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Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
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Published on: November 22, 2021

Evaluation of Mutation Risk Using Patient-Derived Organoids in Patients With Lynch Syndrome.

Youmi Shin1,2, Dong Keon Kim1, Yoojeong Seo1,2

  • 1Division of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.

International Journal of Cancer
|July 10, 2026
PubMed
Summary

Lynch syndrome (LS) patients have varying colorectal cancer (CRC) risks. A new organoid assay using MNNG and O6BG shows differential DNA damage response, aiding LS mutation risk stratification.

Keywords:
Lynch syndromecolorectal cancermutationorganoid

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Lynch syndrome (LS) is an inherited condition increasing colorectal cancer (CRC) risk due to DNA mismatch repair (MMR) gene mutations.
  • Individual CRC risk varies among LS patients with identical MMR mutations, necessitating personalized risk assessment.

Purpose of the Study:

  • To develop a functional assay using patient-derived organoids (PDOs) for assessing mutation risk in Lynch syndrome patients.
  • To evaluate the utility of organoid response to cytotoxic agents for predicting LS-associated cancer risk.

Main Methods:

  • Patient-derived organoids (PDOs) from LS and non-LS individuals were treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), an O6-alkylguanine DNA alkyltransferase (MGMT) inhibitor (O6BG), and an ATR inhibitor.
  • Organoid growth, apoptosis, and DNA damage marker (γH2AX) expression were analyzed to assess cytotoxic effects and DNA damage response.
  • Differential responses between LS-PDOs and non-LS PDOs were compared to identify predictive markers for cancer risk.

Main Results:

  • Non-LS organoids showed significantly higher sensitivity to the combined MNNG, O6BG, and ATR inhibitor treatment compared to LS organoids.
  • LS organoids exhibited higher γH2AX expression after MNNG and O6BG treatment, indicating impaired DNA damage response and potential for mutation accumulation.
  • The assay demonstrated potential for distinguishing between LS and non-LS organoids based on DNA damage response.

Conclusions:

  • A preclinical platform utilizing MNNG and O6BG treatment of PDOs, coupled with DNA damage response measurement, can aid in risk stratification for Lynch syndrome patients.
  • This functional assay offers a novel approach to personalize cancer risk assessment in individuals with hereditary cancer syndromes.
  • Understanding differential DNA damage responses in organoids can guide therapeutic strategies and surveillance protocols for LS patients.