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  - 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  - 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 . .