitizes Resistant Cancer Cells to Classic Chemotherapeutics by Selective Killing of P-glycoprotein Over-expressing Cells
IS  - null
VL  - 48
EP  - S225
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1161
ER  - 

@conference{
author = "Ruždijić, Sabera and Banković, Jasna Z. and Podolski-Renić, Ana and Pešić, Milica and Milošević, Zorica Z. and Tanić, Nikola T and Andra, J",
year = "2012",
journal = "European Journal of Cancer",
title = "NK-lysin Derived Peptide (NK-2) Sensitizes Resistant Cancer Cells to Classic Chemotherapeutics by Selective Killing of P-glycoprotein Over-expressing Cells",
number = "null",
volume = "48",
pages = "S225",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1161"
}

Ruždijić, S., Banković, J. Z., Podolski-Renić, A., Pešić, M., Milošević, Z. Z., Tanić, N. T.,& Andra, J.. (2012). NK-lysin Derived Peptide (NK-2) Sensitizes Resistant Cancer Cells to Classic Chemotherapeutics by Selective Killing of P-glycoprotein Over-expressing Cells. in European Journal of Cancer, 48(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1161

Ruždijić S, Banković JZ, Podolski-Renić A, Pešić M, Milošević ZZ, Tanić NT, Andra J. NK-lysin Derived Peptide (NK-2) Sensitizes Resistant Cancer Cells to Classic Chemotherapeutics by Selective Killing of P-glycoprotein Over-expressing Cells. in European Journal of Cancer. 2012;48(null):null-S225.
https://hdl.handle.net/21.15107/rcub_ibiss_1161 .

Ruždijić, Sabera, Banković, Jasna Z., Podolski-Renić, Ana, Pešić, Milica, Milošević, Zorica Z., Tanić, Nikola T, Andra, J, "NK-lysin Derived Peptide (NK-2) Sensitizes Resistant Cancer Cells to Classic Chemotherapeutics by Selective Killing of P-glycoprotein Over-expressing Cells" in European Journal of Cancer, 48, no. null (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1161 .

TY  - CONF
AU  - Podolski-Renić, Ana
AU  - Pešić, Milica
AU  - Chiourea, M
AU  - Banković, Jasna Z.
AU  - Anđelković, Tijana
AU  - Milošević, Zorica Z.
AU  - Milinković, Vedrana P.
AU  - Gagos, S
AU  - Tanić, Nikola T
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1162
C3  - European Journal of Cancer
T1  - Characterization of Newly Established P-glycoprotein Over-expressing Multi-drug Resistant Human Cancer Cell Lines
IS  - null
VL  - 48
EP  - S244
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1162
ER  - 

@conference{
author = "Podolski-Renić, Ana and Pešić, Milica and Chiourea, M and Banković, Jasna Z. and Anđelković, Tijana and Milošević, Zorica Z. and Milinković, Vedrana P. and Gagos, S and Tanić, Nikola T",
year = "2012",
journal = "European Journal of Cancer",
title = "Characterization of Newly Established P-glycoprotein Over-expressing Multi-drug Resistant Human Cancer Cell Lines",
number = "null",
volume = "48",
pages = "S244",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1162"
}

Podolski-Renić, A., Pešić, M., Chiourea, M., Banković, J. Z., Anđelković, T., Milošević, Z. Z., Milinković, V. P., Gagos, S.,& Tanić, N. T.. (2012). Characterization of Newly Established P-glycoprotein Over-expressing Multi-drug Resistant Human Cancer Cell Lines. in European Journal of Cancer, 48(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1162

Podolski-Renić A, Pešić M, Chiourea M, Banković JZ, Anđelković T, Milošević ZZ, Milinković VP, Gagos S, Tanić NT. Characterization of Newly Established P-glycoprotein Over-expressing Multi-drug Resistant Human Cancer Cell Lines. in European Journal of Cancer. 2012;48(null):null-S244.
https://hdl.handle.net/21.15107/rcub_ibiss_1162 .

Podolski-Renić, Ana, Pešić, Milica, Chiourea, M, Banković, Jasna Z., Anđelković, Tijana, Milošević, Zorica Z., Milinković, Vedrana P., Gagos, S, Tanić, Nikola T, "Characterization of Newly Established P-glycoprotein Over-expressing Multi-drug Resistant Human Cancer Cell Lines" in European Journal of Cancer, 48, no. null (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1162 .

TY  - JOUR
AU  - Milinković, Vedrana P.
AU  - Banković, Jasna Z.
AU  - Rakić, Miodrag L
AU  - Milosević, Nebojsa T
AU  - Stanković, Tijana
AU  - Joković, Milos B
AU  - Milošević, Zorica Z.
AU  - Skender-Gazibara, Milica K
AU  - Podolski-Renić, Ana
AU  - Pešić, Milica
AU  - Ruždijić, Sabera
AU  - Tanić, Nikola T
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1108
AB  - The purpose of this study was to detect the level of genomic instability and p53 alterations in anaplastic astrocytoma and primary glioblastoma patients, and to evaluate their impact on glioma pathogenesis and patients outcome. AP-PCR DNA profiling revealed two types of genetic differences between tumor and normal tissue: qualitative changes which represent accumulation of changes in DNA sequence and are the manifestation of microsatellite and point mutation instability (MIN-PIN) and quantitative changes which represent amplifications or deletions of existing chromosomal material and are the manifestation of chromosomal instability (CIN). Both types of alterations were present in all analyzed samples contributing almost equally to the total level of genomic instability, and showing no differences between histological subtypes. p53 alterations were detected in 40% of samples, predominantly in anaplastic astrocytoma. The higher level of genomic instability was observed in elderly patients (>50 years) and patents with primary glioblastoma. Level of genomic instability had no impact on patients' survival, while presence of p53 alterations seemed to be a favorable prognostic factor in this case. Our results indicate that extensive genomic instability is one of the main features of malignant gliomas. (C) 2012 Elsevier Inc. All rights reserved.
T2  - Experimental and Molecular Pathology
T1  - Genomic instability and p53 alterations in patients with malignant glioma
IS  - 2
VL  - 93
SP  - 67
EP  - 206
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1108
ER  - 

@article{
author = "Milinković, Vedrana P. and Banković, Jasna Z. and Rakić, Miodrag L and Milosević, Nebojsa T and Stanković, Tijana and Joković, Milos B and Milošević, Zorica Z. and Skender-Gazibara, Milica K and Podolski-Renić, Ana and Pešić, Milica and Ruždijić, Sabera and Tanić, Nikola T",
year = "2012",
abstract = "The purpose of this study was to detect the level of genomic instability and p53 alterations in anaplastic astrocytoma and primary glioblastoma patients, and to evaluate their impact on glioma pathogenesis and patients outcome. AP-PCR DNA profiling revealed two types of genetic differences between tumor and normal tissue: qualitative changes which represent accumulation of changes in DNA sequence and are the manifestation of microsatellite and point mutation instability (MIN-PIN) and quantitative changes which represent amplifications or deletions of existing chromosomal material and are the manifestation of chromosomal instability (CIN). Both types of alterations were present in all analyzed samples contributing almost equally to the total level of genomic instability, and showing no differences between histological subtypes. p53 alterations were detected in 40% of samples, predominantly in anaplastic astrocytoma. The higher level of genomic instability was observed in elderly patients (>50 years) and patents with primary glioblastoma. Level of genomic instability had no impact on patients' survival, while presence of p53 alterations seemed to be a favorable prognostic factor in this case. Our results indicate that extensive genomic instability is one of the main features of malignant gliomas. (C) 2012 Elsevier Inc. All rights reserved.",
journal = "Experimental and Molecular Pathology",
title = "Genomic instability and p53 alterations in patients with malignant glioma",
number = "2",
volume = "93",
pages = "67-206",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1108"
}

Milinković, V. P., Banković, J. Z., Rakić, M. L., Milosević, N. T., Stanković, T., Joković, M. B., Milošević, Z. Z., Skender-Gazibara, M. K., Podolski-Renić, A., Pešić, M., Ruždijić, S.,& Tanić, N. T.. (2012). Genomic instability and p53 alterations in patients with malignant glioma. in Experimental and Molecular Pathology, 93(2), 67-206.
https://hdl.handle.net/21.15107/rcub_ibiss_1108

Milinković VP, Banković JZ, Rakić ML, Milosević NT, Stanković T, Joković MB, Milošević ZZ, Skender-Gazibara MK, Podolski-Renić A, Pešić M, Ruždijić S, Tanić NT. Genomic instability and p53 alterations in patients with malignant glioma. in Experimental and Molecular Pathology. 2012;93(2):67-206.
https://hdl.handle.net/21.15107/rcub_ibiss_1108 .

Milinković, Vedrana P., Banković, Jasna Z., Rakić, Miodrag L, Milosević, Nebojsa T, Stanković, Tijana, Joković, Milos B, Milošević, Zorica Z., Skender-Gazibara, Milica K, Podolski-Renić, Ana, Pešić, Milica, Ruždijić, Sabera, Tanić, Nikola T, "Genomic instability and p53 alterations in patients with malignant glioma" in Experimental and Molecular Pathology, 93, no. 2 (2012):67-206,
https://hdl.handle.net/21.15107/rcub_ibiss_1108 .

TY  - CONF
AU  - Banković, Jasna Z.
AU  - Stojsić, Jelena M
AU  - Ruždijić, Sabera
AU  - Tanić, Nikola T
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1431
C3  - Ejc Supplements
T1  - Identification of altered genes associated with non-small cell lung cancer promotion and progression
IS  - 2
VL  - 7
EP  - 110
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1431
ER  - 

@conference{
author = "Banković, Jasna Z. and Stojsić, Jelena M and Ruždijić, Sabera and Tanić, Nikola T",
year = "2009",
journal = "Ejc Supplements",
title = "Identification of altered genes associated with non-small cell lung cancer promotion and progression",
number = "2",
volume = "7",
pages = "110",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1431"
}

Banković, J. Z., Stojsić, J. M., Ruždijić, S.,& Tanić, N. T.. (2009). Identification of altered genes associated with non-small cell lung cancer promotion and progression. in Ejc Supplements, 7(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1431

Banković JZ, Stojsić JM, Ruždijić S, Tanić NT. Identification of altered genes associated with non-small cell lung cancer promotion and progression. in Ejc Supplements. 2009;7(2):null-110.
https://hdl.handle.net/21.15107/rcub_ibiss_1431 .

Banković, Jasna Z., Stojsić, Jelena M, Ruždijić, Sabera, Tanić, Nikola T, "Identification of altered genes associated with non-small cell lung cancer promotion and progression" in Ejc Supplements, 7, no. 2 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1431 .

TY  - CONF
AU  - Anđelković, Tijana
AU  - Pešić, Milica
AU  - Banković, Jasna Z.
AU  - Tanić, Nikola T
AU  - Ruždijić, Sabera
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1580
C3  - Ejc Supplements
T1  - Effect of sulfinosine [(R,S)-2-amino-9-beta-D-ribofuranosylpurine-6-sulfinamide] on lung carcinoma cell lines and its role in overcoming multidrug resistance
IS  - 4
VL  - 5
EP  - 71
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1580
ER  - 

@conference{
author = "Anđelković, Tijana and Pešić, Milica and Banković, Jasna Z. and Tanić, Nikola T and Ruždijić, Sabera",
year = "2007",
journal = "Ejc Supplements",
title = "Effect of sulfinosine [(R,S)-2-amino-9-beta-D-ribofuranosylpurine-6-sulfinamide] on lung carcinoma cell lines and its role in overcoming multidrug resistance",
number = "4",
volume = "5",
pages = "71",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1580"
}

Anđelković, T., Pešić, M., Banković, J. Z., Tanić, N. T.,& Ruždijić, S.. (2007). Effect of sulfinosine [(R,S)-2-amino-9-beta-D-ribofuranosylpurine-6-sulfinamide] on lung carcinoma cell lines and its role in overcoming multidrug resistance. in Ejc Supplements, 5(4).
https://hdl.handle.net/21.15107/rcub_ibiss_1580

Anđelković T, Pešić M, Banković JZ, Tanić NT, Ruždijić S. Effect of sulfinosine [(R,S)-2-amino-9-beta-D-ribofuranosylpurine-6-sulfinamide] on lung carcinoma cell lines and its role in overcoming multidrug resistance. in Ejc Supplements. 2007;5(4):null-71.
https://hdl.handle.net/21.15107/rcub_ibiss_1580 .

Anđelković, Tijana, Pešić, Milica, Banković, Jasna Z., Tanić, Nikola T, Ruždijić, Sabera, "Effect of sulfinosine [(R,S)-2-amino-9-beta-D-ribofuranosylpurine-6-sulfinamide] on lung carcinoma cell lines and its role in overcoming multidrug resistance" in Ejc Supplements, 5, no. 4 (2007),
https://hdl.handle.net/21.15107/rcub_ibiss_1580 .

TY  - CONF
AU  - Banković, Jasna Z.
AU  - Stojsić, Jelena M
AU  - Zunić, Svetlana S
AU  - Selaković, I
AU  - Paunović, V
AU  - Ruždijić, Sabera
AU  - Tanić, Nikola T
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1581
C3  - Ejc Supplements
T1  - Genomic instability in non-small cell lung cancer assessed by arbitrarily primed polymerase chain reaction
IS  - 4
VL  - 5
EP  - 74
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1581
ER  - 

@conference{
author = "Banković, Jasna Z. and Stojsić, Jelena M and Zunić, Svetlana S and Selaković, I and Paunović, V and Ruždijić, Sabera and Tanić, Nikola T",
year = "2007",
journal = "Ejc Supplements",
title = "Genomic instability in non-small cell lung cancer assessed by arbitrarily primed polymerase chain reaction",
number = "4",
volume = "5",
pages = "74",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1581"
}

Banković, J. Z., Stojsić, J. M., Zunić, S. S., Selaković, I., Paunović, V., Ruždijić, S.,& Tanić, N. T.. (2007). Genomic instability in non-small cell lung cancer assessed by arbitrarily primed polymerase chain reaction. in Ejc Supplements, 5(4).
https://hdl.handle.net/21.15107/rcub_ibiss_1581

Banković JZ, Stojsić JM, Zunić SS, Selaković I, Paunović V, Ruždijić S, Tanić NT. Genomic instability in non-small cell lung cancer assessed by arbitrarily primed polymerase chain reaction. in Ejc Supplements. 2007;5(4):null-74.
https://hdl.handle.net/21.15107/rcub_ibiss_1581 .

Banković, Jasna Z., Stojsić, Jelena M, Zunić, Svetlana S, Selaković, I, Paunović, V, Ruždijić, Sabera, Tanić, Nikola T, "Genomic instability in non-small cell lung cancer assessed by arbitrarily primed polymerase chain reaction" in Ejc Supplements, 5, no. 4 (2007),
https://hdl.handle.net/21.15107/rcub_ibiss_1581 .