[5][6][7] 53BP1 is underexpressed in most cases of triple-negative breast cancer.

[8] DNA double-strand breaks (DSBs) are cytotoxic damages that can be repaired either by the homologous recombinational repair (HR) pathway or by the non-homologous end-joining (NHEJ) pathway.

Ordinarily during the G1 phase of the cell cycle, when a sister chromatid is unavailable for HR, NHEJ is the predominant pathway for repairing DNA double-strand breaks (DSBs).

However, as individuals age, recruitment of 53BP1 to DSBs during G1 becomes deficient.

[11] The absence of 53BP1 at such DSBs appears to promote the alternative error-prone repair process Alt-EJ.