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Related Concept Videos

Mutations01:39

Mutations

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...
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...
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...
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...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Related Experiment Video

Updated: Jul 25, 2026

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

Spontaneous DNA damage propels tumorigenicity.

Ilio Vitale1,2, Guido Kroemer3,4,5,6,7,8,9

  • 1Department of Biology, University of Rome "Tor Vergata", Rome 00133, Italy.

Cell Research
|April 1, 2017
PubMed
Summary

DNA damage fuels cancer growth and treatment resistance. A new study reveals an intrinsic source of DNA double-strand breaks that enhances cancer cell aggressiveness and stemness.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Endogenously generated DNA damage is a key driver of cancer development, progression, and therapeutic resistance.
  • Understanding the sources of DNA damage is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To identify novel intrinsic sources of DNA double-strand breaks (DSBs) in malignant cells.
  • To investigate the role of these DSBs in promoting cancer aggressiveness and stemness.

Main Methods:

  • Utilized advanced molecular biology techniques to detect and characterize DNA double-strand breaks.
  • Employed cell-based assays to assess cancer cell aggressiveness and stem-like properties.
  • Investigated the signaling pathways involved in the generation and response to DSBs.

Main Results:

  • Discovered a previously unrecognized intrinsic source of DNA double-strand breaks in cancer cells.
  • Demonstrated that these DSBs significantly enhance cancer cell aggressiveness, including invasion and metastasis.
  • Showed that the identified DSBs promote stemness properties, contributing to tumor initiation and recurrence.

Conclusions:

  • The study identifies a novel intrinsic source of DNA double-strand breaks that actively contributes to cancer malignancy.
  • Targeting this source of DNA damage may represent a promising therapeutic strategy to overcome cancer aggressiveness and stemness.
  • Further research is warranted to explore the clinical implications of these findings for cancer treatment.