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Updated: Jun 9, 2026

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
Published on: June 8, 2018
Epigenetic modifications in double-strand break DNA damage signaling and repair
Dorine Rossetto1, Andrew W Truman, Stephen J Kron
1Laval University Cancer Research Center, Hôtel-Dieu de Québec, Quebec City, Canada.
Abstract:
Factors involved in the cellular response to double-strand break (DSB) DNA damage have been identified as potential therapeutic targets that would greatly sensitize cancer cells to radiotherapy and genotoxic chemotherapy. These targets could disable the repair machinery and/or reinstate normal cell-cycle checkpoint leading to growth arrest, senescence, and apoptosis. It is now clear that a major aspect of the DNA damage response occurs through specific interactions with chromatin structure and its modulation. It implicates highly dynamic posttranslational modifications of histones that are critical for DNA damage recognition and/or signaling, repair of the lesion, and release of cell-cycle arrest. Therefore, drugs that target the enzymes responsible for these modifications, or the protein modules reading them, have very high therapeutic potential. This review presents the current state of knowledge on the different chromatin modifications and their roles in each step of eukaryotic DSB DNA damage response.
Insights
Targeting DNA repair mechanisms, specifically chromatin modifications, can sensitize cancer cells to radiation and chemotherapy. Understanding these processes is key to developing new cancer therapies.
Area of Science:
- Molecular Biology
- Cancer Therapeutics
- Epigenetics
Background:
- Cellular response to DNA damage is crucial for cancer treatment.
- Chromatin structure and histone modifications play a key role in DNA damage response.
- Targeting DNA repair pathways offers therapeutic potential for sensitizing cancer cells.
Purpose of the Study:
- To review the current understanding of chromatin modifications in eukaryotic double-strand break (DSB) DNA damage response.
- To highlight the therapeutic potential of targeting enzymes involved in these modifications.
Main Methods:
- Literature review of current research on DNA damage response and chromatin modulation.
- Analysis of the roles of posttranslational histone modifications in DSB repair and cell-cycle control.
Main Results:
- Specific chromatin modifications are critical for DNA damage recognition, signaling, and repair.
- Modulation of histone modifications can impact cell-cycle checkpoints, leading to growth arrest, senescence, or apoptosis.
- Enzymes regulating these modifications are promising therapeutic targets.
Conclusions:
- Targeting chromatin modifications offers a viable strategy to enhance cancer therapy efficacy.
- Further research into these epigenetic mechanisms can lead to novel anti-cancer drugs.
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