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- W2104405656 abstract "EGFR is often overexpressed in human malignancies and its overexpression is associated with the activation of the Akt pathway leading to anti-apoptotic effects and a lack of sensitivity to many existing cytotoxic therapies. ZRBA1 is a binary targeting molecule, which not only blocks EGFR at the TK domain but also damages DNA. DNA repair mechanisms in cancer cells can however limit the DNA damaging property of this molecule. To further increase the efficacy of ZRBA1, we combined it with ionizing radiation. In this study we have investigated the impact of this novel combination on induction and repair of DNA damage. Using MDA-MB-468 breast cancer cells, we performed comet assays to detect DNA single and double strand breaks induced by drug (36 μM), radiation (4 Gy) and the combination of both treatments at 1 and 24 hr post treatment. In addition, flow cytometry analysis was carried out to quantitate the formation of γH2AX foci in G1 cells at 1 and 24 hr post treatment. Both neutral and alkaline comet assay showed significantly higher DNA breaks in cells treated with ZRBA1 and radiation than in cells treated with radiation or ZRBA1 alone. Importantly, the increase in DNA double strand breaks (DSBs) remained at high levels after 24hr. This was also confirmed with gamma H2AX analysis at 1 and 24 hr post treatment; showing the higher level of DSBs when ZRBA1 and radiation are combined. Similarly, the significant difference in the level of DSBs in the combination group remained as high as 30% vs. 10% and 15 % in the irradiated and drug treated group respectively after 24 hr. Overall our findings suggests that the combination of ZRBA 1 and radiation not only increases the DNA double and single strand breaks but also delays the DNA damage repair process." @default.
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- W2104405656 date "2012-11-01" @default.
- W2104405656 modified "2023-09-27" @default.
- W2104405656 title "Combination of Ionizing Radiation and DNA/EGFR Binary Targeting Molecule Delays DNA Double-Strands Repair" @default.
- W2104405656 doi "https://doi.org/10.1016/j.ijrobp.2012.07.1897" @default.
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