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. 2018 Oct 17;41(1):77–86. doi: 10.3892/or.2018.6803

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Osimertinib causes a delay in DNA damage repair in NCI-H1975 cells. The change in the proportion of cells with positive γ-H2AX foci (A) 2, (B) 24 and (C) 48 h following treatment. (D) Representative images of γ-H2AX foci 48 h following treatment (magnification, ×60). *P<0.05 vs. IR alone. IR, irradiation; DMSO, dimethyl sulfoxide; γ-H2AX, H2A histone family member X.

Figure 3. — Osimertinib causes a delay in DNA damage repair in NCI-H1975 cells. The change in the proportion of cells with positive γ-H2AX foci (A) 2, (B) 24 and (C) 48 h following treatment. (D) Representative images of γ-H2AX foci 48 h following treatment (magnification, ×60). *P<0.05 vs. IR alone. IR, irradiation; DMSO, dimethyl sulfoxide; γ-H2AX, H2A histone family member X.