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Updated: Jan 28, 2026

Targeted DNA Methylation Analysis by Next-generation Sequencing
08:38

Targeted DNA Methylation Analysis by Next-generation Sequencing

Published on: February 24, 2015

38.0K

Targeting DNA Methylation and EZH2 Activity to Overcome Melanoma Resistance to Immunotherapy

Abdullah Al Emran1, Aniruddha Chatterjee2, Euan J Rodger3

  • 1Melanoma Immunology and Oncology Group, The Centenary Institute, University of Sydney, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Australia; These authors contributed equally.

Trends in Immunology
|March 12, 2019
PubMed

Insights

DNA methylation patterns influence cancer immunotherapy. Hypermethylation can hinder immune responses, while hypomethylation may promote tumor evasion, highlighting methylation as a therapeutic target.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Immunology

Background:

  • DNA methylation at CpG sites is a stable epigenetic modification in cancer.
  • Hypermethylation can limit immune checkpoint blockade immunotherapy by suppressing interferon responses.
  • Global hypomethylation is linked to PD-L1 expression, immunosuppression, and epithelial-mesenchymal transition.

Purpose of the Study:

  • To explore how DNA methylation defines cancer patient subgroups.
  • To investigate DNA methylation as a target for tailored cancer treatment combinations.

Main Methods:

  • Exploratory analysis of DNA methylation data.
  • Correlation of methylation states with immune responses and tumor progression.

Main Results:

  • Contrasting roles of DNA hypermethylation and hypomethylation in cancer immunity.
  • DNA methylation's involvement in cytotoxic T cell exhaustion.
  • Identification of potential patient subgroups based on methylation profiles.

Conclusions:

  • DNA methylation patterns significantly impact the tumor microenvironment and response to immunotherapy.
  • Targeting DNA methylation offers a strategy for developing novel, personalized cancer therapies.
Keywords:
DNA methylationPD-L1PD1T cell exhaustionbiomarkerepigenetic remodelingimmune checkpoint blockademelanomaresistanceviral mimicry

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