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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Histone Variants at the Centromere02:30

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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
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Related Experiment Video

Updated: Jan 16, 2026

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
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How structural variation shapes the cancer epigenome.

Signe MacLennan1, Marco A Marra2

  • 1Department of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, Canada; Michael Smith Laboratories, University of British Columbia, Vancouver, Canada; Canada's Michael Smith Genome Sciences Centre, Vancouver, Canada.

Trends in Cancer
|October 1, 2025
PubMed
Summary

Cancer arises from genomic changes. Epigenetic disruptions and structural variations (SV) interact, influencing cancer development and progression. This review covers technologies and research on SV and the epigenome in cancer.

Keywords:
enhancer hijackingextrachromosomal DNAmethylationretrotransposonstopologically associated domainsviral integration

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Area of Science:

  • Oncology
  • Genomics
  • Epigenetics

Background:

  • Cancer develops through genomic alterations leading to malignant properties.
  • Epigenetic disruptions, affecting genome interpretation without altering sequence, are key in cancer.
  • The interplay between structural variation (SV) and epigenetics in cancer is a growing research area.

Purpose of the Study:

  • To review technological advances for simultaneous genome and epigenome profiling in cancer.
  • To highlight recent research on the relationship between SV and the epigenome in cancer.

Main Methods:

  • Review of current technologies for cancer genome and epigenome analysis.
  • Synthesis of recent scientific literature on SV-epigenome interactions in malignancy.

Main Results:

  • Technological advancements enable integrated analysis of genomic and epigenetic changes.
  • Emerging research reveals complex interactions between SV and epigenetic modifications in cancer progression.

Conclusions:

  • Understanding the SV-epigenome axis is crucial for deciphering cancer development.
  • Future research directions involve leveraging new technologies to explore these interactions further.