Cellular pathways that repair chromosomal double-strand breaks (DSBs) have pivotal roles
in cell growth, development and cancer. These DSB repair pathways have been the target of …

DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genomic integrity.
Failure to repair a DSB has deleterious consequences, including genomic instability and cell …

POLQ is a key effector of DSB repair by microhomology-mediated end-joining (MMEJ) and is
overexpressed in many cancers. POLQ inhibitors confer synthetic lethality in HR and …

DNA damage repair (DDR) pathways modulate cancer risk, progression, and therapeutic
response. We systematically analyzed somatic alterations to provide a comprehensive view …

DNA double-strand breaks (DSBs) disrupt the continuity of chromosomes and their repair by
error-free mechanisms is essential to preserve genome integrity. Microhomology-mediated …

Single-strand annealing (SSA) is a DNA double-strand break (DSB) repair pathway that
uses homologous repeats to bridge DSB ends. SSA involving repeats that flank a single …

Genome-embedded ribonucleotides arrest replicative DNA polymerases (Pols) and cause
DNA breaks. Whether mammalian DNA repair Pols efficiently use template ribonucleotides …

Preserving the integrity of the DNA double helix is crucial for the maintenance of genomic
stability. Therefore, DNA double‐strand breaks represent a serious threat to cells. In this …

Targeted cancer therapies represent a milestone towards personalized treatment as they
function via inhibition of cancer-specific alterations. Polymerase θ (POLQ), an error-prone …

Polymerase theta (POLθ) is an error-prone DNA polymerase whose loss is synthetically
lethal in cancer cells bearing breast cancer susceptibility proteins 1 and 2 (BRCA1/2) …