Editorial: Cancer therapeutics: targeting DNA repair pathways

A cell’s genome is constantly challenged by exogenous and endogenous DNA damaging agents and failure to repair this damage can lead to genomic instability and tumorigenesis (Lavin et al., 2005; Jackson and Bartek, 2009). Genomic instability is an established hallmark of cancer and as tumorigenesis progresses, genetic streamlining leads to dysregulation of DNA repair pathways, selecting for cancer cells that have enhanced genomic instability and fitness. Importantly, this tumor evolution commonly leads to dependency on a single DNA repair pathway for survival through inactivation of alternate pathways, highlighting a key molecular weakness of cancer cells (Jeggo et al., 2016). Exploiting this weakness by accurately targeting the remaining or dysregulated DNA repair pathways in cancer cells using the next generation of precision/personalized medicine drugs, provides a therapeutic approach tailored to an individual’s specific tumor profile (Aziz et al., 2012; Kelley et al., 2014; Jekimovs et al., 2014; Biau et al., 2019; Lavin and Yeo, 2020).