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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cancer therapy traditionally targets pathway inhibition.
  • Conditional pathway activation as a vulnerability source is underexplored.
  • Systematic identification of gene-activation-induced lethality is needed.

Purpose of the Study:

  • To systematically identify context-specific gene-activation-induced lethalities in cancer.
  • To explore the pan-cancer vulnerability landscape through pathway activation.

Main Methods:

  • Developed a high-throughput method for simultaneous gain-of-function genetic perturbations across ~500 barcoded cancer cell lines.
  • Queried cancer vulnerability by activating ten key pathway nodes.
  • Validated findings in xenograft and patient-derived organoid models.

Main Results:

  • Revealed selective activation dependencies of MAPK and PI3K pathways linked to specific biomarkers.
  • Discovered novel pathway hyperactivation dependencies in APC-mutant colorectal cancers.
  • Demonstrated that WNT pathway activation via APC knockdown or β-catenin overexpression induced robust anti-tumor effects.

Conclusions:

  • Identified a new class of conditional gene-activation dependencies in cancer.
  • Highlights pathway activation as a potential therapeutic strategy.
  • Suggests biomarker-driven approaches for targeted pathway activation therapies.