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G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma.

Gregory M Kelly1,2, Fares Al-Ejeh1, Robert McCuaig1

  • 1QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 16, 2021
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Summary
This summary is machine-generated.

Inhibiting G9a histone methyltransferase enhances immunotherapy response by increasing LC3B levels, a biomarker predicting patient survival and treatment efficacy in melanoma. This strategy may improve outcomes for more patients receiving checkpoint inhibitors.

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Area of Science:

  • Oncology
  • Epigenetics
  • Immunotherapy

Background:

  • G9a histone methyltransferase has oncogenic roles and its inhibition shows anticancer effects.
  • The impact of G9a inhibition on checkpoint inhibitor blockade response and its utility as a biomarker are understudied.

Purpose of the Study:

  • To investigate if G9a inhibition can enhance checkpoint inhibitor blockade efficacy.
  • To determine if LC3B, a G9a target gene, can predict response to checkpoint inhibitor blockade.

Main Methods:

  • Assessed LC3B's clinical potential as a biomarker using patient tumor biopsies and liquid biopsies.
  • Examined G9a inhibition's efficacy in improving checkpoint inhibitor blockade using a mouse model.

Main Results:

  • Responders to checkpoint inhibitor blockade showed higher tumor LC3B levels and expression.
  • Higher LC3B expression correlated with longer survival and reduced acquired resistance in melanoma patients.
  • G9a inhibition increased LC3B levels, augmented checkpoint inhibitor blockade efficacy, and induced melanoma cell death.

Conclusions:

  • LC3B shows potential as a predictive biomarker for guiding patient selection for checkpoint inhibitor blockade.
  • G9a inhibition represents a strategy to increase the proportion of patients benefiting from immunotherapy.