Figure 1.

Synthetic lethality between PTEN loss and ATM inhibition. Loss of phosphatase and tensin homolog (PTEN) results in increased oxidative stress (reactive oxygen species [ROS]) and DNA damage, resulting in checkpoint activation, DNA repair, and cell survival. In the absence of ataxia telangiectasia mutated (ATM), loss of checkpoints and further DNA damage result in genomic instability and death.