Related Experiment Video
Updated: Jun 14, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
DNA hypomethylation in cancer: epigenetic scars of a neoplastic journey
Charles De Smet1, Axelle Loriot1
1Catholic University of Louvain.
Abstract:
Cytosine methylation is a heritable modification of DNA in mammalian cells, and has a determinant impact on long-term gene repression and genome stability. Genomic methylation patterns, which remain generally stable in the adult, become profoundly altered in most human tumors. While discrete DNA segments become hypermethylated in cancer cells, many more sequences become hypomethylated. This review discusses our current understanding of the mechanisms that lead to DNA hypomethylation in tumors. Evidence suggests that methylation losses are not random, but rather evolve into mosaic hypomethylation patterns. It is proposed that such hypomethylation patterns result from a historical event of transient DNA demethylation, and that transcriptional regulators contribute to determining which regions escape remethylation and remain therefore unmethylated. Finally, possible stages of tumor development during which the transient DNA demethylation process may take place will be discussed.
Insights
DNA hypomethylation, a key change in cancer, involves non-random methylation losses. Transcriptional regulators may influence these patterns during tumor development, suggesting transient DNA demethylation events.
Area of Science:
- Epigenetics
- Cancer Biology
- Genomics
Background:
- Cytosine methylation is a crucial, heritable DNA modification impacting gene repression and genome stability in mammals.
- While generally stable in adults, genomic methylation patterns are significantly altered in most human tumors.
- Cancer cells exhibit both hypermethylated and, more extensively, hypomethylated DNA segments.
Purpose of the Study:
- To review the current understanding of the mechanisms driving DNA hypomethylation in tumors.
- To explore the non-random nature of methylation loss and proposed patterns of mosaic hypomethylation.
- To discuss the potential role of transient DNA demethylation events and transcriptional regulators in establishing these patterns.
Main Methods:
- Literature review of existing research on DNA methylation and cancer.
- Analysis of evidence suggesting mechanisms for DNA hypomethylation in tumor development.
- Discussion of proposed models involving transient demethylation and transcriptional regulation.
Main Results:
- DNA hypomethylation in tumors is extensive and appears to follow non-random, mosaic patterns.
- Evidence suggests these patterns arise from historical transient DNA demethylation events.
- Transcriptional regulators are implicated in determining regions that escape remethylation.
Conclusions:
- DNA hypomethylation in cancer is a complex process, not a random event.
- Transient DNA demethylation followed by selective remethylation, influenced by transcriptional regulators, likely shapes tumor hypomethylation patterns.
- Understanding these mechanisms may reveal critical stages in tumor development.
Related Concept Videos
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Cancers Originate from Somatic Mutations in a Single Cell
Cancers Originate from Somatic Mutations in a Single Cell

