Issues

In response to radiation, ATM drives DNA repair and cell cycle checkpoint controls to protect cancer cells from the lethal consequences of dividing with double strand breaks. Selective suppression of these functions can lower this protective barrier and allow cancer cells to proliferate with unrepaired DNA damage, ultimately leading to catastrophic mitotic events. In this issue, Zimmerman and colleagues introduce two new pharmacological inhibitors of ATM, M3541 and M4076, and show that they effectively enhance the efficacy of certain classes of double-strand-break inducing therapeutic agents and might offer novel combination options for cancer therapy. Read the full manuscript on page 859.