# OnCo record replication-stress (pathway). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)". Whole corpus: https://onco.cc/api/v1/onco.nt
@prefix schema: <https://schema.org/> .
@prefix onco: <https://onco.cc/ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .

<https://onco.cc/pathways/replication-stress/>
  a schema:BioChemEntity ;
  onco:kind "pathway" ;
  schema:identifier "replication-stress" ;
  schema:name "DNA replication stress"@en ;
  schema:description "Cancers copy their DNA too fast and with broken checkpoints, so replication forks stall and collapse. They survive only by leaning on emergency repair kinases such as ATR, CHK1, and WEE1, which is why blocking those kinases can be selectively lethal."@en ;
  schema:url <https://onco.cc/pathways/replication-stress/> ;
  schema:dateModified "2026-09-08"^^xsd:date ;
  schema:sameAs <https://en.wikipedia.org/wiki/Replication_stress> ;
  schema:citation <https://doi.org/10.1016/j.molcel.2022.05.004> ;
  onco:tag "mechanism" ;
  onco:cancers <https://onco.cc/cancers/colorectal/> ;
  onco:technologies <https://onco.cc/technologies/synthetic-lethality-approaches/>, <https://onco.cc/technologies/parp-inhibitor/> ;
  onco:targets <https://onco.cc/targets/atr/>, <https://onco.cc/targets/wee1/>, <https://onco.cc/targets/tp53/>, <https://onco.cc/targets/parp/> ;
  onco:institutions <https://onco.cc/institutions/icr-london/>, <https://onco.cc/institutions/dana-farber/>, <https://onco.cc/institutions/nki/>, <https://onco.cc/institutions/francis-crick/> ;
  onco:pathways <https://onco.cc/pathways/ddr/>, <https://onco.cc/pathways/p53-cell-cycle/>, <https://onco.cc/pathways/myc/> ;
  onco:terms <https://onco.cc/terms/synthetic-lethality/>, <https://onco.cc/terms/genome-instability-mutation/> ;
  onco:keyPapers <https://onco.cc/key-papers/paper-saxena-mol-cell/> .