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Updated: Jul 12, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
Published on: August 21, 2021
DNA damage response: the players, the network and the role in tumor suppression
Rekha Rai1, Guang Peng, Kaiyi Li
1ACTREC (CRI), TMC, Mumbai, Maharashtra, India.
Abstract:
One of the most common features of cancer is genetic instability. In response to numerous DNA-damaging insults, normal cells have evolved a complex mechanism to monitor and repair DNA damage lesions to maintain genomic integrity. The defects in DNA damage response, indeed, have been shown to associate closely with tumorigenesis. This review provides an overview on the molecular events in DNA damage signaling pathway, including cell cycle checkpoint and DNA repair. The recent research discoveries on how dysfunction in DNA damage response contributes to genomic instability and cancer development are also discussed.
Insights
Cancer
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- Genetic instability is a hallmark of cancer.
- Normal cells possess DNA damage response (DDR) mechanisms to maintain genomic integrity.
- Defects in DDR are linked to cancer development.
Purpose of the Study:
- To review the molecular mechanisms of DNA damage signaling pathways.
- To discuss the role of cell cycle checkpoints and DNA repair.
- To explore how DDR dysfunction contributes to cancer.
Main Methods:
- Literature review of DNA damage response pathways.
- Analysis of molecular events in cell cycle checkpoint control.
- Synthesis of research on DNA repair mechanisms.
Main Results:
- Detailed overview of DNA damage signaling pathways.
- Explanation of cell cycle checkpoints and DNA repair processes.
- Discussion of recent findings linking DDR defects to cancer.
Conclusions:
- Dysfunctional DNA damage response is a critical factor in genomic instability and tumorigenesis.
- Understanding DDR pathways is crucial for cancer research and therapy.
- Further research into DDR mechanisms may reveal new therapeutic targets.
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