TY  - JOUR
AU  - Keta, Otilija D.
AU  - Bulat, Tanja M.
AU  - Korićanac, Lela
AU  - Žakula, Jelena
AU  - Cuttone, Giacomo
AU  - Privitera, Giuseppe
AU  - Petrović, Ivan M.
AU  - Ristić-Fira, Aleksandra
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/167
AB  - Molecular targeted cancer therapy is a promising treatment strategy. Considering the central role of the epidermal growth factor receptor in cell proliferation and survival, there are indications that targeted agents like tyrosine kinase inhibitors, i. e., erlotinib, may enhance the antitumor treatment by radiation. The aim of this study is to analyze the inactivation effects of gamma-rays and to test the radiosensitizing potential of erlotinib on human lung adenocarcinoma cells in vitro. Irradiations were performed with doses ranging from 1 Gy to 8 Gy. In order to increase the radiosensitivity of CRL-5876 lung adenocarcinoma cells, the cells were treated with a clinically relevant concentration of 2 mu M erlotinib. The effects of single and combined treatments were monitored using clonogenic survival, cell viability and proliferation assays at different time points. For the detection and visualization of the phosphorylated histone H2AX (gamma-H2AX), an important biological marker of DNA double-strand break formation, fluorescence inununocytochemistry, was performed. The response to the treatment was monitored at four time points: 30 min, 2, 6, and 24 h. Irradiations with gamma-rays resulted in significant cell inactivation regarding all analyzed biological endpoints. Combined treatments revealed consistent cell inactivation. Moreover, compared to gamma-rays alone, elevated levels of gamma-H2AX foci were observed after pretreatment with erlotinib, indicating radiosensitization through impaired DNA repair.
T2  - Nuclear technology and radiation protection
T1  - Radiosensitization of Non-Small Cell Lung Carcinoma By EGFR Inhibition
VL  - 29
IS  - 3
SP  - 233
EP  - 241
DO  - 10.2298/NTRP1403233K
ER  - 

@article{
author = "Keta, Otilija D. and Bulat, Tanja M. and Korićanac, Lela and Žakula, Jelena and Cuttone, Giacomo and Privitera, Giuseppe and Petrović, Ivan M. and Ristić-Fira, Aleksandra",
year = "2014",
abstract = "Molecular targeted cancer therapy is a promising treatment strategy. Considering the central role of the epidermal growth factor receptor in cell proliferation and survival, there are indications that targeted agents like tyrosine kinase inhibitors, i. e., erlotinib, may enhance the antitumor treatment by radiation. The aim of this study is to analyze the inactivation effects of gamma-rays and to test the radiosensitizing potential of erlotinib on human lung adenocarcinoma cells in vitro. Irradiations were performed with doses ranging from 1 Gy to 8 Gy. In order to increase the radiosensitivity of CRL-5876 lung adenocarcinoma cells, the cells were treated with a clinically relevant concentration of 2 mu M erlotinib. The effects of single and combined treatments were monitored using clonogenic survival, cell viability and proliferation assays at different time points. For the detection and visualization of the phosphorylated histone H2AX (gamma-H2AX), an important biological marker of DNA double-strand break formation, fluorescence inununocytochemistry, was performed. The response to the treatment was monitored at four time points: 30 min, 2, 6, and 24 h. Irradiations with gamma-rays resulted in significant cell inactivation regarding all analyzed biological endpoints. Combined treatments revealed consistent cell inactivation. Moreover, compared to gamma-rays alone, elevated levels of gamma-H2AX foci were observed after pretreatment with erlotinib, indicating radiosensitization through impaired DNA repair.",
journal = "Nuclear technology and radiation protection",
title = "Radiosensitization of Non-Small Cell Lung Carcinoma By EGFR Inhibition",
volume = "29",
number = "3",
pages = "233-241",
doi = "10.2298/NTRP1403233K"
}

Keta, O. D., Bulat, T. M., Korićanac, L., Žakula, J., Cuttone, G., Privitera, G., Petrović, I. M.,& Ristić-Fira, A.. (2014). Radiosensitization of Non-Small Cell Lung Carcinoma By EGFR Inhibition. in Nuclear technology and radiation protection, 29(3), 233-241.
https://doi.org/10.2298/NTRP1403233K

Keta OD, Bulat TM, Korićanac L, Žakula J, Cuttone G, Privitera G, Petrović IM, Ristić-Fira A. Radiosensitization of Non-Small Cell Lung Carcinoma By EGFR Inhibition. in Nuclear technology and radiation protection. 2014;29(3):233-241.
doi:10.2298/NTRP1403233K .

Keta, Otilija D., Bulat, Tanja M., Korićanac, Lela, Žakula, Jelena, Cuttone, Giacomo, Privitera, Giuseppe, Petrović, Ivan M., Ristić-Fira, Aleksandra, "Radiosensitization of Non-Small Cell Lung Carcinoma By EGFR Inhibition" in Nuclear technology and radiation protection, 29, no. 3 (2014):233-241,
https://doi.org/10.2298/NTRP1403233K . .