During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

ATR protects stem cell genomes by activating a transcriptional response mediated by totipotency genes, conferring trophoblast differentiation potential, the derepression of which in somatic cells might favour cancer features emergence.

In addition to its role in preventing tumors, the protein p53 appears to participate in a DNA repair process known as the replication-stress response.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.

Protein IGFBP-4 acts as a genotoxic stress mediator that, entering into circulation after its secretion by senescent cells, could promote further senescence phenomena in non-injured cells thus impairing tissues’ homeostasis.

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.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

An investigation into 8-oxodeoxguanosine bypass by archaeal DNA polymerases.

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.