Milovanovic, Zorka

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  • Milovanovic, Zorka (3)
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Author's Bibliography

Prolonged survival after neoadjuvant chemotherapy related with specific molecular alterations in the patients with nonsmall-cell lung carcinoma

Stojsic, Jelena; Stankovic, Tijana; Stojković Burić, Sonja; Milinkovic, Vedrana; Dinić, Jelena; Milosevic, Zorica; Milovanovic, Zorka; Tanić, Nikola; Banković, Jasna Z.

(2015)

TY  - JOUR
AU  - Stojsic, Jelena
AU  - Stankovic, Tijana
AU  - Stojković Burić, Sonja
AU  - Milinkovic, Vedrana
AU  - Dinić, Jelena
AU  - Milosevic, Zorica
AU  - Milovanovic, Zorka
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2005
AB  - Lung cancer is the most common cause of neoplasia-related death
   worldwide. Accounting for approximately 80\% of all lung carcinomas, the
   non-small cell lung carcinoma (NSCLC) is the most common clinical form
   with its two predominant histological types, adenocarcinoma (ADC) and
   squamous cell carcinoma (SCC). Although surgical resection is the most
   favorable treatment for patients with NSCLC, relapse is still high, so
   neoadjuvant chemotherapy (NAC) is an accepted treatment modality. In
   this study we examined whether some of the key molecules associated with
   the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways could have
   predictive and prognostic value for the NAC application. To that end we
   examined the expression status of PTEN, pAKT, pERK and loss of
   heterozygosity (LOH) of PTEN in two groups of NSCLC patients, those who
   received and those who did not receive NAG LOH PTEN and low pERK
   expression is shown to be correlated with the longest survival of
   patients with SCC and ADC, respectively, who received NAC. These results
   point that the application of NAC is beneficial in the NSCLC patients
   with specific molecular alterations which could further help to improve
   constant search for the druggable molecular targets used in personalized
   therapy. (C) 2014 Elsevier Inc. All rights reserved.
T2  - Experimental and Molecular Pathology
T1  - Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma
IS  - 1
VL  - 98
DO  - 10.1016/j.yexmp.2014.11.010
SP  - 27
EP  - 32
ER  - 
@article{
author = "Stojsic, Jelena and Stankovic, Tijana and Stojković Burić, Sonja and Milinkovic, Vedrana and Dinić, Jelena and Milosevic, Zorica and Milovanovic, Zorka and Tanić, Nikola and Banković, Jasna Z.",
year = "2015",
abstract = "Lung cancer is the most common cause of neoplasia-related death
   worldwide. Accounting for approximately 80\% of all lung carcinomas, the
   non-small cell lung carcinoma (NSCLC) is the most common clinical form
   with its two predominant histological types, adenocarcinoma (ADC) and
   squamous cell carcinoma (SCC). Although surgical resection is the most
   favorable treatment for patients with NSCLC, relapse is still high, so
   neoadjuvant chemotherapy (NAC) is an accepted treatment modality. In
   this study we examined whether some of the key molecules associated with
   the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways could have
   predictive and prognostic value for the NAC application. To that end we
   examined the expression status of PTEN, pAKT, pERK and loss of
   heterozygosity (LOH) of PTEN in two groups of NSCLC patients, those who
   received and those who did not receive NAG LOH PTEN and low pERK
   expression is shown to be correlated with the longest survival of
   patients with SCC and ADC, respectively, who received NAC. These results
   point that the application of NAC is beneficial in the NSCLC patients
   with specific molecular alterations which could further help to improve
   constant search for the druggable molecular targets used in personalized
   therapy. (C) 2014 Elsevier Inc. All rights reserved.",
journal = "Experimental and Molecular Pathology",
title = "Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma",
number = "1",
volume = "98",
doi = "10.1016/j.yexmp.2014.11.010",
pages = "27-32"
}
Stojsic, J., Stankovic, T., Stojković Burić, S., Milinkovic, V., Dinić, J., Milosevic, Z., Milovanovic, Z., Tanić, N.,& Banković, J. Z.. (2015). Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma. in Experimental and Molecular Pathology, 98(1), 27-32.
https://doi.org/10.1016/j.yexmp.2014.11.010
Stojsic J, Stankovic T, Stojković Burić S, Milinkovic V, Dinić J, Milosevic Z, Milovanovic Z, Tanić N, Banković JZ. Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma. in Experimental and Molecular Pathology. 2015;98(1):27-32.
doi:10.1016/j.yexmp.2014.11.010 .
Stojsic, Jelena, Stankovic, Tijana, Stojković Burić, Sonja, Milinkovic, Vedrana, Dinić, Jelena, Milosevic, Zorica, Milovanovic, Zorka, Tanić, Nikola, Banković, Jasna Z., "Prolonged survival after neoadjuvant chemotherapy related with specific
 molecular alterations in the patients with nonsmall-cell lung carcinoma" in Experimental and Molecular Pathology, 98, no. 1 (2015):27-32,
https://doi.org/10.1016/j.yexmp.2014.11.010 . .
4
2
4

Genetic alterations in quadruple malignancies of a patient with multiple sclerosis: their role in malignancy development and response to therapy

Milosevic, Zorica; Tanić, Nikola; Banković, Jasna Z.; Stankovic, Tijana; Buta, Marko; Lavrnic, Dragana; Milovanovic, Zorka; Pupic, Gordana; Stojković Burić, Sonja; Milinkovic, Vedrana; Ito, Yasuhiro; Džodić, Radan R.

(2014)

TY  - JOUR
AU  - Milosevic, Zorica
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
AU  - Stankovic, Tijana
AU  - Buta, Marko
AU  - Lavrnic, Dragana
AU  - Milovanovic, Zorka
AU  - Pupic, Gordana
AU  - Stojković Burić, Sonja
AU  - Milinkovic, Vedrana
AU  - Ito, Yasuhiro
AU  - Džodić, Radan R.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2290
AB  - Multiple cancers represent 2.42\% of all human cancers and are mainly
   double or triple cancers. Many possible causes of multiple malignancies
   have been reported such as genetic alterations, exposure to anti-cancer
   chemotherapy, radiotherapy, immunosuppressive therapy and reduced
   immunologic response. We report a female patient with multiple sclerosis
   and quadruple cancers of different embryological origin. Patient was
   diagnosed with stage III (T3, N1a, MO) medullary thyroid carcinoma
   (MTC), multicentric micropapillary thyroid carcinoma, scapular and
   lumbar melanomas (Clark II, Breslow II), and lobular invasive breast
   carcinoma (T1a, NO, MO). All tumors present in our patient except
   micropapillary thyroid carcinomas were investigated for gene alterations
   known to have a key role in cancer promotion and progression. Tumor
   samples were screened for the p16 alterations (loss of heterozygosity
   and homozygous deletions), loss of heterozygosity of PTEN, p53
   alterations (mutational status and loss of heterozygosity) and
   mutational status of RET, HRAS and KRAS. Each type of tumor investigated
   had specific pattern of analyzed genetic alterations. The most prominent
   genetic changes were mutual alterations in PTEN and p53 tumor
   suppressors present in breast cancer and two melanomas. These
   co-alterations could be crucial for promoting development of multiple
   malignancies. Moreover the insertion in 4th codon of HRAS gene was
   common for all tumor types investigated. It represents frameshift
   mutation introducing stop codon at position 5 which prevents synthesis
   of a full-length protein. Since the inactivated RAS enhances sensitivity
   to tamoxifen and radiotherapy this genetic alteration could be
   considered as a good prognostic factor for this patient.
T2  - International Journal of Clinical and Experimental Pathology
T1  - Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy
IS  - 4
VL  - 7
SP  - 1826
EP  - 1833
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_2290
ER  - 
@article{
author = "Milosevic, Zorica and Tanić, Nikola and Banković, Jasna Z. and Stankovic, Tijana and Buta, Marko and Lavrnic, Dragana and Milovanovic, Zorka and Pupic, Gordana and Stojković Burić, Sonja and Milinkovic, Vedrana and Ito, Yasuhiro and Džodić, Radan R.",
year = "2014",
abstract = "Multiple cancers represent 2.42\% of all human cancers and are mainly
   double or triple cancers. Many possible causes of multiple malignancies
   have been reported such as genetic alterations, exposure to anti-cancer
   chemotherapy, radiotherapy, immunosuppressive therapy and reduced
   immunologic response. We report a female patient with multiple sclerosis
   and quadruple cancers of different embryological origin. Patient was
   diagnosed with stage III (T3, N1a, MO) medullary thyroid carcinoma
   (MTC), multicentric micropapillary thyroid carcinoma, scapular and
   lumbar melanomas (Clark II, Breslow II), and lobular invasive breast
   carcinoma (T1a, NO, MO). All tumors present in our patient except
   micropapillary thyroid carcinomas were investigated for gene alterations
   known to have a key role in cancer promotion and progression. Tumor
   samples were screened for the p16 alterations (loss of heterozygosity
   and homozygous deletions), loss of heterozygosity of PTEN, p53
   alterations (mutational status and loss of heterozygosity) and
   mutational status of RET, HRAS and KRAS. Each type of tumor investigated
   had specific pattern of analyzed genetic alterations. The most prominent
   genetic changes were mutual alterations in PTEN and p53 tumor
   suppressors present in breast cancer and two melanomas. These
   co-alterations could be crucial for promoting development of multiple
   malignancies. Moreover the insertion in 4th codon of HRAS gene was
   common for all tumor types investigated. It represents frameshift
   mutation introducing stop codon at position 5 which prevents synthesis
   of a full-length protein. Since the inactivated RAS enhances sensitivity
   to tamoxifen and radiotherapy this genetic alteration could be
   considered as a good prognostic factor for this patient.",
journal = "International Journal of Clinical and Experimental Pathology",
title = "Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy",
number = "4",
volume = "7",
pages = "1826-1833",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_2290"
}
Milosevic, Z., Tanić, N., Banković, J. Z., Stankovic, T., Buta, M., Lavrnic, D., Milovanovic, Z., Pupic, G., Stojković Burić, S., Milinkovic, V., Ito, Y.,& Džodić, R. R.. (2014). Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy. in International Journal of Clinical and Experimental Pathology, 7(4), 1826-1833.
https://hdl.handle.net/21.15107/rcub_ibiss_2290
Milosevic Z, Tanić N, Banković JZ, Stankovic T, Buta M, Lavrnic D, Milovanovic Z, Pupic G, Stojković Burić S, Milinkovic V, Ito Y, Džodić RR. Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy. in International Journal of Clinical and Experimental Pathology. 2014;7(4):1826-1833.
https://hdl.handle.net/21.15107/rcub_ibiss_2290 .
Milosevic, Zorica, Tanić, Nikola, Banković, Jasna Z., Stankovic, Tijana, Buta, Marko, Lavrnic, Dragana, Milovanovic, Zorka, Pupic, Gordana, Stojković Burić, Sonja, Milinkovic, Vedrana, Ito, Yasuhiro, Džodić, Radan R., "Genetic alterations in quadruple malignancies of a patient with multiple
 sclerosis: their role in malignancy development and response to therapy" in International Journal of Clinical and Experimental Pathology, 7, no. 4 (2014):1826-1833,
https://hdl.handle.net/21.15107/rcub_ibiss_2290 .
4

Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to chemosensitize anaplastic thyroid carcinoma

Milosevic, Zorica; Pešić, Milica; Stankovic, Tijana; Dinić, Jelena; Milovanovic, Zorka; Stojsic, Jelena; Džodić, Radan R.; Tanić, Nikola; Banković, Jasna Z.

(2014)

TY  - JOUR
AU  - Milosevic, Zorica
AU  - Pešić, Milica
AU  - Stankovic, Tijana
AU  - Dinić, Jelena
AU  - Milovanovic, Zorka
AU  - Stojsic, Jelena
AU  - Džodić, Radan R.
AU  - Tanić, Nikola
AU  - Banković, Jasna Z.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2133
AB  - Anaplastic thyroid carcinoma (ATC) is a rare, but aggressive and
   chemoresistant tumor with dismal prognosis. Most ATCs harbor mutations
   that activate RAS/MAPK/ERK and PI3K/AKT/mTOR pathways. Therefore, we
   investigated and correlated the expression of phosphatase and tensin
   homolog, pERK, and pAKT proteins as well as mutations of BRAF, RAS, and
   p53 genes in samples of patients with ATC. Furthermore, we evaluated the
   potential of inhibition of these pathways on chemosensitization of ATC
   using 2 thyroid carcinoma cell lines (FRO and SW1736). Our results
   revealed a negative correlation between the activity of RAS-MAPK-ERK and
   PI3K-AKT-mTOR pathways in samples of patients. To be specific, the
   PI3K-AKT-mTOR pathway was suppressed in patients with activated NRAS or
   high pERK expression. In vitro results suggest that the inhibition of
   either RAS-MAPK-ERK or PI3K-AKT-mTOR components may confer sensitivity
   of thyroid cancer cells to classic chemotherapeutics. This may form a
   basis for the development of novel genetic-based therapeutic approach
   for this cancer type.
T2  - Translational Research
T1  - Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma
IS  - 5
VL  - 164
DO  - 10.1016/j.trsl.2014.06.005
SP  - 411
EP  - 423
ER  - 
@article{
author = "Milosevic, Zorica and Pešić, Milica and Stankovic, Tijana and Dinić, Jelena and Milovanovic, Zorka and Stojsic, Jelena and Džodić, Radan R. and Tanić, Nikola and Banković, Jasna Z.",
year = "2014",
abstract = "Anaplastic thyroid carcinoma (ATC) is a rare, but aggressive and
   chemoresistant tumor with dismal prognosis. Most ATCs harbor mutations
   that activate RAS/MAPK/ERK and PI3K/AKT/mTOR pathways. Therefore, we
   investigated and correlated the expression of phosphatase and tensin
   homolog, pERK, and pAKT proteins as well as mutations of BRAF, RAS, and
   p53 genes in samples of patients with ATC. Furthermore, we evaluated the
   potential of inhibition of these pathways on chemosensitization of ATC
   using 2 thyroid carcinoma cell lines (FRO and SW1736). Our results
   revealed a negative correlation between the activity of RAS-MAPK-ERK and
   PI3K-AKT-mTOR pathways in samples of patients. To be specific, the
   PI3K-AKT-mTOR pathway was suppressed in patients with activated NRAS or
   high pERK expression. In vitro results suggest that the inhibition of
   either RAS-MAPK-ERK or PI3K-AKT-mTOR components may confer sensitivity
   of thyroid cancer cells to classic chemotherapeutics. This may form a
   basis for the development of novel genetic-based therapeutic approach
   for this cancer type.",
journal = "Translational Research",
title = "Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma",
number = "5",
volume = "164",
doi = "10.1016/j.trsl.2014.06.005",
pages = "411-423"
}
Milosevic, Z., Pešić, M., Stankovic, T., Dinić, J., Milovanovic, Z., Stojsic, J., Džodić, R. R., Tanić, N.,& Banković, J. Z.. (2014). Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma. in Translational Research, 164(5), 411-423.
https://doi.org/10.1016/j.trsl.2014.06.005
Milosevic Z, Pešić M, Stankovic T, Dinić J, Milovanovic Z, Stojsic J, Džodić RR, Tanić N, Banković JZ. Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma. in Translational Research. 2014;164(5):411-423.
doi:10.1016/j.trsl.2014.06.005 .
Milosevic, Zorica, Pešić, Milica, Stankovic, Tijana, Dinić, Jelena, Milovanovic, Zorka, Stojsic, Jelena, Džodić, Radan R., Tanić, Nikola, Banković, Jasna Z., "Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to
 chemosensitize anaplastic thyroid carcinoma" in Translational Research, 164, no. 5 (2014):411-423,
https://doi.org/10.1016/j.trsl.2014.06.005 . .
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