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  - GEN
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Petrić, Marija
AU  - Radojković, Dragica
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2017
UR  - http://link.springer.com/10.1007/s00418-017-1590-4
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2796
AB  - Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.
T2  - Histochemistry and Cell Biology
T1  - Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells
DO  - 10.1007/s00418-017-1590-4
ER  - 

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

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

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

Divac Rankov, Aleksandra, Ljujić, Mila, Petrić, Marija, Radojković, Dragica, Pešić, Milica, Dinić, Jelena, "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells" in Histochemistry and Cell Biology (2017),
https://doi.org/10.1007/s00418-017-1590-4 . .

TY  - JOUR
AU  - Ljujić, Mila
AU  - Mijatović, Sanja
AU  - Bulatović, Mirna
AU  - Mojić, Marija
AU  - Maksimović-Ivanić, Danijela
AU  - Radojković, Dragica
AU  - Topić, Aleksandra
PY  - 2017
UR  - http://link.springer.com/10.1007/s12253-016-0104-3
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2729
AB  - Increased circulating alpha-1-antitrypsin (AAT) correlates with cancer stage/aggressiveness, but its role in cancer biology is unclear. We revealed antagonistic effect of AAT to cisplatin-induced cytotoxicity in prostate (PC3) and melanoma (A375) cancer cell lines. Moreover, AAT abrogated cytotoxicity of MEK inhibitor U0126 in PC3 cell line. Weaker antagonistic effect of AAT on cytotoxicity of PI3/Akt and NF-kB inhibitors was also observed. In addition, cisplatin increased AAT gene expression in transfected PC3 cells. However, AAT derived from transfected PC3 cells did not antagonize cisplatin-induced cytotoxicity. In conclusion, these results suggest possible association between high circulating AAT and cisplatin resistance.
T2  - Pathology & Oncology Research
T1  - Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines
IS  - 2
VL  - 23
DO  - 10.1007/s12253-016-0104-3
SP  - 335
EP  - 343
ER  - 

@article{
author = "Ljujić, Mila and Mijatović, Sanja and Bulatović, Mirna and Mojić, Marija and Maksimović-Ivanić, Danijela and Radojković, Dragica and Topić, Aleksandra",
year = "2017",
abstract = "Increased circulating alpha-1-antitrypsin (AAT) correlates with cancer stage/aggressiveness, but its role in cancer biology is unclear. We revealed antagonistic effect of AAT to cisplatin-induced cytotoxicity in prostate (PC3) and melanoma (A375) cancer cell lines. Moreover, AAT abrogated cytotoxicity of MEK inhibitor U0126 in PC3 cell line. Weaker antagonistic effect of AAT on cytotoxicity of PI3/Akt and NF-kB inhibitors was also observed. In addition, cisplatin increased AAT gene expression in transfected PC3 cells. However, AAT derived from transfected PC3 cells did not antagonize cisplatin-induced cytotoxicity. In conclusion, these results suggest possible association between high circulating AAT and cisplatin resistance.",
journal = "Pathology & Oncology Research",
title = "Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines",
number = "2",
volume = "23",
doi = "10.1007/s12253-016-0104-3",
pages = "335-343"
}

Ljujić, M., Mijatović, S., Bulatović, M., Mojić, M., Maksimović-Ivanić, D., Radojković, D.,& Topić, A.. (2017). Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines. in Pathology & Oncology Research, 23(2), 335-343.
https://doi.org/10.1007/s12253-016-0104-3

Ljujić M, Mijatović S, Bulatović M, Mojić M, Maksimović-Ivanić D, Radojković D, Topić A. Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines. in Pathology & Oncology Research. 2017;23(2):335-343.
doi:10.1007/s12253-016-0104-3 .

Ljujić, Mila, Mijatović, Sanja, Bulatović, Mirna, Mojić, Marija, Maksimović-Ivanić, Danijela, Radojković, Dragica, Topić, Aleksandra, "Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines" in Pathology & Oncology Research, 23, no. 2 (2017):335-343,
https://doi.org/10.1007/s12253-016-0104-3 . .

TY  - JOUR
AU  - Đorđević, Valentina
AU  - Timotijević, Gordana
AU  - Pruner, Iva
AU  - Radojković, Dragica
AU  - Milovanović, Boško
AU  - Miljković, Đorđe
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/503
AB  - Background: The mutant CCR5Δ32 allele confers resistance to HIV infection. Several hypotheses regarding its origin and persistence in the human population have been proposed. It is assumed that the Δ32 mutation was introduced in Northern or Eastern Europe and that it spread to the south. Although the frequency of CCR5Δ32 was determined in numerous European nations and regions, further data are needed to complete the puzzle of CCR5Δ32 distribution within the continent. Methods: To this end, CCR5Δ32 frequency was determined in a Serbian population (sample size 352). DNA was extracted from peripheral whole blood and polymerase chain reaction specific for CCR5 gene was performed. A reaction product of 263 bp was obtained from the wild­type CCR5 sequence and a product of 231 bp was obtained from the truncated CCR5Δ32 sequence. Results: Overall allele frequency of CCR5Δ32 is 4.55%; 0.57% of individuals in the examined population are homozygous and 8.52% are heterozygous for CCR5Δ32. Conclusions: The determined frequency of the CCR5Δ32 allele in a Serbian population is unexpectedly low, considering ethnically related populations.
AB  - Uvod: Nosioci alela CCR5Δ32 su relativno rezistentni na infekciju HIV-om. Postoji nekoliko hipoteza o poreklu i održanju ovog alela u ljudskoj populaciji. Pretpostavlja se da je mutacija Δ32 nastala u populaciji severne ili istočne Evrope i da se potom proširila ka jugu. Iako je učestalost CCR5Δ32 određena u mnogim evropskim populacijama, dodatni podaci su neophodni za formiranje sveobuhvatne slike o distribuciji CCR5Δ32 u Evropi. Zbog toga smo u našoj studiji odredili učestalost CCR5Δ32 u srpskoj populaciji, za koju do ovog rada nisu postojali takvi podaci. Metode: DNK je izolovana iz periferne krvi 352 osobe. U reakciji lančanog umnožavanja korišćeni su prajmeri specifični za gen CCR5. Dobijen je proizvod od 263 bp na osnovu matrice 'wild type', sekvence CCR5 gena, a proizvod od 231 bp na osnovu okrnjene sekvence gena CCR5 (CCR5Δ32). Ukupna učestalost alela CCR5Δ32 u srpskoj populaciji iznosi 4,55%. Rezultati: Od ukupnog broja analiziranih osoba, identifikovano je 8,52% heterozigotnih i 0,57% homozigotnih nosilaca za ovaj alel. Zaključak: Utvrđena učestalost alela CCR5Δ32 u srpskoj populaciji je neočekivano niska, u poređenju sa učestalošću u ostalim slovenskim populacijama.
T2  - Journal of Medical Biochemistry
T1  - Učestalost alela CCR5Δ32 u srpskoj populaciji
T1  - The frequency of allele CCR5Δ32 in a Serbian population
IS  - 4
VL  - 32
DO  - 10.2478/jomb-2013-0030
SP  - 368
EP  - 374
ER  - 

@article{
author = "Đorđević, Valentina and Timotijević, Gordana and Pruner, Iva and Radojković, Dragica and Milovanović, Boško and Miljković, Đorđe",
year = "2013, 2013",
abstract = "Background: The mutant CCR5Δ32 allele confers resistance to HIV infection. Several hypotheses regarding its origin and persistence in the human population have been proposed. It is assumed that the Δ32 mutation was introduced in Northern or Eastern Europe and that it spread to the south. Although the frequency of CCR5Δ32 was determined in numerous European nations and regions, further data are needed to complete the puzzle of CCR5Δ32 distribution within the continent. Methods: To this end, CCR5Δ32 frequency was determined in a Serbian population (sample size 352). DNA was extracted from peripheral whole blood and polymerase chain reaction specific for CCR5 gene was performed. A reaction product of 263 bp was obtained from the wild­type CCR5 sequence and a product of 231 bp was obtained from the truncated CCR5Δ32 sequence. Results: Overall allele frequency of CCR5Δ32 is 4.55%; 0.57% of individuals in the examined population are homozygous and 8.52% are heterozygous for CCR5Δ32. Conclusions: The determined frequency of the CCR5Δ32 allele in a Serbian population is unexpectedly low, considering ethnically related populations., Uvod: Nosioci alela CCR5Δ32 su relativno rezistentni na infekciju HIV-om. Postoji nekoliko hipoteza o poreklu i održanju ovog alela u ljudskoj populaciji. Pretpostavlja se da je mutacija Δ32 nastala u populaciji severne ili istočne Evrope i da se potom proširila ka jugu. Iako je učestalost CCR5Δ32 određena u mnogim evropskim populacijama, dodatni podaci su neophodni za formiranje sveobuhvatne slike o distribuciji CCR5Δ32 u Evropi. Zbog toga smo u našoj studiji odredili učestalost CCR5Δ32 u srpskoj populaciji, za koju do ovog rada nisu postojali takvi podaci. Metode: DNK je izolovana iz periferne krvi 352 osobe. U reakciji lančanog umnožavanja korišćeni su prajmeri specifični za gen CCR5. Dobijen je proizvod od 263 bp na osnovu matrice 'wild type', sekvence CCR5 gena, a proizvod od 231 bp na osnovu okrnjene sekvence gena CCR5 (CCR5Δ32). Ukupna učestalost alela CCR5Δ32 u srpskoj populaciji iznosi 4,55%. Rezultati: Od ukupnog broja analiziranih osoba, identifikovano je 8,52% heterozigotnih i 0,57% homozigotnih nosilaca za ovaj alel. Zaključak: Utvrđena učestalost alela CCR5Δ32 u srpskoj populaciji je neočekivano niska, u poređenju sa učestalošću u ostalim slovenskim populacijama.",
journal = "Journal of Medical Biochemistry",
title = "Učestalost alela CCR5Δ32 u srpskoj populaciji, The frequency of allele CCR5Δ32 in a Serbian population",
number = "4",
volume = "32",
doi = "10.2478/jomb-2013-0030",
pages = "368-374"
}

Đorđević, V., Timotijević, G., Pruner, I., Radojković, D., Milovanović, B.,& Miljković, Đ.. (2013). Učestalost alela CCR5Δ32 u srpskoj populaciji. in Journal of Medical Biochemistry, 32(4), 368-374.
https://doi.org/10.2478/jomb-2013-0030

Đorđević V, Timotijević G, Pruner I, Radojković D, Milovanović B, Miljković Đ. Učestalost alela CCR5Δ32 u srpskoj populaciji. in Journal of Medical Biochemistry. 2013;32(4):368-374.
doi:10.2478/jomb-2013-0030 .

Đorđević, Valentina, Timotijević, Gordana, Pruner, Iva, Radojković, Dragica, Milovanović, Boško, Miljković, Đorđe, "Učestalost alela CCR5Δ32 u srpskoj populaciji" in Journal of Medical Biochemistry, 32, no. 4 (2013):368-374,
https://doi.org/10.2478/jomb-2013-0030 . .