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. 2019 Jul 31;21(12):1529–1539. doi: 10.1093/neuonc/noz127

Fig. 3.

Fig. 3

TMZ but not afatinib plus thalidomide induce 53BP1 foci formation. (A) GBM12 cells were treated with TMZ (10 μM), afatinib (1 μM) plus etanercept (100 μg/mL), or thalidomide (1 μM) for 24 hours followed by immunofluorescence using antibody against 53BP1 (red). Nuclei are stained with 4′,6′-diamidino-2-phenylindole (blue). (B) Similar experiments were conducted in GBM 9 cells. (C–D) Double-strand breaks repair rates were determined by scoring 53BP1 foci. Data are presented as mean ± SEM of at least 3 independent experiments, ***P < 0.001. (E) Mice with GBM12 or GBM9 tumors were treated with drugs for 48 h followed by removal of tumors. Immunohistochemistry of 53BP1 in representative GBM12 orthotopic tumor sections from vehicle, afatinib, thalidomide, afatinib plus thalidomide, and TMZ group. (F) Quantification of 53BP1-positive in tumor sections. (G) Immunostaining of 53BP1 in brain sections from GBM9 orthotopic mice treated with indicated drugs. (H) Quantification of 53BP1-positive cells in tumor sections. Four random fields in 3 tissue blocks at x400 magnification were scored. Data are presented as mean ± SEM. ***P < 0.001, ****P < 0.0001. Scale bars represent 50 µm.