TY  - JOUR
AU  - Popović, Branka
AU  - Jekić, B.
AU  - Novaković, I.
AU  - Luković, Ljiljana
AU  - Tepavčević, Zvezdana
AU  - Jurišić, Vladimir
AU  - Vukadinović, Miroslav
AU  - Milašin, Jelena
PY  - 2007
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1329
AB  - Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II,III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, [sic].
PB  - Wiley-Blackwell, Hoboken
T2  - Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease
T1  - Bcl-2 expression in oral squamous cell carcinoma
VL  - 1095
SP  - 19
EP  - 25
DO  - 10.1196/annals.1397.003
ER  - 

@article{
author = "Popović, Branka and Jekić, B. and Novaković, I. and Luković, Ljiljana and Tepavčević, Zvezdana and Jurišić, Vladimir and Vukadinović, Miroslav and Milašin, Jelena",
year = "2007",
abstract = "Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II,III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, [sic].",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease",
title = "Bcl-2 expression in oral squamous cell carcinoma",
volume = "1095",
pages = "19-25",
doi = "10.1196/annals.1397.003"
}

Popović, B., Jekić, B., Novaković, I., Luković, L., Tepavčević, Z., Jurišić, V., Vukadinović, M.,& Milašin, J.. (2007). Bcl-2 expression in oral squamous cell carcinoma. in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease
Wiley-Blackwell, Hoboken., 1095, 19-25.
https://doi.org/10.1196/annals.1397.003

Popović B, Jekić B, Novaković I, Luković L, Tepavčević Z, Jurišić V, Vukadinović M, Milašin J. Bcl-2 expression in oral squamous cell carcinoma. in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease. 2007;1095:19-25.
doi:10.1196/annals.1397.003 .

Popović, Branka, Jekić, B., Novaković, I., Luković, Ljiljana, Tepavčević, Zvezdana, Jurišić, Vladimir, Vukadinović, Miroslav, Milašin, Jelena, "Bcl-2 expression in oral squamous cell carcinoma" in Signal Transduction Pathways, Pt C: Cell Signaling in Health & Disease, 1095 (2007):19-25,
https://doi.org/10.1196/annals.1397.003 . .

TY  - JOUR
AU  - Jekić, B.
AU  - Novaković, I.
AU  - Luković, L
AU  - Kuzmanović, M
AU  - Popović, Branka
AU  - Milašin, Jelena
AU  - Bunjevacki, G
AU  - Damnjanović, Tatjana
AU  - Cvjetičanin, S
AU  - Bunjevački, Vera
PY  - 2006
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1314
AB  - Myelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisims underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed nnutations of these genes in a cohort of 35 children with MDS. Single-strand conformation polymorphism polymerase chain reaction analysis performed on FMS codon 969 and TP53 exons 5-9 showed no mutations in the analyzed sequences. Our results Suggest that molecular mechanisms of MDS evolution in children are different from those in adults.
PB  - Elsevier Science Inc, New York
T2  - Cancer Genetics & Cytogenetics
T1  - Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome
VL  - 166
IS  - 2
SP  - 163
EP  - 165
DO  - 10.1016/j.cancergencyto.2005.11.003
ER  - 

@article{
author = "Jekić, B. and Novaković, I. and Luković, L and Kuzmanović, M and Popović, Branka and Milašin, Jelena and Bunjevacki, G and Damnjanović, Tatjana and Cvjetičanin, S and Bunjevački, Vera",
year = "2006",
abstract = "Myelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisims underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed nnutations of these genes in a cohort of 35 children with MDS. Single-strand conformation polymorphism polymerase chain reaction analysis performed on FMS codon 969 and TP53 exons 5-9 showed no mutations in the analyzed sequences. Our results Suggest that molecular mechanisms of MDS evolution in children are different from those in adults.",
publisher = "Elsevier Science Inc, New York",
journal = "Cancer Genetics & Cytogenetics",
title = "Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome",
volume = "166",
number = "2",
pages = "163-165",
doi = "10.1016/j.cancergencyto.2005.11.003"
}

Jekić, B., Novaković, I., Luković, L., Kuzmanović, M., Popović, B., Milašin, J., Bunjevacki, G., Damnjanović, T., Cvjetičanin, S.,& Bunjevački, V.. (2006). Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. in Cancer Genetics & Cytogenetics
Elsevier Science Inc, New York., 166(2), 163-165.
https://doi.org/10.1016/j.cancergencyto.2005.11.003

Jekić B, Novaković I, Luković L, Kuzmanović M, Popović B, Milašin J, Bunjevacki G, Damnjanović T, Cvjetičanin S, Bunjevački V. Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. in Cancer Genetics & Cytogenetics. 2006;166(2):163-165.
doi:10.1016/j.cancergencyto.2005.11.003 .

Jekić, B., Novaković, I., Luković, L, Kuzmanović, M, Popović, Branka, Milašin, Jelena, Bunjevacki, G, Damnjanović, Tatjana, Cvjetičanin, S, Bunjevački, Vera, "Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome" in Cancer Genetics & Cytogenetics, 166, no. 2 (2006):163-165,
https://doi.org/10.1016/j.cancergencyto.2005.11.003 . .

TY  - JOUR
AU  - Jekić, B.
AU  - Novaković, I.
AU  - Luković, L
AU  - Kuzmanović, M
AU  - Popović, Branka
AU  - Pastar, I
AU  - Milašin, Jelena
AU  - Bunjevacki, G
AU  - Bunjevački, Vera
PY  - 2004
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1224
AB  - In children, myelodysplastic syndromes (MDS) represent less then 10% of all hematological malignancies; consequently, molecular genetic studies dealing with this group of patients are scarce. We have analyzed 35 archival bone marrow samples of children with MDS for the presence of mutations in the first and second exons of the NRAS and KRAS2 genes. Mutations were detected with single-strand conformation polymorphism analysis in three patients. One patient harbored a mutation in the second exon of NRAS and two patients in the second exon of KRAS2. Sequencing was performed in two samples and novel mutations were found in both. One patient had a missense mutation in codon 45 of NRAS; the other had a silent mutation in codon 53 and a missense mutation in codon 55 of KRAS2.
PB  - Elsevier Science Inc, New York
T2  - Cancer Genetics & Cytogenetics
T1  - Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes
VL  - 154
IS  - 2
SP  - 180
EP  - 182
DO  - 10.1016/j.cancergencyto.2004.02.025
ER  - 

@article{
author = "Jekić, B. and Novaković, I. and Luković, L and Kuzmanović, M and Popović, Branka and Pastar, I and Milašin, Jelena and Bunjevacki, G and Bunjevački, Vera",
year = "2004",
abstract = "In children, myelodysplastic syndromes (MDS) represent less then 10% of all hematological malignancies; consequently, molecular genetic studies dealing with this group of patients are scarce. We have analyzed 35 archival bone marrow samples of children with MDS for the presence of mutations in the first and second exons of the NRAS and KRAS2 genes. Mutations were detected with single-strand conformation polymorphism analysis in three patients. One patient harbored a mutation in the second exon of NRAS and two patients in the second exon of KRAS2. Sequencing was performed in two samples and novel mutations were found in both. One patient had a missense mutation in codon 45 of NRAS; the other had a silent mutation in codon 53 and a missense mutation in codon 55 of KRAS2.",
publisher = "Elsevier Science Inc, New York",
journal = "Cancer Genetics & Cytogenetics",
title = "Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes",
volume = "154",
number = "2",
pages = "180-182",
doi = "10.1016/j.cancergencyto.2004.02.025"
}

Jekić, B., Novaković, I., Luković, L., Kuzmanović, M., Popović, B., Pastar, I., Milašin, J., Bunjevacki, G.,& Bunjevački, V.. (2004). Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes. in Cancer Genetics & Cytogenetics
Elsevier Science Inc, New York., 154(2), 180-182.
https://doi.org/10.1016/j.cancergencyto.2004.02.025

Jekić B, Novaković I, Luković L, Kuzmanović M, Popović B, Pastar I, Milašin J, Bunjevacki G, Bunjevački V. Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes. in Cancer Genetics & Cytogenetics. 2004;154(2):180-182.
doi:10.1016/j.cancergencyto.2004.02.025 .

Jekić, B., Novaković, I., Luković, L, Kuzmanović, M, Popović, Branka, Pastar, I, Milašin, Jelena, Bunjevacki, G, Bunjevački, Vera, "Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes" in Cancer Genetics & Cytogenetics, 154, no. 2 (2004):180-182,
https://doi.org/10.1016/j.cancergencyto.2004.02.025 . .

TY  - CONF
AU  - Popović, B.
AU  - Milašin, Jelena
AU  - Jekić, B.
AU  - Novaković, I.
PY  - 2002
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1133
PB  - Nature Publishing Group, London
C3  - European Journal of Human Genetics
T1  - The role of H-Ras gene in tumorigenesis of oral squamous cell carcinoma
VL  - 10
SP  - 99
EP  - 99
UR  - https://hdl.handle.net/21.15107/rcub_smile_1133
ER  - 

@conference{
author = "Popović, B. and Milašin, Jelena and Jekić, B. and Novaković, I.",
year = "2002",
publisher = "Nature Publishing Group, London",
journal = "European Journal of Human Genetics",
title = "The role of H-Ras gene in tumorigenesis of oral squamous cell carcinoma",
volume = "10",
pages = "99-99",
url = "https://hdl.handle.net/21.15107/rcub_smile_1133"
}

Popović, B., Milašin, J., Jekić, B.,& Novaković, I.. (2002). The role of H-Ras gene in tumorigenesis of oral squamous cell carcinoma. in European Journal of Human Genetics
Nature Publishing Group, London., 10, 99-99.
https://hdl.handle.net/21.15107/rcub_smile_1133

Popović B, Milašin J, Jekić B, Novaković I. The role of H-Ras gene in tumorigenesis of oral squamous cell carcinoma. in European Journal of Human Genetics. 2002;10:99-99.
https://hdl.handle.net/21.15107/rcub_smile_1133 .

Popović, B., Milašin, Jelena, Jekić, B., Novaković, I., "The role of H-Ras gene in tumorigenesis of oral squamous cell carcinoma" in European Journal of Human Genetics, 10 (2002):99-99,
https://hdl.handle.net/21.15107/rcub_smile_1133 .