TY  - CONF
AU  - Jovanović, Irena
AU  - Nedeljković, Milica
AU  - Medić-Milijić, Nataša
AU  - Spurnić, Igor
AU  - Milovanović, Zorka
AU  - Tomić, Tijana
AU  - Tanić, Nasta
AU  - Tanić, Nikola
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12633
AB  - Background: Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negaƟ ve breast cancer (TNBC) is the most aggressive breast cancer subtype and is associated with high recurrence rates, high incidence of distant metastases and poor overall survival. The aim of this study was to invesƟ gate the role of cludin 3, claudin 4 and claudin 7 in TNBC promoƟ on and progression. Claudins are Ɵ ght juncƟ on (TJ) integral membrane proteins that are key regulators of the paracellular pathway. Materials and methods: This is a retrospecƟ ve analysis of 125 paƟ ents with triple-negaƟ ve breast cancer operated at the InsƟ tute of Oncology and Radiology of Serbia in the period from 2009 to 2014. The expression of claudin 3, 4 and 7 was observed using the immunohistochemical staining method. The Allred scoring system was used with cut-off values: ≤4 and >4 (low/ high expression). Results: Our results showed that the expression of claudins 3 and 4 correlate with higher nuclear gradus and low desease free interval (DFI). More over, the expression of claudin 3 and claudin 4 correlates (Spearman test p˂0.0001). In addiƟ on, high expression of claudin 7 is signifi cantly related to low DFI of paƟ ents (p˂0.005) and distant metastases. Conclusions: We concluded that claudin 3, claudin 4 and claudin 7 have signifi cant impact on TNBC progression. Namely, elevated expression of these proteins signifi cantly correlates with low DFI and distant metastases. In other words, elevated expression of claudins is a bad news for TNBC paƟ ents. Therefore, the expression of claudins could be a good prognosƟ c marker for TNBC paƟ ents and potential target for future therapy protocols.
PB  - Belgrade : Serbian Association for Cancer Research
C3  - Oncology Insights
T1  - Role of claudins 3,4 and 7 in triple negative breast cancer progression
IS  - 1
SP  - 63
EP  - 63
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12633
ER  - 

@conference{
author = "Jovanović, Irena and Nedeljković, Milica and Medić-Milijić, Nataša and Spurnić, Igor and Milovanović, Zorka and Tomić, Tijana and Tanić, Nasta and Tanić, Nikola",
year = "2023",
abstract = "Background: Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negaƟ ve breast cancer (TNBC) is the most aggressive breast cancer subtype and is associated with high recurrence rates, high incidence of distant metastases and poor overall survival. The aim of this study was to invesƟ gate the role of cludin 3, claudin 4 and claudin 7 in TNBC promoƟ on and progression. Claudins are Ɵ ght juncƟ on (TJ) integral membrane proteins that are key regulators of the paracellular pathway. Materials and methods: This is a retrospecƟ ve analysis of 125 paƟ ents with triple-negaƟ ve breast cancer operated at the InsƟ tute of Oncology and Radiology of Serbia in the period from 2009 to 2014. The expression of claudin 3, 4 and 7 was observed using the immunohistochemical staining method. The Allred scoring system was used with cut-off values: ≤4 and >4 (low/ high expression). Results: Our results showed that the expression of claudins 3 and 4 correlate with higher nuclear gradus and low desease free interval (DFI). More over, the expression of claudin 3 and claudin 4 correlates (Spearman test p˂0.0001). In addiƟ on, high expression of claudin 7 is signifi cantly related to low DFI of paƟ ents (p˂0.005) and distant metastases. Conclusions: We concluded that claudin 3, claudin 4 and claudin 7 have signifi cant impact on TNBC progression. Namely, elevated expression of these proteins signifi cantly correlates with low DFI and distant metastases. In other words, elevated expression of claudins is a bad news for TNBC paƟ ents. Therefore, the expression of claudins could be a good prognosƟ c marker for TNBC paƟ ents and potential target for future therapy protocols.",
publisher = "Belgrade : Serbian Association for Cancer Research",
journal = "Oncology Insights",
title = "Role of claudins 3,4 and 7 in triple negative breast cancer progression",
number = "1",
pages = "63-63",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12633"
}

Jovanović, I., Nedeljković, M., Medić-Milijić, N., Spurnić, I., Milovanović, Z., Tomić, T., Tanić, N.,& Tanić, N.. (2023). Role of claudins 3,4 and 7 in triple negative breast cancer progression. in Oncology Insights
Belgrade : Serbian Association for Cancer Research.(1), 63-63.
https://hdl.handle.net/21.15107/rcub_vinar_12633

Jovanović I, Nedeljković M, Medić-Milijić N, Spurnić I, Milovanović Z, Tomić T, Tanić N, Tanić N. Role of claudins 3,4 and 7 in triple negative breast cancer progression. in Oncology Insights. 2023;(1):63-63.
https://hdl.handle.net/21.15107/rcub_vinar_12633 .

Jovanović, Irena, Nedeljković, Milica, Medić-Milijić, Nataša, Spurnić, Igor, Milovanović, Zorka, Tomić, Tijana, Tanić, Nasta, Tanić, Nikola, "Role of claudins 3,4 and 7 in triple negative breast cancer progression" in Oncology Insights, no. 1 (2023):63-63,
https://hdl.handle.net/21.15107/rcub_vinar_12633 .

TY  - CONF
AU  - Ademović, Nejla
AU  - Tomić, Tijana
AU  - Tanić, Nasta
AU  - Milić, Marina
AU  - Rakić, Miodrag
AU  - Tanić, Nikola
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12638
AB  - Introduction: Glioblastoma and Astrocytoma are diff use malignant brain tumors and characterized as the most aggressive and invasive brain cancers. Glioblastoma IDH wild-type is a primary brain tumour that develops de novo, and Astrocytoma IDH mutant is a secondary tumour which arises by progression from lower tumour grades. They are characterized by poor survival, resistance to therapy and poor prognosis which develops as a consequence of genomic instability. Genomic instability also contributes to tumour heterogeneity and provides the genomic diversity necessary for selecƟ on. Materials and methods: 31 paƟ ents with Glioblastoma IDH wild-type and Astrocytoma IDH mutant, grade 3 and 4, were analysed for the presence of genomic instability using AP-PCR, DNA profi ling method. Comparing DNA profi les between tumour Ɵ ssue and normal Ɵ ssue (blood) of the same paƟ ent, we detected qualitaƟ ve and quanƟ taƟ ve changes. QualitaƟ ve changes are detected as the presence and absence of bands and are the manifestaƟ on of microsatellite instability (MIN). QuanƟ taƟ ve changes are the representaƟ on of chromosomal instability (CIN) and are detected as diff erences in the intensity of bands. Survival analyses were performed using Kaplan & Maier test for survival data in relaƟ on to diff erent histological tumour type and genomic instability. StaƟ sƟ cal diff erences were considered signifi cant for p≤ 0,05. Results: PaƟ ents with Glioblastoma IDH wild-type have signifi cantly shorter survival compared to other histological types (p=0,025). For each histological type that we analysed and each type of instability MIN, CIN and total genomic instability, two groups of paƟ ents were made – those with high and low instability. PaƟ ents with Glioblastoma IDH wild-type that have low total genomic instability have signifi cantly shorter survival (p=0,045) compared to other analysed types of brain cancer. PaƟ ents with Astrocytoma IDH mutant grade 4 who have high total genomic instability and high CIN have signifi cantly shorter survival (p=0,018, p=0,007 respecƞ ully). Conclusion: PaƟ ents with Glioblastoma IDH wild-type have shorter survival which makes this tumour the most aggressive and malignat of all analysed tumours. Our results show that low genomic instability in Glioblastoma IDH wild-type and high genomic instability lead by high CIN in Astrocytoma IDH mutant, gradus 4 contribute to shorter survival, which makes genomic instability a potential good prognostic marker
PB  - Belgrade : Serbian Association for Cancer Research
C3  - Oncology Insights
T1  - Genomic instability as a prognostic marker in malignant brain cancer
IS  - 1
SP  - 90
EP  - 91
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12638
ER  - 

@conference{
author = "Ademović, Nejla and Tomić, Tijana and Tanić, Nasta and Milić, Marina and Rakić, Miodrag and Tanić, Nikola",
year = "2023",
abstract = "Introduction: Glioblastoma and Astrocytoma are diff use malignant brain tumors and characterized as the most aggressive and invasive brain cancers. Glioblastoma IDH wild-type is a primary brain tumour that develops de novo, and Astrocytoma IDH mutant is a secondary tumour which arises by progression from lower tumour grades. They are characterized by poor survival, resistance to therapy and poor prognosis which develops as a consequence of genomic instability. Genomic instability also contributes to tumour heterogeneity and provides the genomic diversity necessary for selecƟ on. Materials and methods: 31 paƟ ents with Glioblastoma IDH wild-type and Astrocytoma IDH mutant, grade 3 and 4, were analysed for the presence of genomic instability using AP-PCR, DNA profi ling method. Comparing DNA profi les between tumour Ɵ ssue and normal Ɵ ssue (blood) of the same paƟ ent, we detected qualitaƟ ve and quanƟ taƟ ve changes. QualitaƟ ve changes are detected as the presence and absence of bands and are the manifestaƟ on of microsatellite instability (MIN). QuanƟ taƟ ve changes are the representaƟ on of chromosomal instability (CIN) and are detected as diff erences in the intensity of bands. Survival analyses were performed using Kaplan & Maier test for survival data in relaƟ on to diff erent histological tumour type and genomic instability. StaƟ sƟ cal diff erences were considered signifi cant for p≤ 0,05. Results: PaƟ ents with Glioblastoma IDH wild-type have signifi cantly shorter survival compared to other histological types (p=0,025). For each histological type that we analysed and each type of instability MIN, CIN and total genomic instability, two groups of paƟ ents were made – those with high and low instability. PaƟ ents with Glioblastoma IDH wild-type that have low total genomic instability have signifi cantly shorter survival (p=0,045) compared to other analysed types of brain cancer. PaƟ ents with Astrocytoma IDH mutant grade 4 who have high total genomic instability and high CIN have signifi cantly shorter survival (p=0,018, p=0,007 respecƞ ully). Conclusion: PaƟ ents with Glioblastoma IDH wild-type have shorter survival which makes this tumour the most aggressive and malignat of all analysed tumours. Our results show that low genomic instability in Glioblastoma IDH wild-type and high genomic instability lead by high CIN in Astrocytoma IDH mutant, gradus 4 contribute to shorter survival, which makes genomic instability a potential good prognostic marker",
publisher = "Belgrade : Serbian Association for Cancer Research",
journal = "Oncology Insights",
title = "Genomic instability as a prognostic marker in malignant brain cancer",
number = "1",
pages = "90-91",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12638"
}

Ademović, N., Tomić, T., Tanić, N., Milić, M., Rakić, M.,& Tanić, N.. (2023). Genomic instability as a prognostic marker in malignant brain cancer. in Oncology Insights
Belgrade : Serbian Association for Cancer Research.(1), 90-91.
https://hdl.handle.net/21.15107/rcub_vinar_12638

Ademović N, Tomić T, Tanić N, Milić M, Rakić M, Tanić N. Genomic instability as a prognostic marker in malignant brain cancer. in Oncology Insights. 2023;(1):90-91.
https://hdl.handle.net/21.15107/rcub_vinar_12638 .

Ademović, Nejla, Tomić, Tijana, Tanić, Nasta, Milić, Marina, Rakić, Miodrag, Tanić, Nikola, "Genomic instability as a prognostic marker in malignant brain cancer" in Oncology Insights, no. 1 (2023):90-91,
https://hdl.handle.net/21.15107/rcub_vinar_12638 .

TY  - CONF
AU  - Murganić, Blagoje
AU  - Kazimir, Aleksandar
AU  - Jelača, Sanja
AU  - Tanić, Nikola
AU  - Hey-Hawkins, Evamarie
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12639
AB  - Background: Estrogen receptor-posiƟ ve (ER+) breast cancer accounts for approximately 70% of all cases and, concordantly, anƟ -estrogen therapies present a leading therapeuƟ c choice. InteresƟ ngly, tamoxifen, which is the most commonly used drug, has also been proven eff ecƟ ve in hormone-independent forms of breast cancer, suggesƟ ng the existence of intracellular off -targets. Frequent acquisiƟ on of therapy resistance presents a plaƞ orm for the design of tamoxifen derivaƟ ves with a 2,2’-bipyridine unit enabling the coordinaƟ on of transiƟ on metal moieƟ es, such as copper(II) dichloride. Copper (Cu) is an essenƟ al element involved in the regulaƟ on of cellular growth and development. DisrupƟ on of its delicate homeostasis results in severe toxicity and hard medical condiƟ ons. Increased demand of cancer cells for this micronutrient makes it a valuable candidate for drug design in cancer treatment. The mechanism of acƟ on of Cu complexes is typically based on their ability to induce deadly oxidaƟ ve stress. This study evaluated the effi cacy of a copper–tamoxifen hybrid drug on a panel of breast cancer cell lines with varying receptor expression status. Material and Methods: The viability of breast adenocarcinoma cell lines MCF-7, MDA-MB-361, MDA-MB-231, 4T1 and glioma U251 was esƟ mated by MTT and CV assays. Flow cytometric analysis of cells stained with annexin V-FITC/propidium iodide, ApoStat, acridine orange, dihydrorhodamine 123 (DHR), dihydroethidium (DHE) or 4-amino-5-methylamino-2’,7’-difl uorofl uorescein diacetate (DAF) was used to evaluate cell death, caspase acƟ vity, autophagy, producƟ on of reacƟ ve oxygen and nitrogen species (ROS/RNS), respecƟ vely. Results: The Cu-tamoxifen hybrid drug displayed substanƟ ally higher hormone-receptor (HR) independent cytotoxic acƟ vity compared to previously reported metal complexes with a similar tamoxifen vector. Massive caspase-dependent apoptoƟ c cell death is parƟ ally aƩ enuated by an autophagic process that counteracts death signals. In contrast to the plaƟ num analogue, the copper-based tamoxifen derivaƟ ve reduces ROS/RNS that may be associated with the intracellular accumulaƟ on of the reduced form of CuI which is important for cuproptosis. Conclusion: This study demonstrates the potenƟ al of the copper–tamoxifen hybrid drug as an intriguing alternaƟ ve to commonly used plaƟ num complexes in treatment of cancer. Its safety and effi ciency will be further esƟ mated in vivo
PB  - Belgrade : Serbian Association for Cancer Research
C3  - Oncology Insights
T1  - Potential of Tamoxifen-based Copper(II) Dichloride in Breast Cancer Therapy
IS  - 1
SP  - 95
EP  - 95
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12639
ER  - 

@conference{
author = "Murganić, Blagoje and Kazimir, Aleksandar and Jelača, Sanja and Tanić, Nikola and Hey-Hawkins, Evamarie and Mijatović, Sanja and Maksimović-Ivanić, Danijela",
year = "2023",
abstract = "Background: Estrogen receptor-posiƟ ve (ER+) breast cancer accounts for approximately 70% of all cases and, concordantly, anƟ -estrogen therapies present a leading therapeuƟ c choice. InteresƟ ngly, tamoxifen, which is the most commonly used drug, has also been proven eff ecƟ ve in hormone-independent forms of breast cancer, suggesƟ ng the existence of intracellular off -targets. Frequent acquisiƟ on of therapy resistance presents a plaƞ orm for the design of tamoxifen derivaƟ ves with a 2,2’-bipyridine unit enabling the coordinaƟ on of transiƟ on metal moieƟ es, such as copper(II) dichloride. Copper (Cu) is an essenƟ al element involved in the regulaƟ on of cellular growth and development. DisrupƟ on of its delicate homeostasis results in severe toxicity and hard medical condiƟ ons. Increased demand of cancer cells for this micronutrient makes it a valuable candidate for drug design in cancer treatment. The mechanism of acƟ on of Cu complexes is typically based on their ability to induce deadly oxidaƟ ve stress. This study evaluated the effi cacy of a copper–tamoxifen hybrid drug on a panel of breast cancer cell lines with varying receptor expression status. Material and Methods: The viability of breast adenocarcinoma cell lines MCF-7, MDA-MB-361, MDA-MB-231, 4T1 and glioma U251 was esƟ mated by MTT and CV assays. Flow cytometric analysis of cells stained with annexin V-FITC/propidium iodide, ApoStat, acridine orange, dihydrorhodamine 123 (DHR), dihydroethidium (DHE) or 4-amino-5-methylamino-2’,7’-difl uorofl uorescein diacetate (DAF) was used to evaluate cell death, caspase acƟ vity, autophagy, producƟ on of reacƟ ve oxygen and nitrogen species (ROS/RNS), respecƟ vely. Results: The Cu-tamoxifen hybrid drug displayed substanƟ ally higher hormone-receptor (HR) independent cytotoxic acƟ vity compared to previously reported metal complexes with a similar tamoxifen vector. Massive caspase-dependent apoptoƟ c cell death is parƟ ally aƩ enuated by an autophagic process that counteracts death signals. In contrast to the plaƟ num analogue, the copper-based tamoxifen derivaƟ ve reduces ROS/RNS that may be associated with the intracellular accumulaƟ on of the reduced form of CuI which is important for cuproptosis. Conclusion: This study demonstrates the potenƟ al of the copper–tamoxifen hybrid drug as an intriguing alternaƟ ve to commonly used plaƟ num complexes in treatment of cancer. Its safety and effi ciency will be further esƟ mated in vivo",
publisher = "Belgrade : Serbian Association for Cancer Research",
journal = "Oncology Insights",
title = "Potential of Tamoxifen-based Copper(II) Dichloride in Breast Cancer Therapy",
number = "1",
pages = "95-95",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12639"
}

Murganić, B., Kazimir, A., Jelača, S., Tanić, N., Hey-Hawkins, E., Mijatović, S.,& Maksimović-Ivanić, D.. (2023). Potential of Tamoxifen-based Copper(II) Dichloride in Breast Cancer Therapy. in Oncology Insights
Belgrade : Serbian Association for Cancer Research.(1), 95-95.
https://hdl.handle.net/21.15107/rcub_vinar_12639

Murganić B, Kazimir A, Jelača S, Tanić N, Hey-Hawkins E, Mijatović S, Maksimović-Ivanić D. Potential of Tamoxifen-based Copper(II) Dichloride in Breast Cancer Therapy. in Oncology Insights. 2023;(1):95-95.
https://hdl.handle.net/21.15107/rcub_vinar_12639 .

Murganić, Blagoje, Kazimir, Aleksandar, Jelača, Sanja, Tanić, Nikola, Hey-Hawkins, Evamarie, Mijatović, Sanja, Maksimović-Ivanić, Danijela, "Potential of Tamoxifen-based Copper(II) Dichloride in Breast Cancer Therapy" in Oncology Insights, no. 1 (2023):95-95,
https://hdl.handle.net/21.15107/rcub_vinar_12639 .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Dramićanin, Tatjana
AU  - Ademović, Nejla
AU  - Tomić, Tijana
AU  - Murganić, Blagoje
AU  - Milovanović, Zorka
AU  - Nedeljković, Milica
AU  - Tanić, Nasta
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12956
AB  - Rak dojke (RD) je najčešći tip maligniteta i vodeći uzrok smrti od raka kod žena širom sveta. RD je izuzetno heterogena bolest i stoga su neophodni različiti modaliteti lečenja da bi se pokrile ove razlike. Cilj našeg istraživanja je bio da se ispita uticaj inaktivacije TP53 i PTEN tumor supresorskih gena (TSG) na odgovor RD na različite modalitete lečenja, kao i njihova moguća saradnja u tome, na postoperativnim uzorcima RD. Metode. Pacijentkinje su klasifikovane, na osnovu primenjene adjuvantne terapije, u četiri različite grupe: one koje su primale samo hormonsku terapiju (HT), hormonsku terapiju u kombinaciji sa hemoterapijom (HT/CHT), hormonsku terapiju u kombinaciji sa hemoterapijom i biološkom terapijom (HT/CHT/H) i druge sistemske terapije koje isključuju HT. Funkcionalna inaktivacija TP53 i PTEN TSG je proučavana analizom mutacionog statusa, gubitka heterozigotnosti (LOH) i metilacionog statusa. Rezultati. Naši rezultati su pokazali da je TP53 gen izmenjen kod 63 od 90 pacijenata (70%), dok je učestalost promena PTEN gena bila nešto niža, 54 od 90 (60%). Simultana inaktivacija je detektovana u 43 testirana uzorka (48%) sa značajnom povezanošću između dva analizirana TSG-a. Dalje, pokazali smo da status TP53 ima značajan uticaj na odgovor pacijenata na terapiju. Suprotno ovome, nismo pokazali značajnu asocijaciju između mutacionog statusa PTEN-a i različitih modaliteta lečenja. Međutim, utvrđena je značajna povezanost između primenjenih terapija i simultanih inaktivacija ova dva TSG-a (p = 0,00001). Zaključak. Pacijenti sa wtTP53 pokazuju značajno bolji terapijski odgovor bez obzira na vrstu terapije u poređenju sa nosiocima mutiranog TP53 gena.
AB  - Introduction. Breast cancer (BC) is the most frequent type of malignancy and the leading cause of cancer related death among women worldwide. BC is exceptionally heterogeneous disease and therefore distinct treatment modalities are necessary to address these differences. The aim of our study was to investigate the impact of TP53 and PTEN tumor suppressor genes (TSGs) inactivation on BC response to different treatment modalities and their possible cooperation, on post-operative BC samples.   Methods. Patients were classified, based on applied adjuvant therapy, into four distinct groups: those that received hormonal therapy (HT) only, hormonal therapy combined with chemotherapy (HT/CHT), hormonal therapy combined with chemo and biological therapy (HT/CHT/H), and other systemic therapies that exclude HT. Functional inactivation of TP53 and PTEN TSG’s were studied by mutation, loss of heterozygosity (LOH) and hypermethylation analysis.   Results. Our results revealed that TP53 gene was altered in 63 out of 90 specimens (70%), while the frequency of PTEN alterations was slightly lower, 54 out of 90 (60%). Simultaneous inactivation was detected in 43 tested samples (48%) with significant association between two analyzed TSGs. Further, we found that TP53 status has significant influence on patients’ therapy response. Contrary to this, no significance was found between mutational status of PTEN and various treatment modalities. However, significant association was found between the type of applied therapy and simultaneous alterations of these two TSGs (p = 0.00001).   Conclusion. Patients with wtTP53 show significantly better therapy response regardless of the type of therapy, compared to carriers of altered TPp53 gene.
T2  - Biomedicinska istraživanja
T1  - The impact of TP53 and PTEN tumor suppressor genes on  response to different breast cancer treatment modalities
T1  - Uticaj tumor supresorskih gena TP53 i PTEN na odgovor na različite načine lečenja raka dojke
VL  - 13
IS  - 2
SP  - 105
EP  - 117
DO  - 10.5937/BII2202105T
ER  - 

@article{
author = "Tanić, Nikola and Dramićanin, Tatjana and Ademović, Nejla and Tomić, Tijana and Murganić, Blagoje and Milovanović, Zorka and Nedeljković, Milica and Tanić, Nasta",
year = "2022",
abstract = "Rak dojke (RD) je najčešći tip maligniteta i vodeći uzrok smrti od raka kod žena širom sveta. RD je izuzetno heterogena bolest i stoga su neophodni različiti modaliteti lečenja da bi se pokrile ove razlike. Cilj našeg istraživanja je bio da se ispita uticaj inaktivacije TP53 i PTEN tumor supresorskih gena (TSG) na odgovor RD na različite modalitete lečenja, kao i njihova moguća saradnja u tome, na postoperativnim uzorcima RD. Metode. Pacijentkinje su klasifikovane, na osnovu primenjene adjuvantne terapije, u četiri različite grupe: one koje su primale samo hormonsku terapiju (HT), hormonsku terapiju u kombinaciji sa hemoterapijom (HT/CHT), hormonsku terapiju u kombinaciji sa hemoterapijom i biološkom terapijom (HT/CHT/H) i druge sistemske terapije koje isključuju HT. Funkcionalna inaktivacija TP53 i PTEN TSG je proučavana analizom mutacionog statusa, gubitka heterozigotnosti (LOH) i metilacionog statusa. Rezultati. Naši rezultati su pokazali da je TP53 gen izmenjen kod 63 od 90 pacijenata (70%), dok je učestalost promena PTEN gena bila nešto niža, 54 od 90 (60%). Simultana inaktivacija je detektovana u 43 testirana uzorka (48%) sa značajnom povezanošću između dva analizirana TSG-a. Dalje, pokazali smo da status TP53 ima značajan uticaj na odgovor pacijenata na terapiju. Suprotno ovome, nismo pokazali značajnu asocijaciju između mutacionog statusa PTEN-a i različitih modaliteta lečenja. Međutim, utvrđena je značajna povezanost između primenjenih terapija i simultanih inaktivacija ova dva TSG-a (p = 0,00001). Zaključak. Pacijenti sa wtTP53 pokazuju značajno bolji terapijski odgovor bez obzira na vrstu terapije u poređenju sa nosiocima mutiranog TP53 gena., Introduction. Breast cancer (BC) is the most frequent type of malignancy and the leading cause of cancer related death among women worldwide. BC is exceptionally heterogeneous disease and therefore distinct treatment modalities are necessary to address these differences. The aim of our study was to investigate the impact of TP53 and PTEN tumor suppressor genes (TSGs) inactivation on BC response to different treatment modalities and their possible cooperation, on post-operative BC samples.   Methods. Patients were classified, based on applied adjuvant therapy, into four distinct groups: those that received hormonal therapy (HT) only, hormonal therapy combined with chemotherapy (HT/CHT), hormonal therapy combined with chemo and biological therapy (HT/CHT/H), and other systemic therapies that exclude HT. Functional inactivation of TP53 and PTEN TSG’s were studied by mutation, loss of heterozygosity (LOH) and hypermethylation analysis.   Results. Our results revealed that TP53 gene was altered in 63 out of 90 specimens (70%), while the frequency of PTEN alterations was slightly lower, 54 out of 90 (60%). Simultaneous inactivation was detected in 43 tested samples (48%) with significant association between two analyzed TSGs. Further, we found that TP53 status has significant influence on patients’ therapy response. Contrary to this, no significance was found between mutational status of PTEN and various treatment modalities. However, significant association was found between the type of applied therapy and simultaneous alterations of these two TSGs (p = 0.00001).   Conclusion. Patients with wtTP53 show significantly better therapy response regardless of the type of therapy, compared to carriers of altered TPp53 gene.",
journal = "Biomedicinska istraživanja",
title = "The impact of TP53 and PTEN tumor suppressor genes on  response to different breast cancer treatment modalities, Uticaj tumor supresorskih gena TP53 i PTEN na odgovor na različite načine lečenja raka dojke",
volume = "13",
number = "2",
pages = "105-117",
doi = "10.5937/BII2202105T"
}

Tanić, N., Dramićanin, T., Ademović, N., Tomić, T., Murganić, B., Milovanović, Z., Nedeljković, M.,& Tanić, N.. (2022). The impact of TP53 and PTEN tumor suppressor genes on  response to different breast cancer treatment modalities. in Biomedicinska istraživanja, 13(2), 105-117.
https://doi.org/10.5937/BII2202105T

Tanić N, Dramićanin T, Ademović N, Tomić T, Murganić B, Milovanović Z, Nedeljković M, Tanić N. The impact of TP53 and PTEN tumor suppressor genes on  response to different breast cancer treatment modalities. in Biomedicinska istraživanja. 2022;13(2):105-117.
doi:10.5937/BII2202105T .

Tanić, Nikola, Dramićanin, Tatjana, Ademović, Nejla, Tomić, Tijana, Murganić, Blagoje, Milovanović, Zorka, Nedeljković, Milica, Tanić, Nasta, "The impact of TP53 and PTEN tumor suppressor genes on  response to different breast cancer treatment modalities" in Biomedicinska istraživanja, 13, no. 2 (2022):105-117,
https://doi.org/10.5937/BII2202105T . .

TY  - JOUR
AU  - Nedeljković, Milica
AU  - Tanić, Nasta
AU  - Prvanović, Mirjana
AU  - Milovanović, Zorka
AU  - Tanić, Nikola
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9173
AB  - Background: ATP-binding cassette (ABC) transporters are responsible for the efflux of a wide variety of anti-cancer agents and have been implicated in the chemoresistance of various solid tumors. Chemoresistance is a major cause of therapeutic failure, especially in the highly aggressive triple-negative breast cancer (TNBC) in which, unlike estrogen receptor-expressing (ER+) BC, both endocrine and targeted treatments are ineffectual. We aimed to investigate the level and frequency of expression of the three most important ABC transporter, ABCG2, ABCC1, and ABCB1, according to breast cancer subtype. Methods: We evaluated ABCG2, ABCC1, and ABCB1 protein expressions in 124 primary breast tumors (78 samples were classified as TNBC, while 46 were classified as ER+) by immunohistochemistry and correlated it to clinicopathological characteristics and outcome. Results: All three transporters had significantly higher expression and were more frequently expressed in TNBC compared to ER+ tumors (p < 0.0001). ABCG2 and ABCC1 had a very high level of expression in TNBC that was significantly greater compared to ABCB1 (p < 0.0001). ABCB1 expression was associated with TNBC metastatic spread (p = 0.03). In contrast, TNBC patients with high ABCG2 expression level had significantly longer disease-free interval (p = 0.03) and overall survival (p = 0.007). Conclusion: ABCG2, ABCC1, and ABCB1 expression in breast cancer is subtype-specific and associated with triple-negative tumors. The expression of ABCB1 may be useful as a marker of metastatic spread. Moreover, unexpectedly, our results showed a beneficial effect of ABCG2 expression on TNBC clinical behavior. These findings could have implications for the implementation of future TNBC treatment strategies.
T2  - Breast Cancer
T1  - Friend or foe: ABCG2, ABCC1 and ABCB1 expression in triple-negative breast cancer
VL  - 28
IS  - 3
SP  - 727
EP  - 736
DO  - 10.1007/s12282-020-01210-z
ER  - 

@article{
author = "Nedeljković, Milica and Tanić, Nasta and Prvanović, Mirjana and Milovanović, Zorka and Tanić, Nikola",
year = "2021",
abstract = "Background: ATP-binding cassette (ABC) transporters are responsible for the efflux of a wide variety of anti-cancer agents and have been implicated in the chemoresistance of various solid tumors. Chemoresistance is a major cause of therapeutic failure, especially in the highly aggressive triple-negative breast cancer (TNBC) in which, unlike estrogen receptor-expressing (ER+) BC, both endocrine and targeted treatments are ineffectual. We aimed to investigate the level and frequency of expression of the three most important ABC transporter, ABCG2, ABCC1, and ABCB1, according to breast cancer subtype. Methods: We evaluated ABCG2, ABCC1, and ABCB1 protein expressions in 124 primary breast tumors (78 samples were classified as TNBC, while 46 were classified as ER+) by immunohistochemistry and correlated it to clinicopathological characteristics and outcome. Results: All three transporters had significantly higher expression and were more frequently expressed in TNBC compared to ER+ tumors (p < 0.0001). ABCG2 and ABCC1 had a very high level of expression in TNBC that was significantly greater compared to ABCB1 (p < 0.0001). ABCB1 expression was associated with TNBC metastatic spread (p = 0.03). In contrast, TNBC patients with high ABCG2 expression level had significantly longer disease-free interval (p = 0.03) and overall survival (p = 0.007). Conclusion: ABCG2, ABCC1, and ABCB1 expression in breast cancer is subtype-specific and associated with triple-negative tumors. The expression of ABCB1 may be useful as a marker of metastatic spread. Moreover, unexpectedly, our results showed a beneficial effect of ABCG2 expression on TNBC clinical behavior. These findings could have implications for the implementation of future TNBC treatment strategies.",
journal = "Breast Cancer",
title = "Friend or foe: ABCG2, ABCC1 and ABCB1 expression in triple-negative breast cancer",
volume = "28",
number = "3",
pages = "727-736",
doi = "10.1007/s12282-020-01210-z"
}

Nedeljković, M., Tanić, N., Prvanović, M., Milovanović, Z.,& Tanić, N.. (2021). Friend or foe: ABCG2, ABCC1 and ABCB1 expression in triple-negative breast cancer. in Breast Cancer, 28(3), 727-736.
https://doi.org/10.1007/s12282-020-01210-z

Nedeljković M, Tanić N, Prvanović M, Milovanović Z, Tanić N. Friend or foe: ABCG2, ABCC1 and ABCB1 expression in triple-negative breast cancer. in Breast Cancer. 2021;28(3):727-736.
doi:10.1007/s12282-020-01210-z .

Nedeljković, Milica, Tanić, Nasta, Prvanović, Mirjana, Milovanović, Zorka, Tanić, Nikola, "Friend or foe: ABCG2, ABCC1 and ABCB1 expression in triple-negative breast cancer" in Breast Cancer, 28, no. 3 (2021):727-736,
https://doi.org/10.1007/s12282-020-01210-z . .

TY  - JOUR
AU  - Prvanović, Mirjana
AU  - Nedeljković, Milica
AU  - Tanić, Nasta
AU  - Tomić, Tijana
AU  - Terzić, Tanja
AU  - Milovanović, Zorka
AU  - Maksimović, Zlatko
AU  - Tanić, Nikola
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10064
AB  - Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negative breast cancer (TNBC) is the most aggressive subtype and is associated with high recurrence rates, high incidence of distant metastases, and poor overall survival. The aim of this study was to investigate the PI3K/PTEN/Akt/mTOR pathway as one of the most frequently deregulated pathways in cancer. We aimed to explore the impact of PI3K and mTOR oncogenes as well as the PTEN tumor suppressor on TNBC clinical behavior, prognosis, and multidrug resistance (MDR), using immunohistochemistry and copy number analysis by quantitative real-time PCR. Our results revealed that loss of PTEN and high expression of PI3K and mTOR proteins are associated with poor outcome of TNBC patients. PTEN deletions appeared as a major cause of reduced or absent PTEN expression in TNBC. Importantly, homozygous deletions of PTEN (and not hemizygous deletions) are a potential molecular marker of metastasis formation and good predictors of TNBC outcome. In conclusion, we believe that concurrent examination of PTEN/PI3K/mTOR protein expression may be more useful in predicting TNBC clinical course than the analysis of single protein expression. Specifically, our results showed that PTEN-reduced/PI3K-high/mTOR-high expression constitutes a 'high risk' profile of TNBC.
T2  - Life (Basel, Switzerland)
T1  - Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer.
VL  - 11
IS  - 11
SP  - 1247
DO  - 10.3390/life11111247
ER  - 

@article{
author = "Prvanović, Mirjana and Nedeljković, Milica and Tanić, Nasta and Tomić, Tijana and Terzić, Tanja and Milovanović, Zorka and Maksimović, Zlatko and Tanić, Nikola",
year = "2021",
abstract = "Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negative breast cancer (TNBC) is the most aggressive subtype and is associated with high recurrence rates, high incidence of distant metastases, and poor overall survival. The aim of this study was to investigate the PI3K/PTEN/Akt/mTOR pathway as one of the most frequently deregulated pathways in cancer. We aimed to explore the impact of PI3K and mTOR oncogenes as well as the PTEN tumor suppressor on TNBC clinical behavior, prognosis, and multidrug resistance (MDR), using immunohistochemistry and copy number analysis by quantitative real-time PCR. Our results revealed that loss of PTEN and high expression of PI3K and mTOR proteins are associated with poor outcome of TNBC patients. PTEN deletions appeared as a major cause of reduced or absent PTEN expression in TNBC. Importantly, homozygous deletions of PTEN (and not hemizygous deletions) are a potential molecular marker of metastasis formation and good predictors of TNBC outcome. In conclusion, we believe that concurrent examination of PTEN/PI3K/mTOR protein expression may be more useful in predicting TNBC clinical course than the analysis of single protein expression. Specifically, our results showed that PTEN-reduced/PI3K-high/mTOR-high expression constitutes a 'high risk' profile of TNBC.",
journal = "Life (Basel, Switzerland)",
title = "Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer.",
volume = "11",
number = "11",
pages = "1247",
doi = "10.3390/life11111247"
}

Prvanović, M., Nedeljković, M., Tanić, N., Tomić, T., Terzić, T., Milovanović, Z., Maksimović, Z.,& Tanić, N.. (2021). Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer.. in Life (Basel, Switzerland), 11(11), 1247.
https://doi.org/10.3390/life11111247

Prvanović M, Nedeljković M, Tanić N, Tomić T, Terzić T, Milovanović Z, Maksimović Z, Tanić N. Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer.. in Life (Basel, Switzerland). 2021;11(11):1247.
doi:10.3390/life11111247 .

Prvanović, Mirjana, Nedeljković, Milica, Tanić, Nasta, Tomić, Tijana, Terzić, Tanja, Milovanović, Zorka, Maksimović, Zlatko, Tanić, Nikola, "Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer." in Life (Basel, Switzerland), 11, no. 11 (2021):1247,
https://doi.org/10.3390/life11111247 . .

TY  - JOUR
AU  - Nedeljković, Milica
AU  - Tanić, Nikola
AU  - Dramićanin, Tatjana
AU  - Milovanović, Zorka M.
AU  - Šušnjar, Snežana
AU  - Milinković, Vedrana
AU  - Vujović, Ivana
AU  - Tanić, Nasta
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7683
AB  - © 2018 Milica Nedeljković et al., published by De Gruyter Open 2018. Background: Triple negative breast cancer (TNBC) is characterized by aggressive clinical course and is unresponsive to anti-HER2 and endocrine therapy. TNBC is difficult to treat and is often lethal. Given the need to find new targets for therapy we explored clinicopathological significance of copy number gain of FGFR1 and c-MYC. Our aim was to determine the impact of FGFR1 and c-MYC copy number gain on clinical course and outcome of TNBC. Methods: FGFR1 and c-MYC gene copy number alterations were evaluated in 78 archive TNBC samples using TaqMan based quantitative real time PCR assays. Results: 50% of samples had increased c-MYC copy number. c-MYC copy number gain was associated with TNBC in contrast to ER positive cancers. Our results showed significant correlation between c-MYC copy number gain and high grade of TNBCs. This suggests that c-MYC copy number could be an useful prognostic marker for TNBC patients. c-MYC copy number gain was associated with high pTNM stage as well as lobular and medullary tumor subtypes. 43% of samples had increased FGFR1 copy number. No correlations between FGFR1 copy number gain and clinicopathological variables were observed. Conclusions: We identified c-MYC copy number gain as a prognostic marker for TNBC. Our results indicate that c- MYC may contribute to TNBC progression. We observed no significant association between c-MYC and/or FGFR1 copy number status and patient survival.
T2  - Journal of Medical Biochemistry
T1  - Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer
T1  - Značaj promena broja kopija FGFR1 i c-MYC gena u trostruko negativnim karcinomima dojke
VL  - 37
IS  - 2
SP  - 1
EP  - 8
DO  - 10.1515/jomb-2018-0012
ER  - 

@article{
author = "Nedeljković, Milica and Tanić, Nikola and Dramićanin, Tatjana and Milovanović, Zorka M. and Šušnjar, Snežana and Milinković, Vedrana and Vujović, Ivana and Tanić, Nasta",
year = "2018",
abstract = "© 2018 Milica Nedeljković et al., published by De Gruyter Open 2018. Background: Triple negative breast cancer (TNBC) is characterized by aggressive clinical course and is unresponsive to anti-HER2 and endocrine therapy. TNBC is difficult to treat and is often lethal. Given the need to find new targets for therapy we explored clinicopathological significance of copy number gain of FGFR1 and c-MYC. Our aim was to determine the impact of FGFR1 and c-MYC copy number gain on clinical course and outcome of TNBC. Methods: FGFR1 and c-MYC gene copy number alterations were evaluated in 78 archive TNBC samples using TaqMan based quantitative real time PCR assays. Results: 50% of samples had increased c-MYC copy number. c-MYC copy number gain was associated with TNBC in contrast to ER positive cancers. Our results showed significant correlation between c-MYC copy number gain and high grade of TNBCs. This suggests that c-MYC copy number could be an useful prognostic marker for TNBC patients. c-MYC copy number gain was associated with high pTNM stage as well as lobular and medullary tumor subtypes. 43% of samples had increased FGFR1 copy number. No correlations between FGFR1 copy number gain and clinicopathological variables were observed. Conclusions: We identified c-MYC copy number gain as a prognostic marker for TNBC. Our results indicate that c- MYC may contribute to TNBC progression. We observed no significant association between c-MYC and/or FGFR1 copy number status and patient survival.",
journal = "Journal of Medical Biochemistry",
title = "Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer, Značaj promena broja kopija FGFR1 i c-MYC gena u trostruko negativnim karcinomima dojke",
volume = "37",
number = "2",
pages = "1-8",
doi = "10.1515/jomb-2018-0012"
}

Nedeljković, M., Tanić, N., Dramićanin, T., Milovanović, Z. M., Šušnjar, S., Milinković, V., Vujović, I.,& Tanić, N.. (2018). Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer. in Journal of Medical Biochemistry, 37(2), 1-8.
https://doi.org/10.1515/jomb-2018-0012

Nedeljković M, Tanić N, Dramićanin T, Milovanović ZM, Šušnjar S, Milinković V, Vujović I, Tanić N. Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer. in Journal of Medical Biochemistry. 2018;37(2):1-8.
doi:10.1515/jomb-2018-0012 .

Nedeljković, Milica, Tanić, Nikola, Dramićanin, Tatjana, Milovanović, Zorka M., Šušnjar, Snežana, Milinković, Vedrana, Vujović, Ivana, Tanić, Nasta, "Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer" in Journal of Medical Biochemistry, 37, no. 2 (2018):1-8,
https://doi.org/10.1515/jomb-2018-0012 . .

TY  - JOUR
AU  - Stanković, Tijana
AU  - Milinković, Vedrana
AU  - Banković, Jasna Z.
AU  - Dinić, Jelena
AU  - Tanić, Nasta
AU  - Dramićanin, Tatjana
AU  - Tanić, Nikola
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/143
AB  - p53, p16 and PTEN are the most commonly altered tumor suppressor genes in human cancers. In the present study, we compared the presence of individual and multiple alterations of these tumor suppressors in non-small cell lung carcinoma (NSCLC), glioma and breast carcinoma, in order to evaluate specificity of each tumor type regarding the number of altered genes, as well as their combinations. We tested the mutational status, loss of heterozygosity and methylation status of these genes. Effects of gene alterations on patients survival were also assessed. In NSCLC samples, single gene alterations occurred rarely, while there was considerable increase in incidence of double gene alterations. Furthermore, coexistence of aberrant p53, PTEN and p16 was the most frequent and had significant adverse effect on the survival of NSCLC patients. On the contrary, in glioma and breast cancer specimens, substantial number of cases had aberrant single gene only. Moreover, glioma and breast carcinoma also differ in genotypes that were predominant. Specifically, in glioma samples, prevalent were co-alterations of PTEN and p16, followed by aberrant only PTEN. In breast cancer samples, alterations in all three genes as well as in p53 and p16 were the most common. Moreover, PTEN was altered exclusively with aberrant p53, with statistically significant correlation among them. Overall, our results suggest that NSCLC, glioma and breast cancer need different approaches in molecular diagnosis and treatment with particular attention toward the number and combination of targeted genes. (C) 2014 Elsevier Masson SAS. All rights reserved.
T2  - Biomedicine and Pharmacotherapy
T1  - Comparative analyses of individual and multiple alterations of p53, PTEN and p16 in non-small cell lung carcinoma, glioma and breast carcinoma samples
VL  - 68
IS  - 5
SP  - 521
EP  - 526
DO  - 10.1016/j.biopha.2014.03.014
ER  - 

@article{
author = "Stanković, Tijana and Milinković, Vedrana and Banković, Jasna Z. and Dinić, Jelena and Tanić, Nasta and Dramićanin, Tatjana and Tanić, Nikola",
year = "2014",
abstract = "p53, p16 and PTEN are the most commonly altered tumor suppressor genes in human cancers. In the present study, we compared the presence of individual and multiple alterations of these tumor suppressors in non-small cell lung carcinoma (NSCLC), glioma and breast carcinoma, in order to evaluate specificity of each tumor type regarding the number of altered genes, as well as their combinations. We tested the mutational status, loss of heterozygosity and methylation status of these genes. Effects of gene alterations on patients survival were also assessed. In NSCLC samples, single gene alterations occurred rarely, while there was considerable increase in incidence of double gene alterations. Furthermore, coexistence of aberrant p53, PTEN and p16 was the most frequent and had significant adverse effect on the survival of NSCLC patients. On the contrary, in glioma and breast cancer specimens, substantial number of cases had aberrant single gene only. Moreover, glioma and breast carcinoma also differ in genotypes that were predominant. Specifically, in glioma samples, prevalent were co-alterations of PTEN and p16, followed by aberrant only PTEN. In breast cancer samples, alterations in all three genes as well as in p53 and p16 were the most common. Moreover, PTEN was altered exclusively with aberrant p53, with statistically significant correlation among them. Overall, our results suggest that NSCLC, glioma and breast cancer need different approaches in molecular diagnosis and treatment with particular attention toward the number and combination of targeted genes. (C) 2014 Elsevier Masson SAS. All rights reserved.",
journal = "Biomedicine and Pharmacotherapy",
title = "Comparative analyses of individual and multiple alterations of p53, PTEN and p16 in non-small cell lung carcinoma, glioma and breast carcinoma samples",
volume = "68",
number = "5",
pages = "521-526",
doi = "10.1016/j.biopha.2014.03.014"
}

Stanković, T., Milinković, V., Banković, J. Z., Dinić, J., Tanić, N., Dramićanin, T.,& Tanić, N.. (2014). Comparative analyses of individual and multiple alterations of p53, PTEN and p16 in non-small cell lung carcinoma, glioma and breast carcinoma samples. in Biomedicine and Pharmacotherapy, 68(5), 521-526.
https://doi.org/10.1016/j.biopha.2014.03.014

Stanković T, Milinković V, Banković JZ, Dinić J, Tanić N, Dramićanin T, Tanić N. Comparative analyses of individual and multiple alterations of p53, PTEN and p16 in non-small cell lung carcinoma, glioma and breast carcinoma samples. in Biomedicine and Pharmacotherapy. 2014;68(5):521-526.
doi:10.1016/j.biopha.2014.03.014 .

Stanković, Tijana, Milinković, Vedrana, Banković, Jasna Z., Dinić, Jelena, Tanić, Nasta, Dramićanin, Tatjana, Tanić, Nikola, "Comparative analyses of individual and multiple alterations of p53, PTEN and p16 in non-small cell lung carcinoma, glioma and breast carcinoma samples" in Biomedicine and Pharmacotherapy, 68, no. 5 (2014):521-526,
https://doi.org/10.1016/j.biopha.2014.03.014 . .

TY  - JOUR
AU  - Tanić, Nasta
AU  - Milinković, Vedrana
AU  - Dramićanin, Tatjana
AU  - Nedeljković, Milica
AU  - Stanković, Tijana
AU  - Milovanović, Zorka M.
AU  - Šušnjar, Snežana
AU  - Milošević, Verica
AU  - Šošić-Jurjević, Branka
AU  - Džodić, Radan R.
AU  - Tanić, Nikola
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5745
AB  - Background: Breast cancer is the most common form of cancer in women. It arises from multiple genetic changes in oncogenes and tumor suppressor genes. Among so far studied oncogenes relatively few, including epdermal growth factor receptor (EGFR), cyclinD1 (CCND1) and c-myc, have been found to play an important role in progression of this type of human malignancy. The aim of this study was to examine the prognostic potential of CCND1, c-myc and EGFR amplification and their possible cooperation in breast carcinogenesis. Methods: Copy number analyses of CCND1 and c-myc genes were done by TaqMan based quantitative real time PCR. Amplification status of EGFR was determined by differential PCR. Results: Amplification of CCND1, c-myc and EGFR oncogene has been found in 20.4%, 26.5% and 26.5% of breast cancer cases, respectively. Analysis showed that amplification of CCND1 oncogene was significantly associated with the stage II of disease while amplification of EGFR gene was significantly associated with overexpression of HER-2/neu. Tumour stage and expression of HER-2/neu appeared to be significant predictors of patients outcome. Stage I patients lived significantly longer then stage III patients (p=0.04) while patients with HER-2/neu overexpression had worse prognoses and lived significantly shorter (p=0.001). Finally, survival of patients who underwent hormone therapy only was significantly longer (p=0.001) then survival of the rest of patients. Conclusions: Amplification of CCND1 or EGFR oncogene is associated with the progression of breast cancer and bad prognosis. No co-ordination in amplification of CCND1, c-myc and EGFR oncogenes were established in this cohort of breast cancer patients.
T2  - Journal of Medical Biochemistry
T1  - Amplification of Cycline D1, C-Myc and Egfr Oncogenes in Tumour Samples of Breast Cancer Patients
VL  - 32
IS  - 4
DO  - 10.2478/jomb-2014-0005
ER  - 

@article{
author = "Tanić, Nasta and Milinković, Vedrana and Dramićanin, Tatjana and Nedeljković, Milica and Stanković, Tijana and Milovanović, Zorka M. and Šušnjar, Snežana and Milošević, Verica and Šošić-Jurjević, Branka and Džodić, Radan R. and Tanić, Nikola",
year = "2013",
abstract = "Background: Breast cancer is the most common form of cancer in women. It arises from multiple genetic changes in oncogenes and tumor suppressor genes. Among so far studied oncogenes relatively few, including epdermal growth factor receptor (EGFR), cyclinD1 (CCND1) and c-myc, have been found to play an important role in progression of this type of human malignancy. The aim of this study was to examine the prognostic potential of CCND1, c-myc and EGFR amplification and their possible cooperation in breast carcinogenesis. Methods: Copy number analyses of CCND1 and c-myc genes were done by TaqMan based quantitative real time PCR. Amplification status of EGFR was determined by differential PCR. Results: Amplification of CCND1, c-myc and EGFR oncogene has been found in 20.4%, 26.5% and 26.5% of breast cancer cases, respectively. Analysis showed that amplification of CCND1 oncogene was significantly associated with the stage II of disease while amplification of EGFR gene was significantly associated with overexpression of HER-2/neu. Tumour stage and expression of HER-2/neu appeared to be significant predictors of patients outcome. Stage I patients lived significantly longer then stage III patients (p=0.04) while patients with HER-2/neu overexpression had worse prognoses and lived significantly shorter (p=0.001). Finally, survival of patients who underwent hormone therapy only was significantly longer (p=0.001) then survival of the rest of patients. Conclusions: Amplification of CCND1 or EGFR oncogene is associated with the progression of breast cancer and bad prognosis. No co-ordination in amplification of CCND1, c-myc and EGFR oncogenes were established in this cohort of breast cancer patients.",
journal = "Journal of Medical Biochemistry",
title = "Amplification of Cycline D1, C-Myc and Egfr Oncogenes in Tumour Samples of Breast Cancer Patients",
volume = "32",
number = "4",
doi = "10.2478/jomb-2014-0005"
}

Tanić, N., Milinković, V., Dramićanin, T., Nedeljković, M., Stanković, T., Milovanović, Z. M., Šušnjar, S., Milošević, V., Šošić-Jurjević, B., Džodić, R. R.,& Tanić, N.. (2013). Amplification of Cycline D1, C-Myc and Egfr Oncogenes in Tumour Samples of Breast Cancer Patients. in Journal of Medical Biochemistry, 32(4).
https://doi.org/10.2478/jomb-2014-0005

Tanić N, Milinković V, Dramićanin T, Nedeljković M, Stanković T, Milovanović ZM, Šušnjar S, Milošević V, Šošić-Jurjević B, Džodić RR, Tanić N. Amplification of Cycline D1, C-Myc and Egfr Oncogenes in Tumour Samples of Breast Cancer Patients. in Journal of Medical Biochemistry. 2013;32(4).
doi:10.2478/jomb-2014-0005 .

Tanić, Nasta, Milinković, Vedrana, Dramićanin, Tatjana, Nedeljković, Milica, Stanković, Tijana, Milovanović, Zorka M., Šušnjar, Snežana, Milošević, Verica, Šošić-Jurjević, Branka, Džodić, Radan R., Tanić, Nikola, "Amplification of Cycline D1, C-Myc and Egfr Oncogenes in Tumour Samples of Breast Cancer Patients" in Journal of Medical Biochemistry, 32, no. 4 (2013),
https://doi.org/10.2478/jomb-2014-0005 . .

TY  - JOUR
AU  - Tanić, Nasta
AU  - Milašin, Jelena
AU  - Dramićanin, Tatjana
AU  - Bošković, Maja
AU  - Vukadinovic, Miroslav
AU  - Milošević, Verica
AU  - Tanić, Nikola
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5747
AB  - Background: Head and neck squamous cell carcinoma, including oral cancer, is the sixth most common cancer worldwide. Despite advances in surgery and treatment, the 5-year survival rate has not improved significantly. There fore, reliable molecular markers for oral cancer progression are badly needed. Methods: We conducted a copy number analysis to estimate amplification status of c-myc, cycD1 and EGFR oncogenes, mutational PCR-SSCP analysis to determine activation of H-ras oncogene and inactivation of TP53 tumour suppressor gene and methylation specific PCR analysis to evaluate hypermethylation of p16 and MGMT genes. Results: c-myc oncogene was amplified in 56.7%, cycD1 in 20% and EGFR in 16.7% of Oral Squamous Cell Carcinoma (OSCC) cases while H-ras was activated in 33.3% of samples. Amplification of c-myc was significantly associated with the tumour grade 2. Interestingly, EGFR and H-ras alterations were mutually exclusive. p16 and MGMT were inactivated by hypermethylation in 30% and 13.3% of cases. Co-alteration of cycD1 and p16 were not observed in any of the analyzed samples. TP53 was inactivated in 56.7% of samples and was significantly associated with progression of OSCC, grade 2 and stage 2. Moreover, TP53 and c-myc oncogene were simultaneously altered in grade 2 OSCC. Conclusions: The most promising marker of OSCC progression remains the TP53 tumour suppressor, which is the most frequently mutated gene in oral cancers. Since there is synergism between TP53 and c-myc, it seems that co-alteration of these two genes could be also a good marker of OSCC progression from grade1 to grade 2 tumours.
T2  - Journal of Medical Biochemistry
T1  - TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION
VL  - 32
IS  - 4
SP  - 380
EP  - 388
DO  - 10.2478/jomb-2014-0009
ER  - 

@article{
author = "Tanić, Nasta and Milašin, Jelena and Dramićanin, Tatjana and Bošković, Maja and Vukadinovic, Miroslav and Milošević, Verica and Tanić, Nikola",
year = "2013",
abstract = "Background: Head and neck squamous cell carcinoma, including oral cancer, is the sixth most common cancer worldwide. Despite advances in surgery and treatment, the 5-year survival rate has not improved significantly. There fore, reliable molecular markers for oral cancer progression are badly needed. Methods: We conducted a copy number analysis to estimate amplification status of c-myc, cycD1 and EGFR oncogenes, mutational PCR-SSCP analysis to determine activation of H-ras oncogene and inactivation of TP53 tumour suppressor gene and methylation specific PCR analysis to evaluate hypermethylation of p16 and MGMT genes. Results: c-myc oncogene was amplified in 56.7%, cycD1 in 20% and EGFR in 16.7% of Oral Squamous Cell Carcinoma (OSCC) cases while H-ras was activated in 33.3% of samples. Amplification of c-myc was significantly associated with the tumour grade 2. Interestingly, EGFR and H-ras alterations were mutually exclusive. p16 and MGMT were inactivated by hypermethylation in 30% and 13.3% of cases. Co-alteration of cycD1 and p16 were not observed in any of the analyzed samples. TP53 was inactivated in 56.7% of samples and was significantly associated with progression of OSCC, grade 2 and stage 2. Moreover, TP53 and c-myc oncogene were simultaneously altered in grade 2 OSCC. Conclusions: The most promising marker of OSCC progression remains the TP53 tumour suppressor, which is the most frequently mutated gene in oral cancers. Since there is synergism between TP53 and c-myc, it seems that co-alteration of these two genes could be also a good marker of OSCC progression from grade1 to grade 2 tumours.",
journal = "Journal of Medical Biochemistry",
title = "TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION",
volume = "32",
number = "4",
pages = "380-388",
doi = "10.2478/jomb-2014-0009"
}

Tanić, N., Milašin, J., Dramićanin, T., Bošković, M., Vukadinovic, M., Milošević, V.,& Tanić, N.. (2013). TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION. in Journal of Medical Biochemistry, 32(4), 380-388.
https://doi.org/10.2478/jomb-2014-0009

Tanić N, Milašin J, Dramićanin T, Bošković M, Vukadinovic M, Milošević V, Tanić N. TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION. in Journal of Medical Biochemistry. 2013;32(4):380-388.
doi:10.2478/jomb-2014-0009 .

Tanić, Nasta, Milašin, Jelena, Dramićanin, Tatjana, Bošković, Maja, Vukadinovic, Miroslav, Milošević, Verica, Tanić, Nikola, "TP53 AND C-MYC CO-ALTERATIONS - A HALLMARK OF ORAL CANCER PROGRESSION" in Journal of Medical Biochemistry, 32, no. 4 (2013):380-388,
https://doi.org/10.2478/jomb-2014-0009 . .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Milovanović, Zorka M.
AU  - Tanić, Nasta
AU  - Džodić, Radan R.
AU  - Juranic, Zorica
AU  - Šušnjar, Snežana
AU  - Plesinac-Karapandzic, Vesna
AU  - Tatic, Svetislav
AU  - Dramićanin, Tatjana
AU  - Davidović, Radoslav S.
AU  - Dimitrijević, Bogomir B.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5073
AB  - Tamoxifen is a standard therapeutical treatment in patients with estrogen receptor positive breast carcinoma. However, less than 50% of estrogen receptor positive breast cancers do not respond to tamoxifen treatment whereas 40% of tumors that initially respond to treatment develop resistance over time. The underlying mechanisms for tamoxifen resistance are probably multifactorial but remain largely unknown. The primary aim of this study was to investigate the impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen by analyzing loss of heterozygosity (LOH) and immunohystochemical expression of PTEN in 49 primary breast carcinomas of patients treated with tamoxifen as the only adjuvant therapy. The effect of PTEN inactivation on breast cancer progression and disease outcome was also analyzed. Reduced or completely lost PTEN expression was observed in 55.1% of samples, while 63.3% of samples displayed LOH of PTEN gene. Inactivation of PTEN immunoexpression significantly correlated with the PTEN loss of heterozygosity, suggesting LOH as the most important genetic mechanism for the reduction or complete loss of PTEN expression in primary breast carcinoma. Most importantly, LOH of PTEN and consequential reduction of its immunoexpression showed significant correlation with the recurrence of the disease. Besides, our study revealed that LOH of PTEN tumor suppressor was significantly associated with shorter disease free survival, breast cancer specific survival and overall survival. In summary, our results imply that LOH of PTEN could be used as a good prognostic characteristic for the outcome of breast cancer patients treated with tamoxifen.
T2  - Cancer Biology and Therapy
T1  - The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients
VL  - 13
IS  - 12
SP  - 1165
EP  - 1174
DO  - 10.4161/cbt.21346
ER  - 

@article{
author = "Tanić, Nikola and Milovanović, Zorka M. and Tanić, Nasta and Džodić, Radan R. and Juranic, Zorica and Šušnjar, Snežana and Plesinac-Karapandzic, Vesna and Tatic, Svetislav and Dramićanin, Tatjana and Davidović, Radoslav S. and Dimitrijević, Bogomir B.",
year = "2012",
abstract = "Tamoxifen is a standard therapeutical treatment in patients with estrogen receptor positive breast carcinoma. However, less than 50% of estrogen receptor positive breast cancers do not respond to tamoxifen treatment whereas 40% of tumors that initially respond to treatment develop resistance over time. The underlying mechanisms for tamoxifen resistance are probably multifactorial but remain largely unknown. The primary aim of this study was to investigate the impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen by analyzing loss of heterozygosity (LOH) and immunohystochemical expression of PTEN in 49 primary breast carcinomas of patients treated with tamoxifen as the only adjuvant therapy. The effect of PTEN inactivation on breast cancer progression and disease outcome was also analyzed. Reduced or completely lost PTEN expression was observed in 55.1% of samples, while 63.3% of samples displayed LOH of PTEN gene. Inactivation of PTEN immunoexpression significantly correlated with the PTEN loss of heterozygosity, suggesting LOH as the most important genetic mechanism for the reduction or complete loss of PTEN expression in primary breast carcinoma. Most importantly, LOH of PTEN and consequential reduction of its immunoexpression showed significant correlation with the recurrence of the disease. Besides, our study revealed that LOH of PTEN tumor suppressor was significantly associated with shorter disease free survival, breast cancer specific survival and overall survival. In summary, our results imply that LOH of PTEN could be used as a good prognostic characteristic for the outcome of breast cancer patients treated with tamoxifen.",
journal = "Cancer Biology and Therapy",
title = "The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients",
volume = "13",
number = "12",
pages = "1165-1174",
doi = "10.4161/cbt.21346"
}

Tanić, N., Milovanović, Z. M., Tanić, N., Džodić, R. R., Juranic, Z., Šušnjar, S., Plesinac-Karapandzic, V., Tatic, S., Dramićanin, T., Davidović, R. S.,& Dimitrijević, B. B.. (2012). The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients. in Cancer Biology and Therapy, 13(12), 1165-1174.
https://doi.org/10.4161/cbt.21346

Tanić N, Milovanović ZM, Tanić N, Džodić RR, Juranic Z, Šušnjar S, Plesinac-Karapandzic V, Tatic S, Dramićanin T, Davidović RS, Dimitrijević BB. The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients. in Cancer Biology and Therapy. 2012;13(12):1165-1174.
doi:10.4161/cbt.21346 .

Tanić, Nikola, Milovanović, Zorka M., Tanić, Nasta, Džodić, Radan R., Juranic, Zorica, Šušnjar, Snežana, Plesinac-Karapandzic, Vesna, Tatic, Svetislav, Dramićanin, Tatjana, Davidović, Radoslav S., Dimitrijević, Bogomir B., "The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients" in Cancer Biology and Therapy, 13, no. 12 (2012):1165-1174,
https://doi.org/10.4161/cbt.21346 . .

TY  - JOUR
AU  - Roganović, Jelena
AU  - Radenković, Miroslav
AU  - Tanić, Nikola
AU  - Tanić, Nasta
AU  - Petrović, Nina
AU  - Stojić, Dragica Lj.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4480
AB  - The aim of this study was to assess the effect of type 1 diabetes mellitus (induced by a single intravenous injection of 100 mg kg(-1) of alloxan) on acetylcholine (ACh)-induced relaxation in isolated rabbit parotid gland feeding artery. Isometric force measurements and quantification of inducible nitric oxide synthase (iNOS) mRNA by real-time RT-PCR were made in parotid artery rings from diabetic and control rabbits. Acetylcholine induced concentration- and endothelium-dependent vasorelaxation that was significantly decreased in parotid artery rings from diabetic rabbits. Schild analysis of the ACh vasorelaxant effect, in the presence of selective muscarinic receptor antagonists, revealed involvement of the M(3) receptor subtype in parotid artery rings from both control and diabetic rabbits, with no change in antagonist affinity constants. The inhibitory effects of indomethacin, a non-selective inhibitor of cyclooxygenase, and of high potassium, an inhibitor of hyperpolarization, on ACh vasorelaxation were increased. The effect of N(G)-nitro-L-arginine, a non-selective inhibitor of NOS, was decreased in diabetes. S-methylisothiourea, a selective inhibitor of iNOS, significantly reduced ACh vasorelaxation only in parotid artery rings from diabetic rabbits. Also, up-regulation of iNOS mRNA expression was detected in parotid artery rings from diabetic rabbits. These results suggest that in parotid artery rings from diabetic rabbits, impaired endothelium-dependent vasorelaxation to ACh appears to be caused by the loss of a nitric oxide-mediated component and increased iNOS expression, and is unlikely to be caused by a change at the M(3) receptor level.
T2  - European Journal of Oral Sciences
T1  - Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit
VL  - 119
IS  - 5
SP  - 352
EP  - 360
DO  - 10.1111/j.1600-0722.2011.00851.x
ER  - 

@article{
author = "Roganović, Jelena and Radenković, Miroslav and Tanić, Nikola and Tanić, Nasta and Petrović, Nina and Stojić, Dragica Lj.",
year = "2011",
abstract = "The aim of this study was to assess the effect of type 1 diabetes mellitus (induced by a single intravenous injection of 100 mg kg(-1) of alloxan) on acetylcholine (ACh)-induced relaxation in isolated rabbit parotid gland feeding artery. Isometric force measurements and quantification of inducible nitric oxide synthase (iNOS) mRNA by real-time RT-PCR were made in parotid artery rings from diabetic and control rabbits. Acetylcholine induced concentration- and endothelium-dependent vasorelaxation that was significantly decreased in parotid artery rings from diabetic rabbits. Schild analysis of the ACh vasorelaxant effect, in the presence of selective muscarinic receptor antagonists, revealed involvement of the M(3) receptor subtype in parotid artery rings from both control and diabetic rabbits, with no change in antagonist affinity constants. The inhibitory effects of indomethacin, a non-selective inhibitor of cyclooxygenase, and of high potassium, an inhibitor of hyperpolarization, on ACh vasorelaxation were increased. The effect of N(G)-nitro-L-arginine, a non-selective inhibitor of NOS, was decreased in diabetes. S-methylisothiourea, a selective inhibitor of iNOS, significantly reduced ACh vasorelaxation only in parotid artery rings from diabetic rabbits. Also, up-regulation of iNOS mRNA expression was detected in parotid artery rings from diabetic rabbits. These results suggest that in parotid artery rings from diabetic rabbits, impaired endothelium-dependent vasorelaxation to ACh appears to be caused by the loss of a nitric oxide-mediated component and increased iNOS expression, and is unlikely to be caused by a change at the M(3) receptor level.",
journal = "European Journal of Oral Sciences",
title = "Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit",
volume = "119",
number = "5",
pages = "352-360",
doi = "10.1111/j.1600-0722.2011.00851.x"
}

Roganović, J., Radenković, M., Tanić, N., Tanić, N., Petrović, N.,& Stojić, D. Lj.. (2011). Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit. in European Journal of Oral Sciences, 119(5), 352-360.
https://doi.org/10.1111/j.1600-0722.2011.00851.x

Roganović J, Radenković M, Tanić N, Tanić N, Petrović N, Stojić DL. Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit. in European Journal of Oral Sciences. 2011;119(5):352-360.
doi:10.1111/j.1600-0722.2011.00851.x .

Roganović, Jelena, Radenković, Miroslav, Tanić, Nikola, Tanić, Nasta, Petrović, Nina, Stojić, Dragica Lj., "Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit" in European Journal of Oral Sciences, 119, no. 5 (2011):352-360,
https://doi.org/10.1111/j.1600-0722.2011.00851.x . .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Tanić, Nikola
AU  - Milašin, Jelena
AU  - Vukadinovic, Miroslav
AU  - Dimitrijević, Bogomir B.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3692
AB  - Leukoplakias, clinically identifiable premalignant lesions, often precede oral squamous cell carcinoma (OSCC). Identification of leukoplakias that have the potential for transformation to malignancy is a key clinical problem. The aim of this study was to assess genomic instability, and to detect tumor-specific genomic alterations, in leukoplakias. Genomic instability was analyzed by comparing the DNA fingerprints of 32 leukoplakias with those of paired normal tissue. In addition, the mutational status of the p53 gene was analyzed using polymerase chain reaction-single-stranded conformational polymorphism (PCR-SSCP) and polymerase chain reaction-heteroduplex DNA (PCR-HET), and the mutations were subsequently confirmed by DNA sequencing. Moderate-to-significant genomic instability was detected in all leukoplakias analysed. Nine unique amplicons, present in leukoplakias but not in normal tissue, were retrieved and successfully characterized. The p53 gene was mutated in 40.6% of patients. Four patients with moderate instability and mutated p53 developed OSCC. The data obtained in this study support and concretize the thesis that premalignant lesions possess many of the alterations found in cancer before the development of a malignant phenotype. Inactivation or mutation of the p53 tumor-suppressor might be an early event contributing to genomic instability and increasing the risk of malignant transformation.
T2  - European Journal of Oral Sciences
T1  - Genomic instability and tumor-specific DNA alterations in oral leukoplakias
VL  - 117
IS  - 3
SP  - 231
EP  - 237
DO  - 10.1111/j.1600-0722.2009.00624.x
ER  - 

@article{
author = "Tanić, Nikola and Tanić, Nikola and Milašin, Jelena and Vukadinovic, Miroslav and Dimitrijević, Bogomir B.",
year = "2009",
abstract = "Leukoplakias, clinically identifiable premalignant lesions, often precede oral squamous cell carcinoma (OSCC). Identification of leukoplakias that have the potential for transformation to malignancy is a key clinical problem. The aim of this study was to assess genomic instability, and to detect tumor-specific genomic alterations, in leukoplakias. Genomic instability was analyzed by comparing the DNA fingerprints of 32 leukoplakias with those of paired normal tissue. In addition, the mutational status of the p53 gene was analyzed using polymerase chain reaction-single-stranded conformational polymorphism (PCR-SSCP) and polymerase chain reaction-heteroduplex DNA (PCR-HET), and the mutations were subsequently confirmed by DNA sequencing. Moderate-to-significant genomic instability was detected in all leukoplakias analysed. Nine unique amplicons, present in leukoplakias but not in normal tissue, were retrieved and successfully characterized. The p53 gene was mutated in 40.6% of patients. Four patients with moderate instability and mutated p53 developed OSCC. The data obtained in this study support and concretize the thesis that premalignant lesions possess many of the alterations found in cancer before the development of a malignant phenotype. Inactivation or mutation of the p53 tumor-suppressor might be an early event contributing to genomic instability and increasing the risk of malignant transformation.",
journal = "European Journal of Oral Sciences",
title = "Genomic instability and tumor-specific DNA alterations in oral leukoplakias",
volume = "117",
number = "3",
pages = "231-237",
doi = "10.1111/j.1600-0722.2009.00624.x"
}

Tanić, N., Tanić, N., Milašin, J., Vukadinovic, M.,& Dimitrijević, B. B.. (2009). Genomic instability and tumor-specific DNA alterations in oral leukoplakias. in European Journal of Oral Sciences, 117(3), 231-237.
https://doi.org/10.1111/j.1600-0722.2009.00624.x

Tanić N, Tanić N, Milašin J, Vukadinovic M, Dimitrijević BB. Genomic instability and tumor-specific DNA alterations in oral leukoplakias. in European Journal of Oral Sciences. 2009;117(3):231-237.
doi:10.1111/j.1600-0722.2009.00624.x .

Tanić, Nikola, Tanić, Nikola, Milašin, Jelena, Vukadinovic, Miroslav, Dimitrijević, Bogomir B., "Genomic instability and tumor-specific DNA alterations in oral leukoplakias" in European Journal of Oral Sciences, 117, no. 3 (2009):231-237,
https://doi.org/10.1111/j.1600-0722.2009.00624.x . .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Stanojević, Boban
AU  - Tanić, Nikola
AU  - Schaefer, Stephan
AU  - Niesters, Hubert G. M.
AU  - Božić, Milena
AU  - Dimitrijević, Bogomir B.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3789
AB  - Hepatitis B virus (HBV) infection is a global health problem associated with severe liver disorders. Viral load and HBV genotype affect the clinical outcome, guide antiviral therapy and provide long term prognosis for HBV infected patients. Various types of detection and quantitation assays are currently in use with a different effectiveness. The aim of this study was to develop a method that would provide simultaneous identification and quantitation of genotypes A and D in a single-tube reaction. Sera from infected patients were analyzed by a TaqMan based real time PCR. Optimized reagents were used for HBV DNA quantitation while the genotypes A and D were quantified separately by our design of the assay. Multiplex real time PCR was achieved and was specific for HBV genotypes A and D within a single-tube reaction. Simulation of mixed virus populations was identified reproducibly in vitro. Quantitation of these individual genotypes was exceptionally reliable, so much so that the sum of individual genotypes was equal to the total viral load determined in a separate reaction. Therefore, a straightforward, conceptually simple and reliable approach to issues involving HBV genotypes A and D is submitted. Identity and exact titer of these genotypes in the Caucasian population can now be determined easily. (C) 2009 Elsevier B.V. All rights reserved.
T2  - Journal of Virological Methods
T1  - Concurrent quantitation of the A and D genotypes of hepatitis B virus
VL  - 161
IS  - 2
SP  - 265
EP  - 270
DO  - 10.1016/j.jviromet.2009.06.022
ER  - 

@article{
author = "Tanić, Nikola and Stanojević, Boban and Tanić, Nikola and Schaefer, Stephan and Niesters, Hubert G. M. and Božić, Milena and Dimitrijević, Bogomir B.",
year = "2009",
abstract = "Hepatitis B virus (HBV) infection is a global health problem associated with severe liver disorders. Viral load and HBV genotype affect the clinical outcome, guide antiviral therapy and provide long term prognosis for HBV infected patients. Various types of detection and quantitation assays are currently in use with a different effectiveness. The aim of this study was to develop a method that would provide simultaneous identification and quantitation of genotypes A and D in a single-tube reaction. Sera from infected patients were analyzed by a TaqMan based real time PCR. Optimized reagents were used for HBV DNA quantitation while the genotypes A and D were quantified separately by our design of the assay. Multiplex real time PCR was achieved and was specific for HBV genotypes A and D within a single-tube reaction. Simulation of mixed virus populations was identified reproducibly in vitro. Quantitation of these individual genotypes was exceptionally reliable, so much so that the sum of individual genotypes was equal to the total viral load determined in a separate reaction. Therefore, a straightforward, conceptually simple and reliable approach to issues involving HBV genotypes A and D is submitted. Identity and exact titer of these genotypes in the Caucasian population can now be determined easily. (C) 2009 Elsevier B.V. All rights reserved.",
journal = "Journal of Virological Methods",
title = "Concurrent quantitation of the A and D genotypes of hepatitis B virus",
volume = "161",
number = "2",
pages = "265-270",
doi = "10.1016/j.jviromet.2009.06.022"
}

Tanić, N., Stanojević, B., Tanić, N., Schaefer, S., Niesters, H. G. M., Božić, M.,& Dimitrijević, B. B.. (2009). Concurrent quantitation of the A and D genotypes of hepatitis B virus. in Journal of Virological Methods, 161(2), 265-270.
https://doi.org/10.1016/j.jviromet.2009.06.022

Tanić N, Stanojević B, Tanić N, Schaefer S, Niesters HGM, Božić M, Dimitrijević BB. Concurrent quantitation of the A and D genotypes of hepatitis B virus. in Journal of Virological Methods. 2009;161(2):265-270.
doi:10.1016/j.jviromet.2009.06.022 .

Tanić, Nikola, Stanojević, Boban, Tanić, Nikola, Schaefer, Stephan, Niesters, Hubert G. M., Božić, Milena, Dimitrijević, Bogomir B., "Concurrent quantitation of the A and D genotypes of hepatitis B virus" in Journal of Virological Methods, 161, no. 2 (2009):265-270,
https://doi.org/10.1016/j.jviromet.2009.06.022 . .

TY  - JOUR
AU  - Gavrilović, Ljubica
AU  - Spasojević, Nataša
AU  - Tanić, Nikola
AU  - Dronjak, Slađana
PY  - 2008
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3629
AB  - OBJECTIVE: Isolation of adult animals represents a form of psychsocial stress that produces sympatho-adrenomedullar activation. The aim of this work was to investigate the changes in gene expression and protein levels of catecholamine biosynthetic enzymes: tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) in the adrenal medulla of naive control and chronically (12 weeks) socially isolated adult Wistar rat males and the response of these animals to additional immobilization stress (2 h). METHODS: TH, DBH and PNMT mRNA levels were quantified by quantitative real-time RT-PCR (qRT-PCR). TH, DBH and PNMT immunoproteins were assayed by Western Blot. RESULTS: In chronically isolated rats, gene expression levels of catecholamine biosynthetic enzymes in the adrenal medulla were decreased, but only TH mRNA was significantly decreased. However, protein levels of TH, DBH and PNMT of these animals were elevated by 55%, 20% and 18%, respectively, in relation to the corresponding control. Naive control and chronically socially isolated rats exposed to additional 2-h-immobilization showed increased gene expression of the examined enzymes, the increase being greater in socially isolated rats as compared to the controls. Additional immobilization of naive controls did not affect TH, DBH and PNMT protein levels. In contrast, this stress produced increased TH, DBH and PNMT protein levels in long-term socially isolated rats. CONCLUSION: We can conclud that psychosocial stress expressed a differential influence on gene expression and protein levels of catecholamine biosynthetic enzymes in the adrenal medulla of adult rats. The results indicate a possible adaptation of catecholamine-synthesizing system at the level of TH gene expression in adrenal medulla of chronically isolated animals.
T2  - Neuroendocrinology Letters
T1  - Chronic isolation of adult rats decreases gene expression of catecholamine biosynthetic enzymes in adrenal medulla
VL  - 29
IS  - 6
SP  - 1015
EP  - 1020
UR  - https://hdl.handle.net/21.15107/rcub_vinar_3629
ER  - 

@article{
author = "Gavrilović, Ljubica and Spasojević, Nataša and Tanić, Nikola and Dronjak, Slađana",
year = "2008",
abstract = "OBJECTIVE: Isolation of adult animals represents a form of psychsocial stress that produces sympatho-adrenomedullar activation. The aim of this work was to investigate the changes in gene expression and protein levels of catecholamine biosynthetic enzymes: tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) in the adrenal medulla of naive control and chronically (12 weeks) socially isolated adult Wistar rat males and the response of these animals to additional immobilization stress (2 h). METHODS: TH, DBH and PNMT mRNA levels were quantified by quantitative real-time RT-PCR (qRT-PCR). TH, DBH and PNMT immunoproteins were assayed by Western Blot. RESULTS: In chronically isolated rats, gene expression levels of catecholamine biosynthetic enzymes in the adrenal medulla were decreased, but only TH mRNA was significantly decreased. However, protein levels of TH, DBH and PNMT of these animals were elevated by 55%, 20% and 18%, respectively, in relation to the corresponding control. Naive control and chronically socially isolated rats exposed to additional 2-h-immobilization showed increased gene expression of the examined enzymes, the increase being greater in socially isolated rats as compared to the controls. Additional immobilization of naive controls did not affect TH, DBH and PNMT protein levels. In contrast, this stress produced increased TH, DBH and PNMT protein levels in long-term socially isolated rats. CONCLUSION: We can conclud that psychosocial stress expressed a differential influence on gene expression and protein levels of catecholamine biosynthetic enzymes in the adrenal medulla of adult rats. The results indicate a possible adaptation of catecholamine-synthesizing system at the level of TH gene expression in adrenal medulla of chronically isolated animals.",
journal = "Neuroendocrinology Letters",
title = "Chronic isolation of adult rats decreases gene expression of catecholamine biosynthetic enzymes in adrenal medulla",
volume = "29",
number = "6",
pages = "1015-1020",
url = "https://hdl.handle.net/21.15107/rcub_vinar_3629"
}

Gavrilović, L., Spasojević, N., Tanić, N.,& Dronjak, S.. (2008). Chronic isolation of adult rats decreases gene expression of catecholamine biosynthetic enzymes in adrenal medulla. in Neuroendocrinology Letters, 29(6), 1015-1020.
https://hdl.handle.net/21.15107/rcub_vinar_3629

Gavrilović L, Spasojević N, Tanić N, Dronjak S. Chronic isolation of adult rats decreases gene expression of catecholamine biosynthetic enzymes in adrenal medulla. in Neuroendocrinology Letters. 2008;29(6):1015-1020.
https://hdl.handle.net/21.15107/rcub_vinar_3629 .

Gavrilović, Ljubica, Spasojević, Nataša, Tanić, Nikola, Dronjak, Slađana, "Chronic isolation of adult rats decreases gene expression of catecholamine biosynthetic enzymes in adrenal medulla" in Neuroendocrinology Letters, 29, no. 6 (2008):1015-1020,
https://hdl.handle.net/21.15107/rcub_vinar_3629 .

TY  - JOUR
AU  - Mandušić, Vesna
AU  - Nikolić-Vukosavljević, Dragica
AU  - Tanić, Nikola
AU  - Kanjer, Ksenija
AU  - Nešković-Konstantinović, Zora
AU  - Celeketic, Dusica
AU  - Dimitrijević, Bogomir B.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/2576
AB  - Purpose In addition to Estrogen Receptor alpha (ER alpha) and Progesterone Receptor (PR), the Second Estrogen Receptor (ER beta) appears to play an important role not only in estrogen signaling, but also in the pathogenesis of cancer in estrogen dependent tissues. The existence of various isoforms and splice variants of both ERs additionally complicates elucidation of their physiological role and involvement in the process of carcinogenesis. Methods In this study, the expression of ER beta 1 mRNA (wild type of beta receptor) and splice variant ER beta Delta 5 mRNA (which codes for truncated protein) was measured by the quantitative RT-PCR (q RT-PCR) in the 60 samples of Breast Cancer (BC) and correlated with ER alpha and PR protein levels and with clinical and histopathological parameters. Results We found the inverse correlation of ER beta Delta 5 mRNA expression with the levels of PR and ER alpha proteins in the group of postmenopausal patients; we also report the lower expression of ER beta 1 and ER beta Delta 5 mRNA in the larger tumors ( GT 20 mm, T2, and T3) than in smaller ones ( LT = 20 mm, T1). The decrease of ER beta Delta 5 mRNA expression in larger tumors is found to arise from ER-positive breast carcinomas. In addition, the portion of tumors with concomitant high expression of both transcripts matches up the known percentage of tumors resistant to endocrine therapy in patients with different ER/PR status. Conclusions As far as we know, this is the first study in which ER beta Delta 5 mRNA splice variant was quantified by realtime RT-PCR in the clinical samples of breast cancer tissue. Until now, the focus of clinical reports was the level of ER beta 1, ER beta 2, and ER beta 5 isoforms. The higher expression of ER beta Delta 5 mRNA is associated with the indicators of low biological aggressiveness of tumor (low tumor size within ER-positive status in our study) suggesting that the uncontrolled local tumor growth may occur as the expression of ER beta Delta 5 mRNA decreases in estrogen-dependent breast cancer.
T2  - Journal of Cancer Research and Clinical Oncology
T1  - Expression of estrogen receptor beta wt isoform (ER beta 1) and ER beta Delta 5 splice variant mRNAs in sporadic breast cancer
VL  - 133
IS  - 8
SP  - 571
EP  - 579
DO  - 10.1007/s00432-007-0209-x
ER  - 

@article{
author = "Mandušić, Vesna and Nikolić-Vukosavljević, Dragica and Tanić, Nikola and Kanjer, Ksenija and Nešković-Konstantinović, Zora and Celeketic, Dusica and Dimitrijević, Bogomir B.",
year = "2007",
abstract = "Purpose In addition to Estrogen Receptor alpha (ER alpha) and Progesterone Receptor (PR), the Second Estrogen Receptor (ER beta) appears to play an important role not only in estrogen signaling, but also in the pathogenesis of cancer in estrogen dependent tissues. The existence of various isoforms and splice variants of both ERs additionally complicates elucidation of their physiological role and involvement in the process of carcinogenesis. Methods In this study, the expression of ER beta 1 mRNA (wild type of beta receptor) and splice variant ER beta Delta 5 mRNA (which codes for truncated protein) was measured by the quantitative RT-PCR (q RT-PCR) in the 60 samples of Breast Cancer (BC) and correlated with ER alpha and PR protein levels and with clinical and histopathological parameters. Results We found the inverse correlation of ER beta Delta 5 mRNA expression with the levels of PR and ER alpha proteins in the group of postmenopausal patients; we also report the lower expression of ER beta 1 and ER beta Delta 5 mRNA in the larger tumors ( GT 20 mm, T2, and T3) than in smaller ones ( LT = 20 mm, T1). The decrease of ER beta Delta 5 mRNA expression in larger tumors is found to arise from ER-positive breast carcinomas. In addition, the portion of tumors with concomitant high expression of both transcripts matches up the known percentage of tumors resistant to endocrine therapy in patients with different ER/PR status. Conclusions As far as we know, this is the first study in which ER beta Delta 5 mRNA splice variant was quantified by realtime RT-PCR in the clinical samples of breast cancer tissue. Until now, the focus of clinical reports was the level of ER beta 1, ER beta 2, and ER beta 5 isoforms. The higher expression of ER beta Delta 5 mRNA is associated with the indicators of low biological aggressiveness of tumor (low tumor size within ER-positive status in our study) suggesting that the uncontrolled local tumor growth may occur as the expression of ER beta Delta 5 mRNA decreases in estrogen-dependent breast cancer.",
journal = "Journal of Cancer Research and Clinical Oncology",
title = "Expression of estrogen receptor beta wt isoform (ER beta 1) and ER beta Delta 5 splice variant mRNAs in sporadic breast cancer",
volume = "133",
number = "8",
pages = "571-579",
doi = "10.1007/s00432-007-0209-x"
}

Mandušić, V., Nikolić-Vukosavljević, D., Tanić, N., Kanjer, K., Nešković-Konstantinović, Z., Celeketic, D.,& Dimitrijević, B. B.. (2007). Expression of estrogen receptor beta wt isoform (ER beta 1) and ER beta Delta 5 splice variant mRNAs in sporadic breast cancer. in Journal of Cancer Research and Clinical Oncology, 133(8), 571-579.
https://doi.org/10.1007/s00432-007-0209-x

Mandušić V, Nikolić-Vukosavljević D, Tanić N, Kanjer K, Nešković-Konstantinović Z, Celeketic D, Dimitrijević BB. Expression of estrogen receptor beta wt isoform (ER beta 1) and ER beta Delta 5 splice variant mRNAs in sporadic breast cancer. in Journal of Cancer Research and Clinical Oncology. 2007;133(8):571-579.
doi:10.1007/s00432-007-0209-x .

Mandušić, Vesna, Nikolić-Vukosavljević, Dragica, Tanić, Nikola, Kanjer, Ksenija, Nešković-Konstantinović, Zora, Celeketic, Dusica, Dimitrijević, Bogomir B., "Expression of estrogen receptor beta wt isoform (ER beta 1) and ER beta Delta 5 splice variant mRNAs in sporadic breast cancer" in Journal of Cancer Research and Clinical Oncology, 133, no. 8 (2007):571-579,
https://doi.org/10.1007/s00432-007-0209-x . .

TY  - JOUR
AU  - Mandušić, Vesna
AU  - Krtolica-Žikić, Koviljka
AU  - Nikolić-Vukosavljević, Dragica
AU  - Popov-Celeketic, D.
AU  - Plećaš, D.
AU  - Boricic, I.
AU  - Dimitrijević, Bogomir B.
AU  - Tanić, Nikola
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3414
T2  - Archives of Biological Sciences
T1  - Transcriptional ratio of estrogen receptor beta mRNAs in carcinomas and in normal tissues.
VL  - 59
IS  - 2
SP  - 15P
EP  - 16P
DO  - 10.2298/ABS070215PM
ER  - 

@article{
author = "Mandušić, Vesna and Krtolica-Žikić, Koviljka and Nikolić-Vukosavljević, Dragica and Popov-Celeketic, D. and Plećaš, D. and Boricic, I. and Dimitrijević, Bogomir B. and Tanić, Nikola",
year = "2007",
journal = "Archives of Biological Sciences",
title = "Transcriptional ratio of estrogen receptor beta mRNAs in carcinomas and in normal tissues.",
volume = "59",
number = "2",
pages = "15P-16P",
doi = "10.2298/ABS070215PM"
}

Mandušić, V., Krtolica-Žikić, K., Nikolić-Vukosavljević, D., Popov-Celeketic, D., Plećaš, D., Boricic, I., Dimitrijević, B. B.,& Tanić, N.. (2007). Transcriptional ratio of estrogen receptor beta mRNAs in carcinomas and in normal tissues.. in Archives of Biological Sciences, 59(2), 15P-16P.
https://doi.org/10.2298/ABS070215PM

Mandušić V, Krtolica-Žikić K, Nikolić-Vukosavljević D, Popov-Celeketic D, Plećaš D, Boricic I, Dimitrijević BB, Tanić N. Transcriptional ratio of estrogen receptor beta mRNAs in carcinomas and in normal tissues.. in Archives of Biological Sciences. 2007;59(2):15P-16P.
doi:10.2298/ABS070215PM .

Mandušić, Vesna, Krtolica-Žikić, Koviljka, Nikolić-Vukosavljević, Dragica, Popov-Celeketic, D., Plećaš, D., Boricic, I., Dimitrijević, Bogomir B., Tanić, Nikola, "Transcriptional ratio of estrogen receptor beta mRNAs in carcinomas and in normal tissues." in Archives of Biological Sciences, 59, no. 2 (2007):15P-16P,
https://doi.org/10.2298/ABS070215PM . .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Brkić, G
AU  - Dimitrijević, Bogomir B.
AU  - Dedović-Tanić, Nasta
AU  - Gefen, N
AU  - Benharroch, D
AU  - Gopas, J
PY  - 2006
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3032
AB  - Background: Malignant melanoma resistance to chemotherapy remains a major limitation to treatment. Our aim was to identify genes associated with drug resistance, in order to better understand the molecular events underlying the drug-resistant phenotype. Materials and Methods: A human melanoma cell line and its drug-resistant variants obtained by selection with MNNG or 6-thioguanine were used. Alterations in gene expression were characterized by differential display reverse transcription-polymerase chain reaction (DDRT-PCR). Prominent mRNA fragments present in selected variants and not in the parental cells were identified and characterized by cloning and sequencing. Differential expression was confirmed by real-time RT-PCR. Results: Three functionally distinct transcriptional products were demonstrated: the chaperonin subunit TCP 1-zeta-6A (CCT6A), the hyaluronan receptor CD44 and LPPR-2, the lipid phosphate phosphatase-related protein type-2. Conclusion: Genes with altered expression were identified in drug-resistant variants. The identified molecules may provide new insights into the molecular basis for melanoma resistance to chemotherapy.
T2  - Anticancer Research
T1  - Identification of differentially expressed mRNA transcripts in drug-resistant versus parental human melanoma cell lines
VL  - 26
IS  - 3A
SP  - 2137
EP  - 2142
UR  - https://hdl.handle.net/21.15107/rcub_vinar_3032
ER  - 

@article{
author = "Tanić, Nikola and Brkić, G and Dimitrijević, Bogomir B. and Dedović-Tanić, Nasta and Gefen, N and Benharroch, D and Gopas, J",
year = "2006",
abstract = "Background: Malignant melanoma resistance to chemotherapy remains a major limitation to treatment. Our aim was to identify genes associated with drug resistance, in order to better understand the molecular events underlying the drug-resistant phenotype. Materials and Methods: A human melanoma cell line and its drug-resistant variants obtained by selection with MNNG or 6-thioguanine were used. Alterations in gene expression were characterized by differential display reverse transcription-polymerase chain reaction (DDRT-PCR). Prominent mRNA fragments present in selected variants and not in the parental cells were identified and characterized by cloning and sequencing. Differential expression was confirmed by real-time RT-PCR. Results: Three functionally distinct transcriptional products were demonstrated: the chaperonin subunit TCP 1-zeta-6A (CCT6A), the hyaluronan receptor CD44 and LPPR-2, the lipid phosphate phosphatase-related protein type-2. Conclusion: Genes with altered expression were identified in drug-resistant variants. The identified molecules may provide new insights into the molecular basis for melanoma resistance to chemotherapy.",
journal = "Anticancer Research",
title = "Identification of differentially expressed mRNA transcripts in drug-resistant versus parental human melanoma cell lines",
volume = "26",
number = "3A",
pages = "2137-2142",
url = "https://hdl.handle.net/21.15107/rcub_vinar_3032"
}

Tanić, N., Brkić, G., Dimitrijević, B. B., Dedović-Tanić, N., Gefen, N., Benharroch, D.,& Gopas, J.. (2006). Identification of differentially expressed mRNA transcripts in drug-resistant versus parental human melanoma cell lines. in Anticancer Research, 26(3A), 2137-2142.
https://hdl.handle.net/21.15107/rcub_vinar_3032

Tanić N, Brkić G, Dimitrijević BB, Dedović-Tanić N, Gefen N, Benharroch D, Gopas J. Identification of differentially expressed mRNA transcripts in drug-resistant versus parental human melanoma cell lines. in Anticancer Research. 2006;26(3A):2137-2142.
https://hdl.handle.net/21.15107/rcub_vinar_3032 .

Tanić, Nikola, Brkić, G, Dimitrijević, Bogomir B., Dedović-Tanić, Nasta, Gefen, N, Benharroch, D, Gopas, J, "Identification of differentially expressed mRNA transcripts in drug-resistant versus parental human melanoma cell lines" in Anticancer Research, 26, no. 3A (2006):2137-2142,
https://hdl.handle.net/21.15107/rcub_vinar_3032 .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Vujošević, Mladen
AU  - Dedović-Tanić, Nasta
AU  - Dimitrijević, Bogomir B.
PY  - 2005
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/2866
AB  - Most B chromosomes are heavily heterochromatic, promoting the general idea that they are genetically inert. The B chromosomes of Apodemus flavicollis are euchromatic and show a high degree of homology with the chromosomes. The euchromatic nature of chromosomes in A. flavicollis suggests that they may carry active genes and have transcriptional activity. We applied the differential display reverse transcription-polymerase chain reaction (DD RT-PCR) in order to analyze and compare gene expression in animals possessing chromosomes and animals without B chromosomes. After a second and third round of amplification, three cDNA fragments were differentially expressed in +B mice compared with 0B animals. These cDNAs were Chaperonin containing TCP-1, subunit 6b (zeta) (CCT6B), Fragile histidine triad gene (FHIT) and hypothetical gene XP transcript. The differential expression pattern was confirmed by Real Time RT-PCR. We suggest that altered expression of these important genes is due to the presence of B chromosomes. In elevating the expression of these genes, B chromosomes of A. flavicollis affect some of the crucial processes in the cell. The significance of these effects and the nature of B chromosomes of A. flavicollis are discussed in the context of the data presented.
T2  - Chromosoma
T1  - Differential gene expression in yellow-necked mice Apodemus flavicollis (Rodentia, Mammalia) with and without B chromosomes
VL  - 113
IS  - 8
SP  - 418
EP  - 427
DO  - 10.1007/s00412-004-0327-z
ER  - 

@article{
author = "Tanić, Nikola and Vujošević, Mladen and Dedović-Tanić, Nasta and Dimitrijević, Bogomir B.",
year = "2005",
abstract = "Most B chromosomes are heavily heterochromatic, promoting the general idea that they are genetically inert. The B chromosomes of Apodemus flavicollis are euchromatic and show a high degree of homology with the chromosomes. The euchromatic nature of chromosomes in A. flavicollis suggests that they may carry active genes and have transcriptional activity. We applied the differential display reverse transcription-polymerase chain reaction (DD RT-PCR) in order to analyze and compare gene expression in animals possessing chromosomes and animals without B chromosomes. After a second and third round of amplification, three cDNA fragments were differentially expressed in +B mice compared with 0B animals. These cDNAs were Chaperonin containing TCP-1, subunit 6b (zeta) (CCT6B), Fragile histidine triad gene (FHIT) and hypothetical gene XP transcript. The differential expression pattern was confirmed by Real Time RT-PCR. We suggest that altered expression of these important genes is due to the presence of B chromosomes. In elevating the expression of these genes, B chromosomes of A. flavicollis affect some of the crucial processes in the cell. The significance of these effects and the nature of B chromosomes of A. flavicollis are discussed in the context of the data presented.",
journal = "Chromosoma",
title = "Differential gene expression in yellow-necked mice Apodemus flavicollis (Rodentia, Mammalia) with and without B chromosomes",
volume = "113",
number = "8",
pages = "418-427",
doi = "10.1007/s00412-004-0327-z"
}

Tanić, N., Vujošević, M., Dedović-Tanić, N.,& Dimitrijević, B. B.. (2005). Differential gene expression in yellow-necked mice Apodemus flavicollis (Rodentia, Mammalia) with and without B chromosomes. in Chromosoma, 113(8), 418-427.
https://doi.org/10.1007/s00412-004-0327-z

Tanić N, Vujošević M, Dedović-Tanić N, Dimitrijević BB. Differential gene expression in yellow-necked mice Apodemus flavicollis (Rodentia, Mammalia) with and without B chromosomes. in Chromosoma. 2005;113(8):418-427.
doi:10.1007/s00412-004-0327-z .

Tanić, Nikola, Vujošević, Mladen, Dedović-Tanić, Nasta, Dimitrijević, Bogomir B., "Differential gene expression in yellow-necked mice Apodemus flavicollis (Rodentia, Mammalia) with and without B chromosomes" in Chromosoma, 113, no. 8 (2005):418-427,
https://doi.org/10.1007/s00412-004-0327-z . .

TY  - JOUR
AU  - Brkić, G
AU  - Gopas, J
AU  - Tanić, Nikola
AU  - Dedović-Tanić, Nasta
AU  - Benharroch, D
AU  - Finkelstein-Jaworowsky, E
AU  - Kedar, I
AU  - Dimitrijević, Bogomir B.
PY  - 2003
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/2652
AB  - Destabilization of the genome seems to be an important step in the generation of drug resistance. Since malignant melanoma is extremely resistant to chemotherapy, we used human melanoma cell lines as a model to investigate the putative role of genomic instability in the appearance of drug resistance. Drug-resistant variants were obtained with MNNG, BiCNU, doxorubicin and 6-thioguanine selection of melanoma cell lines. Genomic alterations in variant cells were detected by arbitrarily primed PCR of Alu-I digested DNA (Alu-I-AP-PCR). Two differential DNA bands from 6-TG-resistant cell variants were sequenced. One is homologous to intron 25 of the neural cell adhesion molecule L1 and the second to endogenous retroviral LTR sequences. We have shown that drug-resistant melanoma cell lines accumulate genomic alterations that are efficiently detected by Alu I-AP-PCR and that drug-resistant variants show genomic instability, including variations in LTR sequences, which may be associated with the appearance of the drug resistance phenotype.
T2  - Anticancer Research
T1  - Genomic instability in drug-resistant human melanoma cell lines detected by Alu-I-arbitrary-primed PCR
VL  - 23
IS  - 3B
SP  - 2601
EP  - 2608
UR  - https://hdl.handle.net/21.15107/rcub_vinar_2652
ER  - 

@article{
author = "Brkić, G and Gopas, J and Tanić, Nikola and Dedović-Tanić, Nasta and Benharroch, D and Finkelstein-Jaworowsky, E and Kedar, I and Dimitrijević, Bogomir B.",
year = "2003",
abstract = "Destabilization of the genome seems to be an important step in the generation of drug resistance. Since malignant melanoma is extremely resistant to chemotherapy, we used human melanoma cell lines as a model to investigate the putative role of genomic instability in the appearance of drug resistance. Drug-resistant variants were obtained with MNNG, BiCNU, doxorubicin and 6-thioguanine selection of melanoma cell lines. Genomic alterations in variant cells were detected by arbitrarily primed PCR of Alu-I digested DNA (Alu-I-AP-PCR). Two differential DNA bands from 6-TG-resistant cell variants were sequenced. One is homologous to intron 25 of the neural cell adhesion molecule L1 and the second to endogenous retroviral LTR sequences. We have shown that drug-resistant melanoma cell lines accumulate genomic alterations that are efficiently detected by Alu I-AP-PCR and that drug-resistant variants show genomic instability, including variations in LTR sequences, which may be associated with the appearance of the drug resistance phenotype.",
journal = "Anticancer Research",
title = "Genomic instability in drug-resistant human melanoma cell lines detected by Alu-I-arbitrary-primed PCR",
volume = "23",
number = "3B",
pages = "2601-2608",
url = "https://hdl.handle.net/21.15107/rcub_vinar_2652"
}

Brkić, G., Gopas, J., Tanić, N., Dedović-Tanić, N., Benharroch, D., Finkelstein-Jaworowsky, E., Kedar, I.,& Dimitrijević, B. B.. (2003). Genomic instability in drug-resistant human melanoma cell lines detected by Alu-I-arbitrary-primed PCR. in Anticancer Research, 23(3B), 2601-2608.
https://hdl.handle.net/21.15107/rcub_vinar_2652

Brkić G, Gopas J, Tanić N, Dedović-Tanić N, Benharroch D, Finkelstein-Jaworowsky E, Kedar I, Dimitrijević BB. Genomic instability in drug-resistant human melanoma cell lines detected by Alu-I-arbitrary-primed PCR. in Anticancer Research. 2003;23(3B):2601-2608.
https://hdl.handle.net/21.15107/rcub_vinar_2652 .

Brkić, G, Gopas, J, Tanić, Nikola, Dedović-Tanić, Nasta, Benharroch, D, Finkelstein-Jaworowsky, E, Kedar, I, Dimitrijević, Bogomir B., "Genomic instability in drug-resistant human melanoma cell lines detected by Alu-I-arbitrary-primed PCR" in Anticancer Research, 23, no. 3B (2003):2601-2608,
https://hdl.handle.net/21.15107/rcub_vinar_2652 .

TY  - JOUR
AU  - Tanić, Nikola
AU  - Dedović-Tanić, Nasta
AU  - Vujošević, Mladen
AU  - Dimitrijević, Bogomir B.
PY  - 2000
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/2325
AB  - Using AP-PCR-based DNA profiling we examined some structural features of B chromosomes from yellow-necked mice Apodemus flavicollis. Mice harboring one,two, or three or lacking B chromosomes were examined. Chromosomal structure was scanned for variant bands by using a series of arbitrary primers and From these, informative bands were selected. The selection:criteria used were the ability to differentiate between individuals of the species, to detect markers common For both A and B chromosomes, and, importantly, to differentiate between A- and B-chromosome sets. In addition to primers, profiling conditions were found to be critical for meeting the selection criteria. Primers and analysis conditions that demonstrated structural characteristics unique to the B-chromosome set are described. These characteristics included variant bands as qualitative parameters and altered electrophoretic band-intensities as quantitative distinctions estimated by integration of densitometric profiles of electrophoretograms. B chromosome-specific molecular markers are easy to detect by AP-PCR-based DNA profiling in the presence of a full set of A chromosomes. Models for the origin of yellow-necked mouse B chromosomes are discussed in the context of presented data.
T2  - Genome Research
T1  - DNA profiling of B chromosomes from the yellow-necked mouse Apodemus flavicollis (Rodentia, Mammalia)
VL  - 10
IS  - 1
SP  - 55
EP  - 61
UR  - https://hdl.handle.net/21.15107/rcub_vinar_2325
ER  - 

@article{
author = "Tanić, Nikola and Dedović-Tanić, Nasta and Vujošević, Mladen and Dimitrijević, Bogomir B.",
year = "2000",
abstract = "Using AP-PCR-based DNA profiling we examined some structural features of B chromosomes from yellow-necked mice Apodemus flavicollis. Mice harboring one,two, or three or lacking B chromosomes were examined. Chromosomal structure was scanned for variant bands by using a series of arbitrary primers and From these, informative bands were selected. The selection:criteria used were the ability to differentiate between individuals of the species, to detect markers common For both A and B chromosomes, and, importantly, to differentiate between A- and B-chromosome sets. In addition to primers, profiling conditions were found to be critical for meeting the selection criteria. Primers and analysis conditions that demonstrated structural characteristics unique to the B-chromosome set are described. These characteristics included variant bands as qualitative parameters and altered electrophoretic band-intensities as quantitative distinctions estimated by integration of densitometric profiles of electrophoretograms. B chromosome-specific molecular markers are easy to detect by AP-PCR-based DNA profiling in the presence of a full set of A chromosomes. Models for the origin of yellow-necked mouse B chromosomes are discussed in the context of presented data.",
journal = "Genome Research",
title = "DNA profiling of B chromosomes from the yellow-necked mouse Apodemus flavicollis (Rodentia, Mammalia)",
volume = "10",
number = "1",
pages = "55-61",
url = "https://hdl.handle.net/21.15107/rcub_vinar_2325"
}

Tanić, N., Dedović-Tanić, N., Vujošević, M.,& Dimitrijević, B. B.. (2000). DNA profiling of B chromosomes from the yellow-necked mouse Apodemus flavicollis (Rodentia, Mammalia). in Genome Research, 10(1), 55-61.
https://hdl.handle.net/21.15107/rcub_vinar_2325

Tanić N, Dedović-Tanić N, Vujošević M, Dimitrijević BB. DNA profiling of B chromosomes from the yellow-necked mouse Apodemus flavicollis (Rodentia, Mammalia). in Genome Research. 2000;10(1):55-61.
https://hdl.handle.net/21.15107/rcub_vinar_2325 .

Tanić, Nikola, Dedović-Tanić, Nasta, Vujošević, Mladen, Dimitrijević, Bogomir B., "DNA profiling of B chromosomes from the yellow-necked mouse Apodemus flavicollis (Rodentia, Mammalia)" in Genome Research, 10, no. 1 (2000):55-61,
https://hdl.handle.net/21.15107/rcub_vinar_2325 .