TY  - JOUR
AU  - Brajić, Ivana
AU  - Skodrić, Sanja
AU  - Milenković, S.
AU  - Tepavčević, Zvezdana
AU  - Soldatović, Ivan
AU  - Čolić, Snježana
AU  - Milašin, Jelena
AU  - Andrić, Miroslav
PY  - 2016
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/2140
AB  - ObjectivesThe aim of this study was to investigate survivin, cyclin D1, and p21hras expression in keratocystic odontogenic tumors before and after decompression, as well as in pericoronal follicles. A potential correlation between the expression levels of these proteins was also investigated. Materials and methodsWe analyzed eighteen keratocystic tumors treated by decompression and subsequent enucleation along with seven pericoronal follicles using immunohistochemistry. ResultsKeratocystic tumor samples, both before and after decompression, were positive for each of the investigated proteins. In pericoronal follicles, survivin exhibited cytoplasmic staining in contrast to nuclear staining in keratocystic tumors. Cyclin D1 expression was negative in pericoronal follicles, and p21hras expression was similar in both groups. Survivin showed significantly higher expression after decompression, while cyclin D1 and p21hras remained unchanged (P=0.039, P=0.255, P=0.913, respectively). There was no correlation between these proteins neither before nor after decompression. ConclusionsWithin the limits of the study, we can conclude that following decompression, keratocystic odontogenic tumors preserve distinct immunohistochemical profiles of cyclin D1 and p21hras expression, despite substantial reduction in size of the lesions. Significant increase of survivin expression after decompression might be attributed to higher level of epithelial proliferation caused by this procedure.
PB  - Wiley-Blackwell, Hoboken
T2  - Oral Diseases
T1  - Survivin, cyclin D1, and p21hras in keratocystic odontogenic tumors before and after decompression
VL  - 22
IS  - 3
SP  - 220
EP  - 225
DO  - 10.1111/odi.12414
ER  - 

@article{
author = "Brajić, Ivana and Skodrić, Sanja and Milenković, S. and Tepavčević, Zvezdana and Soldatović, Ivan and Čolić, Snježana and Milašin, Jelena and Andrić, Miroslav",
year = "2016",
abstract = "ObjectivesThe aim of this study was to investigate survivin, cyclin D1, and p21hras expression in keratocystic odontogenic tumors before and after decompression, as well as in pericoronal follicles. A potential correlation between the expression levels of these proteins was also investigated. Materials and methodsWe analyzed eighteen keratocystic tumors treated by decompression and subsequent enucleation along with seven pericoronal follicles using immunohistochemistry. ResultsKeratocystic tumor samples, both before and after decompression, were positive for each of the investigated proteins. In pericoronal follicles, survivin exhibited cytoplasmic staining in contrast to nuclear staining in keratocystic tumors. Cyclin D1 expression was negative in pericoronal follicles, and p21hras expression was similar in both groups. Survivin showed significantly higher expression after decompression, while cyclin D1 and p21hras remained unchanged (P=0.039, P=0.255, P=0.913, respectively). There was no correlation between these proteins neither before nor after decompression. ConclusionsWithin the limits of the study, we can conclude that following decompression, keratocystic odontogenic tumors preserve distinct immunohistochemical profiles of cyclin D1 and p21hras expression, despite substantial reduction in size of the lesions. Significant increase of survivin expression after decompression might be attributed to higher level of epithelial proliferation caused by this procedure.",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Oral Diseases",
title = "Survivin, cyclin D1, and p21hras in keratocystic odontogenic tumors before and after decompression",
volume = "22",
number = "3",
pages = "220-225",
doi = "10.1111/odi.12414"
}

Brajić, I., Skodrić, S., Milenković, S., Tepavčević, Z., Soldatović, I., Čolić, S., Milašin, J.,& Andrić, M.. (2016). Survivin, cyclin D1, and p21hras in keratocystic odontogenic tumors before and after decompression. in Oral Diseases
Wiley-Blackwell, Hoboken., 22(3), 220-225.
https://doi.org/10.1111/odi.12414

Brajić I, Skodrić S, Milenković S, Tepavčević Z, Soldatović I, Čolić S, Milašin J, Andrić M. Survivin, cyclin D1, and p21hras in keratocystic odontogenic tumors before and after decompression. in Oral Diseases. 2016;22(3):220-225.
doi:10.1111/odi.12414 .

Brajić, Ivana, Skodrić, Sanja, Milenković, S., Tepavčević, Zvezdana, Soldatović, Ivan, Čolić, Snježana, Milašin, Jelena, Andrić, Miroslav, "Survivin, cyclin D1, and p21hras in keratocystic odontogenic tumors before and after decompression" in Oral Diseases, 22, no. 3 (2016):220-225,
https://doi.org/10.1111/odi.12414 . .

TY  - JOUR
AU  - Andrić, Miroslav
AU  - Nikolić, Nadja
AU  - Bosković, Marija
AU  - Miličić, Biljana
AU  - Skodrić, Sanja
AU  - Basta-Jovanović, Gordana
AU  - Milašin, Jelena
PY  - 2012
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1755
AB  - Several single nucleotide polymorphisms in survivin gene promoters, notably -31G/C, have been shown to modulate the expression and activity of the survivin protein. Consequently, the -31G/C polymorphism has been identified as a risk factor for the development of several types of tumors. The aim of this study was to investigate a possible association between the -31G/C polymorphism and the risk for keratocystic odontogenic tumor (KCOT) development. DNA from 52 biopsy specimens of KCOTs and from 82 buccal swabs of healthy individuals was subjected to PCR restriction fragment length polymorphism analysis to identify individual genotypes. The distribution of genotypes in KCOT and control groups, respectively, was: GG: 30 (57.7%) vs. 26 (31.7%); CG: 17 (32.7%) vs. 45 (54.9%); and CC: 5 (9.6%) vs. 11 (13.4%), respectively. These differences were statistically significant. The G allele was more common in the KCOT group than in the control group: 76 (74%) vs. 96 (59%), respectively. Logistic regression analysis showed that GC heterozygotes had a considerably decreased susceptibility for KCOTs compared with GG homozygotes. The same was true for GC+CC vs. GG. The GG genotype of the -31G/C polymorphism might be a risk factor for KCOT development.
PB  - Wiley-Blackwell, Hoboken
T2  - European Journal of Oral Sciences
T1  - Survivin gene promoter polymorphism-31G/C as a risk factor for keratocystic odontogenic tumor development
VL  - 120
IS  - 1
SP  - 9
EP  - 13
DO  - 10.1111/j.1600-0722.2011.00919.x
ER  - 

@article{
author = "Andrić, Miroslav and Nikolić, Nadja and Bosković, Marija and Miličić, Biljana and Skodrić, Sanja and Basta-Jovanović, Gordana and Milašin, Jelena",
year = "2012",
abstract = "Several single nucleotide polymorphisms in survivin gene promoters, notably -31G/C, have been shown to modulate the expression and activity of the survivin protein. Consequently, the -31G/C polymorphism has been identified as a risk factor for the development of several types of tumors. The aim of this study was to investigate a possible association between the -31G/C polymorphism and the risk for keratocystic odontogenic tumor (KCOT) development. DNA from 52 biopsy specimens of KCOTs and from 82 buccal swabs of healthy individuals was subjected to PCR restriction fragment length polymorphism analysis to identify individual genotypes. The distribution of genotypes in KCOT and control groups, respectively, was: GG: 30 (57.7%) vs. 26 (31.7%); CG: 17 (32.7%) vs. 45 (54.9%); and CC: 5 (9.6%) vs. 11 (13.4%), respectively. These differences were statistically significant. The G allele was more common in the KCOT group than in the control group: 76 (74%) vs. 96 (59%), respectively. Logistic regression analysis showed that GC heterozygotes had a considerably decreased susceptibility for KCOTs compared with GG homozygotes. The same was true for GC+CC vs. GG. The GG genotype of the -31G/C polymorphism might be a risk factor for KCOT development.",
publisher = "Wiley-Blackwell, Hoboken",
journal = "European Journal of Oral Sciences",
title = "Survivin gene promoter polymorphism-31G/C as a risk factor for keratocystic odontogenic tumor development",
volume = "120",
number = "1",
pages = "9-13",
doi = "10.1111/j.1600-0722.2011.00919.x"
}

Andrić, M., Nikolić, N., Bosković, M., Miličić, B., Skodrić, S., Basta-Jovanović, G.,& Milašin, J.. (2012). Survivin gene promoter polymorphism-31G/C as a risk factor for keratocystic odontogenic tumor development. in European Journal of Oral Sciences
Wiley-Blackwell, Hoboken., 120(1), 9-13.
https://doi.org/10.1111/j.1600-0722.2011.00919.x

Andrić M, Nikolić N, Bosković M, Miličić B, Skodrić S, Basta-Jovanović G, Milašin J. Survivin gene promoter polymorphism-31G/C as a risk factor for keratocystic odontogenic tumor development. in European Journal of Oral Sciences. 2012;120(1):9-13.
doi:10.1111/j.1600-0722.2011.00919.x .

Andrić, Miroslav, Nikolić, Nadja, Bosković, Marija, Miličić, Biljana, Skodrić, Sanja, Basta-Jovanović, Gordana, Milašin, Jelena, "Survivin gene promoter polymorphism-31G/C as a risk factor for keratocystic odontogenic tumor development" in European Journal of Oral Sciences, 120, no. 1 (2012):9-13,
https://doi.org/10.1111/j.1600-0722.2011.00919.x . .