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Targeting DNA Damage Response and Replication Stress in Pancreatic Cancer.

Stephan B Dreyer1, Rosie Upstill-Goddard2, Viola Paulus-Hock3

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Pancreatic cancer (PC) therapies are challenging. This study identifies biomarkers for DNA damage response (DDR) deficiency and replication stress, guiding new targeted treatments for PC.

Keywords:
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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Pancreatic cancer (PC) remains a highly lethal malignancy with limited therapeutic options.
  • Developing novel, biomarker-driven strategies is crucial for improving PC treatment outcomes.

Purpose of the Study:

  • To investigate the association between DNA damage response (DDR), replication stress, and therapeutic response in PC.
  • To establish a biomarker-driven strategy targeting DDR and replication stress for PC treatment.

Main Methods:

  • Interrogation of transcriptome, genome, proteome, and functional characteristics of 61 PC patient-derived cell lines.
  • Validation in patient-derived xenografts and human PC organoids.
  • Development of novel signatures for DDR deficiency and replication stress.

Main Results:

  • Biomarkers for DDR deficiency, including homologous recombination deficiency, correlate with response to platinum and PARP inhibitor therapies.
  • A novel replication stress signature predicts response to ATR and WEE1 inhibitor treatments.
  • Replication stress is prevalent in the squamous subtype of PC and independent of DDR deficiency.

Conclusions:

  • DDR deficiency and replication stress are distinct pathways in PC, offering therapeutic opportunities.
  • Targeting DDR and replication stress provides a promising avenue for novel PC therapies, even in DDR-proficient tumors or post-platinum treatment.