"Collaborative DNA Repair System Unlocks Potential Breast Cancer Prevention"
A study investigates how tumors adapt to tolerate DNA damage caused by replication stress through alterations in DNA damage response (DDR) genes. The findings suggest that MRE11, a DNA repair protein, plays a crucial role in suppressing breast tumorigenesis driven by MYC overexpression and p53 deficiency by promoting cGAS activation and initiating downstream innate immune responses. MRE11 was found to stimulate cGAS activation by antagonizing nucleosome sequestration, leading to the suppression of tumor growth and increased proliferation despite heightened genome instability. This study provides insights into the mechanisms involved in transducing DNA damage signals to activate cGAS and initiate innate immune responses during tumorigenesis.