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Updated: Jan 25, 2026

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Loss of Msh2 and a single-radiation hit induce common, genome-wide, and persistent epigenetic changes in the

Maria Herberg1, Susann Siebert2,3, Marianne Quaas1,4

  • 1Interdisciplinary Center for Bioinformatics (IZBI), Leipzig University, Leipzig, Germany.

Clinical Epigenetics
|April 29, 2019
PubMed
Abstract

Insights

Mismatch repair deficiency alters histone methylation, increasing colorectal cancer risk. Radiation causes similar epigenetic changes in normal mice, but not in those with MMR deficiency.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Genomics

Background:

  • Mismatch repair (MMR)-deficiency is linked to increased colorectal cancer risk.
  • Investigating the epigenetic landscape in MMR-deficient mice before tumor onset is crucial.
  • Understanding radiation's impact on epigenetic profiles in this context is key.

Purpose of the Study:

  • To determine if tumors develop on a normal or disturbed epigenetic background in MMR-deficient mice.
  • To assess how radiation affects these epigenetic profiles.
  • To quantify genome-wide histone H3 methylation profiles.

Main Methods:

  • Analysis of histone H3 methylation profiles.
  • Comparison between MMR-deficient (Msh2-/-) and wild-type (Msh2+/+) mice.
  • Assessment of young, radiated, and untreated mice before tumor onset.

Main Results:

  • Histone H3 methylation increases in Msh2-/- mice compared to controls.
  • Specific histone marks (H3K4me3, H3K36me3) accumulate at certain genes.
  • Radiation induces similar epigenetic changes in wild-type mice but not in Msh2-/- mice.

Conclusions:

  • MMR deficiency leads to genome-wide histone methylation changes before tumor development.
  • These epigenetic alterations precede tumor formation.
  • Radiation-induced epigenetic changes resemble those in MMR deficiency and persist as a signature.
Keywords:
Histone H3 methylationIntestineMismatch repair deficiencyMsh2Radiation

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