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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

Using DNA methylation patterns to infer tumor ancestry.

You Jin Hong1, Paul Marjoram, Darryl Shibata

  • 1Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.

Plos One
|August 17, 2010
PubMed
Summary

Epigenetic variation in most colorectal cancers (CRCs) suggests a single clonal expansion, not multiple. DNA methylation patterns support a molecular clock hypothesis for tumor growth.

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Area of Science:

  • Oncology
  • Genomics
  • Epigenetics

Background:

  • Understanding human tumor growth is limited by the impracticality of serial observations.
  • Genomic variation within tumors offers a method to reconstruct cancer histories.
  • The "molecular clock hypothesis" posits greater variation indicates more time since the last clonal expansion.

Purpose of the Study:

  • To evaluate if DNA methylation patterns in colorectal cancers (CRCs) are consistent with a single clonal expansion.
  • To test the "molecular clock hypothesis" in primary human CRCs.

Main Methods:

  • Analysis of passenger DNA methylation patterns from opposite sides of 12 primary CRCs.
  • Comparison of empirical data with epigenomic data simulated under various single clonal expansion scenarios.

Main Results:

  • A single clonal expansion model explained the epigenetic variation in 11 out of 12 CRCs.
  • Eight CRCs exhibited symmetric growth, with cells equally related regardless of sampling location.
  • Three CRCs showed asymmetric growth, explainable by differential cell division within tumor regions.

Conclusions:

  • Epigenetic variation in primary CRCs is predominantly explained by a single clonal expansion event.
  • The findings challenge the notion of frequent, sequential clonal expansions in early tumor development.