Skip to main content
. 2019 Nov 14;11(11):1789. doi: 10.3390/cancers11111789

Figure 2.

Figure 2

Linking processing of clustered DNA damage and its biological consequences. (a) Formation of fluorescent γH2AX–OGG1 clusters in normal human bronchial epithelial cells at 1 h post-irradiation with heavy ions of varying LETs (adapted from [178]). Colocalization parameter (Pclc) values (as described in Section 3.5.2) increase with increasing LET; (b) induction of complex DNA damage and biological consequences in mammalian cells. Long-term consequences of DNA damage include different forms of genomic instability, which significantly contribute to carcinogenesis. Furthermore, processing of unrepaired or persistent clustered DNA damage promotes cell death. Activation of DNA damage response (DDR) and repair machinery can trigger the extracellular release of diverse signatures of ‘Danger’ signals or damage-associated molecular patterns (DAMPs: ATP, short DNAs/RNAs, ROS, heat shock proteins (HSPs) and others) [179].