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, 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 . .