Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

3.9K
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...
3.9K
Base Excision Repair01:54

Base Excision Repair

23.3K
One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
23.3K
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

7.2K
Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
7.2K
Base-pairing and DNA Repair02:27

Base-pairing and DNA Repair

67.3K
67.3K
Overview of DNA Repair02:25

Overview of DNA Repair

32.0K
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...
32.0K
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

276
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).
276

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Facilitating access to clinical data from a randomized controlled trial of complex adaptive design.

BMC research notes·2026
Same author

Beyond Viral Control: Tenofovir's Hidden Impact on Blood-Brain Barrier Endothelial Cells.

Microcirculation (New York, N.Y. : 1994)·2026
Same author

A Phase I Study of Copanlisib and Venetoclax in Patients With Relapsed or Refractory Diffuse Large B-Cell Lymphoma.

Clinical lymphoma, myeloma & leukemia·2026
Same author

Systematic infectome-phenome profiling reveals cryptococcal infection-associated proteins driving immune system remodeling and immunization potential.

iScience·2026
Same author

Chitosan-hyaluronic acid engineered polycaprolactone nanoparticles enhance curcumin antiplasmodial activity and preserve blood-brain barrier integrity.

Journal of biomaterials science. Polymer edition·2026
Same author

Development of a prediction model for acute kidney injury in critically ill patients with advanced colorectal cancer based on white blood cell-related indicators.

Frontiers in oncology·2026

Related Experiment Video

Updated: Oct 4, 2025

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

18.3K

Role for Nucleotide Excision Repair Gene Variants in Oxaliplatin-Induced Peripheral Neuropathy.

Hannah West1, Michelle Coffey1, Michael J Wagner1

  • 1Hannah West, Michelle Coffey, James P. Colley, Richard A. Adams, Rebecca Harris, and Jeremy P. Cheadle, School of Medicine, Cardiff University, Cardiff; Oliver Fleck, North West Cancer Research Institute, Bangor University, Bangor; Timothy S. Maughan, Cancer Research UK/Medical Research Council Oxford Institute for Radiation Oncology, University of Oxford, Oxford; David Fisher and Richard S. Kaplan, Medical Research Council Clinical Trials Unit, London, United Kingdom; Michael J. Wagner, Institute for Pharmacogenomics and Individualized Therapy, University of North Carolina, Chapel Hill, NC; and Howard L. McLeod, DeBartolo Family Personalized Medicine Institute, Moffitt Cancer Center, Tampa, FL.

JCO Precision Oncology
|February 9, 2022
PubMed
Summary

Genetic variations in nucleotide excision repair (NER) genes, specifically ERCC4 and ERCC6, are linked to oxaliplatin-induced peripheral neuropathy (PNAO) in colorectal cancer patients. These findings offer mechanistic insights into PNAO development.

More Related Videos

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays
04:07

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays

Published on: February 24, 2023

1.8K
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

880

Related Experiment Videos

Last Updated: Oct 4, 2025

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

18.3K
Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays
04:07

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays

Published on: February 24, 2023

1.8K
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

880

Area of Science:

  • Oncology
  • Genetics
  • Toxicology

Background:

  • Oxaliplatin is a key chemotherapy for advanced colorectal cancer.
  • Oxaliplatin-induced peripheral neuropathy (PNAO) is a common dose-limiting toxicity.
  • The underlying molecular mechanisms of PNAO are not fully understood.

Purpose of the Study:

  • To investigate the genetic and cellular mechanisms of oxaliplatin-induced peripheral neuropathy (PNAO).
  • To identify specific genes associated with PNAO susceptibility.

Main Methods:

  • Exome resequencing of DNA from patients with PNAO.
  • Sanger sequencing and targeted genotyping of ERCC4 and ERCC6 genes.
  • Functional assays in yeast and human cell lines to assess DNA repair capacity.

Main Results:

  • A novel germline mutation in the ERCC4 gene was identified in a patient with PNAO.
  • Rare nonsynonymous variants in ERCC4 and ERCC6 genes were significantly over-represented in patients with PNAO.
  • Defective DNA repair function was observed for several ERCC4 variants.
  • Approximately 22% of PNAO patients carried specific ERCC4 or ERCC6 variants.

Conclusions:

  • Nucleotide excision repair (NER) genes play a significant role in PNAO.
  • Genetic variations in NER genes contribute to oxaliplatin toxicity.
  • Mechanistic insights into PNAO are provided, potentially guiding future treatment strategies.