It has long been known that cancer cells, compared to their non-neoplastic counterparts, constitutively exhibit increased levels of replication stress, i.e. the slowing or stalling of replication fork progression due to various endogenous and exogenous stresses.1 Early on it was also discovered that increased replication stress in tumour cells is often associated with increased ataxia telangiectasia and Rad3-related checkpoint (ATR) activity in these cells, which is considered to be a survival advantage in tumour development.
It has long been known that cancer cells, compared to their non-neoplastic counterparts, constitutively exhibit increased levels of replication stress, i.e. the slowing or stalling of replication fork progression due to various endogenous and exogenous stresses.1 Early on it was also discovered that increased replication stress in tumour cells is often associated with increased ataxia telangiectasia and Rad3-related checkpoint (ATR) activity in these cells, which is considered to be a survival advantage in tumour development.