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Related Concept Videos

Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Mutations01:39

Mutations

Overview
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...

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Related Experiment Video

Updated: May 25, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

DNA damage by X-rays and their impact on replication processes.

Ann Christin Parplys1, Eva Petermann, Cordula Petersen

  • 1Center of Oncology, University Medical Center Hamburg-Eppendorf, Germany.

Radiotherapy and Oncology : Journal of the European Society for Therapeutic Radiology and Oncology
|February 14, 2012
PubMed
Summary
This summary is machine-generated.

Combining radiotherapy with agents that induce DNA damage or inhibit checkpoint signaling can enhance tumor radiosensitivity during S phase. This approach shows promise for improving cancer treatment outcomes.

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Last Updated: May 25, 2026

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Radiotherapy

Background:

  • Replication-dependent radiosensitization is a promising cancer therapy strategy.
  • Cell cycle checkpoints during S phase are crucial for genomic stability after irradiation.
  • The impact of different DNA damage types on replication fork function is not well understood.

Purpose of the Study:

  • To investigate the effects of various DNA-damaging agents on replication fork functionality in tumor cells.
  • To understand how different types of DNA damage influence cell cycle checkpoint signaling.

Main Methods:

  • U2OS cells were treated with methyl methanesulfonate, hydrogen peroxide, Topotecan, Mitomycin C, or ionizing radiation.
  • Analysis included Chk1 phosphorylation, origin firing, replication fork progression, and cell cycle distribution.

Main Results:

  • Chk1 phosphorylation extent and duration varied with damage type, correlating with replication initiation inhibition.
  • Ionizing radiation, high hydrogen peroxide, and Topotecan significantly impacted replication elongation.
  • Prolonged Chk1 phosphorylation and strong replication elongation inhibition led to G2 arrest.

Conclusions:

  • Radiosensitivity in S phase can be enhanced by combining irradiation with agents causing secondary double-strand breaks (DSBs) or inhibiting checkpoint signaling.
  • Inhibitors of Poly (ADP-ribose) polymerase (PARP) or Chk1 are potential agents for combination therapy.