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DNA Methylation in Cancer: Progress and Challenges

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 741

Special Issue Editor


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Special Issue Information

Dear Colleagues,

DNA methylation abnormalities are frequent in cancer, including altered cytosine methylation in CpG dinucleotide residues and other pairs, such as CpA, although much less is known about the latter. The impact of alterations in DNA methylation on cancer onset and progression is very topical, especially in relation to aggressive cancer characteristics like metastasis, drug-resistance, altered anti-tumor immune responses, and enhanced tumor growth. The technologies for investigating genome-wide methylation have rapidly evolved in recent years, including bisulfite sequencing approaches. These developments could enhance this field, potentially allowing a higher sensitivity for detecting methylation alterations in smaller amounts of DNA.

In this Special Issue, we are looking to receive review articles and original research shaping our understanding of the role of DNA methylation alterations in cancer, as well as contributions which could potentially influence future research directions in this important area of cancer biology.

Prof. Dr. Michael Eccles
Guest Editor

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Keywords

  • DNA methylation
  • cancer
  • hypomethylation
  • hypermethylation
  • epigenetics
  • tumor onset
  • tumor progression
  • technologies

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Published Papers (1 paper)

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Review

20 pages, 901 KB  
Review
Epigenetic Deregulation of Transposable Elements Links Developmental Processes and Tumorigenesis
by Chiemi Lynch-Sutherland, Peter Stockwell, Aniruddha Chatterjee, Michael R. Eccles and Erin Macaulay
Int. J. Mol. Sci. 2026, 27(6), 2690; https://doi.org/10.3390/ijms27062690 - 16 Mar 2026
Viewed by 309
Abstract
Dedifferentiation—the acquisition of an early developmental state—is a hallmark of cancer. However, the underlying mechanisms that lead to cancer-associated dedifferentiation are not fully understood. Transposable elements (TEs) are becoming increasingly recognised as important regulators of development and disease. The recruitment of TE sequences [...] Read more.
Dedifferentiation—the acquisition of an early developmental state—is a hallmark of cancer. However, the underlying mechanisms that lead to cancer-associated dedifferentiation are not fully understood. Transposable elements (TEs) are becoming increasingly recognised as important regulators of development and disease. The recruitment of TE sequences has played an important role in placental evolution, and TE-derived genes play critical roles in placental development. Although important biological differences exist between tumours and the placenta, the placenta shares certain features with tumours, including the capacity to invade surrounding tissue and modulate the maternal immune response. In this regard, TEs have been implicated in cancer development, and are documented to contribute to oncogenesis through multiple different mechanisms. Moreover, cancers reacquire an epigenetic landscape, which is reflective of early development, and which corresponds to increased phenotypic plasticity, including facilitating the activation of early developmental genes. Many cancers can repurpose developmental genes, including TE-associated genes, which may contribute to pathways involved in invasion and metastasis. Determining whether TE activation is a consequence of broader epigenetic reprogramming or actively contributes to dedifferentiation will be important for understanding cancer biology and may facilitate improvements in cancer diagnosis and treatment. Full article
(This article belongs to the Special Issue DNA Methylation in Cancer: Progress and Challenges)
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