Systematic analyses of natural variants and artificial mutants establish functional landscapes of BRCA1 for homology-directed repair (HDR) and therapy resistance and identify the BRCA1-PALB2 interaction as a key control point for HDR pathway choice.

Small molecule inhibitors identified in a biophysical high-throughout screening assay confirm the importance of the interaction between single-stranded DNA and the protein RAD52 for the survival of BRCA2-depleted cells.

53BP1 and BRCA1 antagonistically control a temporal choice of two distinct pathways to restart stalled replication forks in a DNA double stand repair-independent manner.

MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.

Genetic and biochemical analysis reveal a variant in HSF2BP causing POI and C19ORF57/BRME1 as an interactor and stabilizer of HSF2BP by forming a complex with BRCA2, RAD51, RPA and PALB2.

p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.

Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

The unraveling of distinct mammary tumor hierarchies in various mouse models of breast cancer emphasizes the need to account for specific cell states with potentially varying therapeutic vulnerabilities in tumors.

Identification of PARP1 trapping as the major contributor of PARP1 inhibitor-induced innate immune response.