David C. Michael, Vice President of Institutional Relations of the Oxford University Biotechnology Society and Doctoral Researcher at the University of Oxford, shared a post on LinkedIn:

“Cancer is not only due to mutations in DNA. Sometimes the problem is how genes are activated or deactivated. That is the world of epigenetics.

I am pleased to share that our new article has just been published in Epigenomics.

Epigenetic dysregulation is now recognized as a hallmark of cancer, and DNA methyltransferase inhibitors (DNMTis) were among the first epigenetic therapies approved for clinical use in hematological cancers. Instead of altering the genetic code, these drugs act by reversing abnormal DNA methylation, thereby reactivating silenced tumor suppressor genes and increasing the visibility of the tumor to the immune system.

In this review, we explore:

• The clinical evolution of DNMT inhibitors such as azacitidine and decitabine.
• Why monotherapy usually has problems in solid tumors
• The growing promise of combination therapies (e.g., with immunotherapy or targeted therapies)
• Emerging directions, including next-generation DNMTis and biomarker-guided treatment

The field of epigenetic therapy is evolving rapidly, particularly as we move toward precision oncology and combination-based approaches. A deeper mechanistic understanding of DNMT inhibitors will be critical to unlocking their full potential in this regard.

I thank my supervisor and co-author. Parinaz Mehdipour, and grateful for the support of colleagues in the Mehdipour laboratory, the Ludwig Institute for Cancer Research, and the Oxford University.

“I hope this review serves as a useful resource for researchers and clinicians working at the intersection of epigenetics, drug development, and cancer therapy.”

Qualification: DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions

Authors: David C. Michael, Parinaz Mehdipour

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