DNA and RNA methylation is implicated in normal and aberrant hematopoiesis.
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These epigenetic marks are exploited in cancer to evade immune surveillance.
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DNA hypomethylating agents can reactivate innate and adaptive immune responses.
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Modulating RNA methylation may enhance activation of the immune system.
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Novel DNA/RNA methylation therapies may improve outcomes for hematological cancers.
Whilst DNA cytosine methylation is the oldest and most well-studied epigenetic modification, basking in its glory days, it may be soon overshadowed by the new kid on the block: RNA adenosine methylation. This juxtaposition is indeed superficial, and a deep exploration toward the fundamental requirements for these essential epigenetic marks provides a clear perspective on their converging and synergistic roles. The recent discovery that both of these modifications are essential for preventing inappropriate activation of the intracellular innate immune responses to endogenous transcripts has provided a lot of interest in targeting them therapeutically as a means to improve cancer immunogenicity. Here we discuss the potential physiological function for DNA and RNA methylation in normal hematopoiesis and how these pervasive epigenetic marks are exploited in cancer, and provide suggestions for future research with a focus on leveraging this knowledge to uncover novel therapeutic targets.
