Cells have evolved a complex network of biochemical pathways, collectively known as the
DNA damage response (DDR), to prevent detrimental mutations from being passed on to …

The major pathways of DNA double-strand break (DSB) repair are crucial for maintaining
genomic stability. However, if deployed in an inappropriate cellular context, these same …

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 …

Many clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-
associated protein 9 (Cas9)-based genome editing technologies take advantage of Cas …

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 double-strand breaks (DSBs) are deleterious lesions that challenge genome integrity.
To mitigate this threat, human cells rely on the activity of multiple DNA repair machineries …

Nonhomologous end-joining (NHEJ) and homologous recombination (HR) are the primary
pathways for repairing DNA double-strand breaks (DSBs) during interphase, whereas …

Genome editing technologies operate by inducing site-specific DNA perturbations that are
resolved by cellular DNA repair pathways. Products of genome editors include DNA breaks …

Eukaryotic cells deploy overlapping repair pathways to resolve DNA damage.
Advancements in genome editing take advantage of these pathways to produce permanent …

DNA polymerase theta (POLθ or POLQ) is synthetic lethal with homologous recombination
(HR) deficiency and is thus a candidate target for HR-deficient cancers. Through high …