Figure 5
Figure 5. Blunting Myc-evoked ROS preserves a latent DDR machinery in vivo. (A) DNA damage sites visualized as γ-H2AX foci in cytospin preparations of Eμ-myc control lymphomas that formed with and without lifelong exposure to NAC; quantification (left) and representative examples (right). Original magnification, × 1000. (B) Spontaneous apoptosis by fluorescence-based TUNEL staining in cytospin preparations of preneoplastic Eμ-myc transgenic B cells (exposure to NAC as in panel A). Original magnification, × 200. (C) Immunoblot analysis of Atm, Atm-P-S1987, p53, p53-P-S18, and tubulin as a loading control in NAC-protected control lymphomas; basal (−) and induced (+) levels 5 hours after ADR in vitro. All quantitative data are mean ± SD; *P < .05; NS indicates not significant.

Blunting Myc-evoked ROS preserves a latent DDR machinery in vivo. (A) DNA damage sites visualized as γ-H2AX foci in cytospin preparations of Eμ-myc control lymphomas that formed with and without lifelong exposure to NAC; quantification (left) and representative examples (right). Original magnification, × 1000. (B) Spontaneous apoptosis by fluorescence-based TUNEL staining in cytospin preparations of preneoplastic Eμ-myc transgenic B cells (exposure to NAC as in panel A). Original magnification, × 200. (C) Immunoblot analysis of Atm, Atm-P-S1987, p53, p53-P-S18, and tubulin as a loading control in NAC-protected control lymphomas; basal (−) and induced (+) levels 5 hours after ADR in vitro. All quantitative data are mean ± SD; *P < .05; NS indicates not significant.

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