Fig. 3
From: Defective DNA damage repair leads to frequent catastrophic genomic events in murine and human tumors
Analysis of brain tissue from early postnatal stages (P8) up to tumor formation (P80) in XRCC4/p53-deficient mice (Nestin-cre p53−/− Xrcc4c/−) and control animals (Nestin-cre p53−/− Xrcc4c/+). a Upper panels, H&E staining of cerebellum sections shows the location of the tumor at P80 (magnification, ×100). Middle and lower panels, representative immunofluorescence stainings for DSB markers gH2AX and 53BP1 and for terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (magnification, ×100; insets, ×200, and ×600). Representative images for 11 analyzed cerebella are shown. Analysis of brain sections at intermediate stages (P60) are shown in Supplementary Figure 5. b Quantification of the number of cells positive for gH2AX, 53BP1, and TUNEL, respectively. CBL cerebellum; p8+, p53−/− Xrcc4c/+, p8−, p53−/− Xrcc4c/−. Between 4 and 12 sections per animal were analyzed, with 8 animals in the XRCC4-deficient group and 3 animals in the XRCC4-proficient group). Unpaired t-tests were done to test for significance
