TY  - JOUR
AU  - Tanić, Nasta
AU  - Milašin, Jelena
AU  - Dramićanin, Tatjana
AU  - Bošković, Maja
AU  - Vukadinović, Miroslav
AU  - Milošević, Verica
AU  - Tanić, Nikola
PY  - 2013
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1780
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. Therefore, 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%, cycDI 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 cycDI 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.
AB  - Uvod: Skvamocelularni karcinomi glave i vrata (HNSCC) uključujući i skvamocelularni karcinom usne duplje (OSCC) ubrajaju se u šest najčešćih tipova humanih maligniteta. Uprkos značajnim napredcima u hirurškom i terapijskom tretmanu, stopa petogodišnjeg preživljavanja kod ovog tipa maligniteta nije značajnije popravljena. Upravo zato, definisanje pouzdanih molekularnih markera progresije kod OSSC predstavlja apsolutni prioritetet. Metode: Amplifikacioni status c-myc, cycD1 i EGFR gena određen je pomoću eseja za detekciju broja genskih kopija, aktivacija H-ras onkogena i inaktivacija TP53 tumor supresora određena je PCR-SSCP mutacionom analizom, a hipermetilacija promotora p16 i MGMT gena je ispitana metil specifičnim PCR-om (MSP). Rezultati: Amplifikacija c-myc onkogena detektovana je kod 56,7%, cycD1 onkogena kod 20%, a EGFR onkogena kod 16,7% analiziranih oralnih skvamocelularnih carcinoma. Istovremeno, mutaciona aktivacija H-ras onkogena detektovana je kod 33,3% ispitanih uzoraka. Amplifikovani c-myc, statistički značajno korelira sa gradusom 2 OSCC. Posebno intrigantan je bio nalaz po kom se onkogene aktivacije u EGFR i H-ras genu međusobno isključuju. Hipermetilacija promotora p16 gena detektovana je kod 30%, a MGMT kod 13,3% analiziranih uzoraka. Ko-alteracije cycDI i p16 gena nisu zapažene ni u jednom od analiziranih uzoraka. Inaktivacija TP53 gena detektovana je kod 56,7% uzoraka i utvrđeno je da statistički značajno korelira sa gradusom 2 i statusom 2 OSCC. Pored ovoga, utvrđeno je da statistički značajan broj uzoraka gradusa 2, sa aktiviranim TP53 genom ima istovremeno aktiviran i c-myc onkogen. Zaključak: TP53, najčešće mutirani gen u oralnim karcinomima, ostaje za sada i najpouzdaniji marker progresije kod OSCC. Obzirom na detektovani sinergizam između TP53 i c-myc gena, možemo reći da su istovremene promene u ova dva gena još pouzdaniji pokazatelj progresije OSSC iz gradusa 1 u gradus 2.
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - TP53 and c-myc Co-alterations: A hallmark of oral cancer progression
T1  - Simultana alteracija TP53 i c-myc gena - obeležje progresije oralnih karcinoma
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 Vukadinović, 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. Therefore, 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%, cycDI 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 cycDI 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., Uvod: Skvamocelularni karcinomi glave i vrata (HNSCC) uključujući i skvamocelularni karcinom usne duplje (OSCC) ubrajaju se u šest najčešćih tipova humanih maligniteta. Uprkos značajnim napredcima u hirurškom i terapijskom tretmanu, stopa petogodišnjeg preživljavanja kod ovog tipa maligniteta nije značajnije popravljena. Upravo zato, definisanje pouzdanih molekularnih markera progresije kod OSSC predstavlja apsolutni prioritetet. Metode: Amplifikacioni status c-myc, cycD1 i EGFR gena određen je pomoću eseja za detekciju broja genskih kopija, aktivacija H-ras onkogena i inaktivacija TP53 tumor supresora određena je PCR-SSCP mutacionom analizom, a hipermetilacija promotora p16 i MGMT gena je ispitana metil specifičnim PCR-om (MSP). Rezultati: Amplifikacija c-myc onkogena detektovana je kod 56,7%, cycD1 onkogena kod 20%, a EGFR onkogena kod 16,7% analiziranih oralnih skvamocelularnih carcinoma. Istovremeno, mutaciona aktivacija H-ras onkogena detektovana je kod 33,3% ispitanih uzoraka. Amplifikovani c-myc, statistički značajno korelira sa gradusom 2 OSCC. Posebno intrigantan je bio nalaz po kom se onkogene aktivacije u EGFR i H-ras genu međusobno isključuju. Hipermetilacija promotora p16 gena detektovana je kod 30%, a MGMT kod 13,3% analiziranih uzoraka. Ko-alteracije cycDI i p16 gena nisu zapažene ni u jednom od analiziranih uzoraka. Inaktivacija TP53 gena detektovana je kod 56,7% uzoraka i utvrđeno je da statistički značajno korelira sa gradusom 2 i statusom 2 OSCC. Pored ovoga, utvrđeno je da statistički značajan broj uzoraka gradusa 2, sa aktiviranim TP53 genom ima istovremeno aktiviran i c-myc onkogen. Zaključak: TP53, najčešće mutirani gen u oralnim karcinomima, ostaje za sada i najpouzdaniji marker progresije kod OSCC. Obzirom na detektovani sinergizam između TP53 i c-myc gena, možemo reći da su istovremene promene u ova dva gena još pouzdaniji pokazatelj progresije OSSC iz gradusa 1 u gradus 2.",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "TP53 and c-myc Co-alterations: A hallmark of oral cancer progression, Simultana alteracija TP53 i c-myc gena - obeležje progresije oralnih karcinoma",
volume = "32",
number = "4",
pages = "380-388",
doi = "10.2478/jomb-2014-0009"
}

Tanić, N., Milašin, J., Dramićanin, T., Bošković, M., Vukadinović, M., Milošević, V.,& Tanić, N.. (2013). TP53 and c-myc Co-alterations: A hallmark of oral cancer progression. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 32(4), 380-388.
https://doi.org/10.2478/jomb-2014-0009

Tanić N, Milašin J, Dramićanin T, Bošković M, Vukadinović 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, Vukadinović, 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  - Roganović, Jelena
AU  - Radenković, Miroslav
AU  - Tanić, Nikola
AU  - Tanić, Nasta
AU  - Petrović, Nina
AU  - Stojić, Dragica
PY  - 2011
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1625
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.
PB  - Wiley, Hoboken
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",
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.",
publisher = "Wiley, Hoboken",
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.. (2011). Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit. in European Journal of Oral Sciences
Wiley, Hoboken., 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 D. 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, "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  - Dedović-Tanić, Nasta
AU  - Popović, Brandon
AU  - Kosanović, Rade
AU  - Milašin, Jelena
PY  - 2011
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1670
AB  - Oral squamous cell carcinomas (OSCCs) are associated with poor prognosis, and despite advances in therapy approaches, no major improvement in survival has been achieved in the recent years. Efforts are now directed toward finding new biological markers that could predict tumor behavior more accurately. OSCCs, as the majority of malignant tumors, arise from progressive accumulation of genetic and epigenetic lesions, transforming normal cells into malignant. In this paper, an analysis of current studies directed to understanding the underlying mechanisms of OSCC pathogenesis was presented. The emphasis was put on mutational analysis of cancer genes, as well as on the role of viral infections and methylation processes in OSCC. Finally, an overview of studies that tried to determine the possibility for developing OSCC was given.
AB  - Oralne skvamocelularne karcinome (OSCK) odlikuje uglavnom loša prognoza i, uprkos pomacima u terapijskim postupcima, poslednjih godina nije ostvaren napredak u preživljavanju osoba s ovim tumorom. Velike nade se polažu u molekularnu medicinu i pronalaženje novih bioloških markera pomoću kojih bi preciznije nego što to dopuštaju klinički i histopatološki parametri moglo da se predvidi ponašanje tumora. OSCK, kao i većina drugih malignih oboljenja, rezultat su postupne akumulacije raznovrsnih genetičkih i epigenetičkih promena u ćelijama, koje od normalnih postaju neoplastične. U ovom radu dat je presek nekih od pravaca istraživanja na polju molekularne biologije oralnih karcinoma, s osvrtom na studije koje se bave ispitivanjem somatskih mutacija u kancerskim genima, učešćem onkogenih virusa u patogenezi i značaju procesa metilacije za OSCK. Takođe su pomenute studije posvećene utvrđivanju eventualnog postojanja predispozicije za razvoj OSCK.
PB  - Srpsko lekarsko društvo - Stomatološka sekcija, Beograd
T2  - Stomatološki glasnik Srbije
T1  - Moleculobiological characteristics of oral squamous cell carcinomas
T1  - Molekularnobiološke osobine oralnih skvamocelularnih karcinoma
VL  - 58
IS  - 2
SP  - 67
EP  - 74
DO  - 10.2298/SGS1102067T
ER  - 

@article{
author = "Tanić, Nikola and Dedović-Tanić, Nasta and Popović, Brandon and Kosanović, Rade and Milašin, Jelena",
year = "2011",
abstract = "Oral squamous cell carcinomas (OSCCs) are associated with poor prognosis, and despite advances in therapy approaches, no major improvement in survival has been achieved in the recent years. Efforts are now directed toward finding new biological markers that could predict tumor behavior more accurately. OSCCs, as the majority of malignant tumors, arise from progressive accumulation of genetic and epigenetic lesions, transforming normal cells into malignant. In this paper, an analysis of current studies directed to understanding the underlying mechanisms of OSCC pathogenesis was presented. The emphasis was put on mutational analysis of cancer genes, as well as on the role of viral infections and methylation processes in OSCC. Finally, an overview of studies that tried to determine the possibility for developing OSCC was given., Oralne skvamocelularne karcinome (OSCK) odlikuje uglavnom loša prognoza i, uprkos pomacima u terapijskim postupcima, poslednjih godina nije ostvaren napredak u preživljavanju osoba s ovim tumorom. Velike nade se polažu u molekularnu medicinu i pronalaženje novih bioloških markera pomoću kojih bi preciznije nego što to dopuštaju klinički i histopatološki parametri moglo da se predvidi ponašanje tumora. OSCK, kao i većina drugih malignih oboljenja, rezultat su postupne akumulacije raznovrsnih genetičkih i epigenetičkih promena u ćelijama, koje od normalnih postaju neoplastične. U ovom radu dat je presek nekih od pravaca istraživanja na polju molekularne biologije oralnih karcinoma, s osvrtom na studije koje se bave ispitivanjem somatskih mutacija u kancerskim genima, učešćem onkogenih virusa u patogenezi i značaju procesa metilacije za OSCK. Takođe su pomenute studije posvećene utvrđivanju eventualnog postojanja predispozicije za razvoj OSCK.",
publisher = "Srpsko lekarsko društvo - Stomatološka sekcija, Beograd",
journal = "Stomatološki glasnik Srbije",
title = "Moleculobiological characteristics of oral squamous cell carcinomas, Molekularnobiološke osobine oralnih skvamocelularnih karcinoma",
volume = "58",
number = "2",
pages = "67-74",
doi = "10.2298/SGS1102067T"
}

Tanić, N., Dedović-Tanić, N., Popović, B., Kosanović, R.,& Milašin, J.. (2011). Moleculobiological characteristics of oral squamous cell carcinomas. in Stomatološki glasnik Srbije
Srpsko lekarsko društvo - Stomatološka sekcija, Beograd., 58(2), 67-74.
https://doi.org/10.2298/SGS1102067T

Tanić N, Dedović-Tanić N, Popović B, Kosanović R, Milašin J. Moleculobiological characteristics of oral squamous cell carcinomas. in Stomatološki glasnik Srbije. 2011;58(2):67-74.
doi:10.2298/SGS1102067T .

Tanić, Nikola, Dedović-Tanić, Nasta, Popović, Brandon, Kosanović, Rade, Milašin, Jelena, "Moleculobiological characteristics of oral squamous cell carcinomas" in Stomatološki glasnik Srbije, 58, no. 2 (2011):67-74,
https://doi.org/10.2298/SGS1102067T . .

TY  - JOUR
AU  - Tanić, Nasta
AU  - Tanić, Nikola
AU  - Milašin, Jelena
AU  - Vukadinović, Miroslav
AU  - Dimitrijević, Bogomir
PY  - 2009
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1483
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.
PB  - Wiley, Hoboken
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, Nasta and Tanić, Nikola and Milašin, Jelena and Vukadinović, Miroslav and Dimitrijević, Bogomir",
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.",
publisher = "Wiley, Hoboken",
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., Vukadinović, M.,& Dimitrijević, B.. (2009). Genomic instability and tumor-specific DNA alterations in oral leukoplakias. in European Journal of Oral Sciences
Wiley, Hoboken., 117(3), 231-237.
https://doi.org/10.1111/j.1600-0722.2009.00624.x

Tanić N, Tanić N, Milašin J, Vukadinović M, Dimitrijević B. 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, Nasta, Tanić, Nikola, Milašin, Jelena, Vukadinović, Miroslav, Dimitrijević, Bogomir, "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 . .