Bernard S. Lopez

TL;DR: The main DSB repair mechanisms are presented and the importance of the fine tuning of this network for genome stability maintenance and for tumor protection in fine is discussed.

TL;DR: Low levels of replication stress, which are not detected by cell surveillance, allow cells to progress through the cell cycle, resulting in aberrant mitosis and chromosome instability, and underline the essential role of HR facing endogenous stress at the interface between replication and mitosis for protection against spontaneous general chromosome instability.

TL;DR: The links of replication, DNA damage and DDR defects to innate immunity activation by pro-inflammatory paracrine effects are reviewed, highlighting the implications for human syndromes and immunotherapies.

TL;DR: This review will focus on non‐programmed genome rearrangements generated by DSB repair, in somatic cells, and discusses chromothripsis, which is the shattering of a localized region of the genome followed by erratic rejoining.

TL;DR: In this article, the authors identify oxidative stress as a major endogenous source of replication speed deceleration in homologous recombination-defective cells, and they show that the treatment of these cells with the antioxidant Nacetyl-cysteine or the maintenance of the cells at low O2 levels (3%) rescues both the replication fork speed, as monitored by single-molecule analysis (molecular combing), and the associated mitotic extra centrosome frequency.