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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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Quantifying replication stress in cancer without proliferation confounding.

Philipp Jungk1, Maik Kschischo1

  • 1Institute for Computer Science, University of Koblenz, Koblenz, Rhineland-Palatinate, Germany.

Cell Stress
|November 24, 2025
PubMed
Summary
This summary is machine-generated.

We developed a new gene expression signature (TRSS) to accurately measure replication stress (RS) independently of cell proliferation. This signature reveals a link between RS and DNA repair pathways, specifically non-homologous end-joining (NHEJ).

Keywords:
cell proliferationchromosomal instabilitygene expression signaturesmismatch repairnon-homologous end-joiningreplication stress

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Area of Science:

  • Genomic instability and cancer biology
  • DNA replication and repair mechanisms

Background:

  • Replication stress (RS) drives genomic instability and cancer, but its link to proliferation is complex.
  • Current RS signatures are biased by oncogene activity, overestimating proliferation-associated changes.
  • A proliferation-independent measure is needed to accurately assess RS in diverse cellular contexts.

Purpose of the Study:

  • To develop and validate a novel gene expression signature for robustly quantifying replication stress (RS).
  • To disentangle genuine RS transcriptional profiles from confounding cell cycle and proliferation signals.
  • To investigate the relationship between RS and DNA repair pathways in patient data.

Main Methods:

  • Development and validation of a novel gene expression signature, the tumorigenic RS signature (TRSS).
  • TRSS was designed to predict RS independently of oncogene activity and proliferation status.
  • Application of TRSS to experimental and clinical samples, including patient data analysis.

Main Results:

  • The developed TRSS accurately measures RS across diverse cellular contexts, independent of proliferation bias.
  • Analysis of patient data using TRSS revealed an association between elevated RS and the non-homologous end-joining (NHEJ) DNA repair pathway.
  • Elevated RS correlated with expression of mismatch repair genes MSH2 and MSH6, suggesting a potential shift towards NHEJ repair.

Conclusions:

  • The TRSS provides a refined, proliferation-independent method for quantifying replication stress.
  • This study highlights a novel link between replication stress and the non-homologous end-joining DNA repair pathway.
  • Findings suggest that RS may influence the choice of DNA repair pathways, impacting genomic stability in cancer.