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

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.0K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.0K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

9.9K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.9K
Overview of DNA Repair02:25

Overview of DNA Repair

33.3K
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...
33.3K
Overview of DNA Repair02:25

Overview of DNA Repair

9.5K
9.5K
Overview of Cell Death01:30

Overview of Cell Death

9.2K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
9.2K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

4.9K
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...
4.9K

You might also read

Related Articles

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

Sort by
Same author

FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination.

Proceedings of the National Academy of Sciences of the United States of America·2020
Same author

DNA damage-induced cell death relies on SLFN11-dependent cleavage of distinct type II tRNAs.

Nature structural & molecular biology·2018
Same author

Nuclear respiratory factor 1 promotes spheroid survival and mesenchymal transition in mammary epithelial cells.

Oncogene·2018
Same author

Extracellular vesicles transfer nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander effects.

Molecular biology of the cell·2018
Same author

EnABLing microprocessor for apoptosis.

Molecular & cellular oncology·2016
Same author

Loss of histone variant macroH2A2 expression associates with progression of anal neoplasm.

Journal of clinical pathology·2015

Related Experiment Video

Updated: Jan 1, 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

4.0K

Cell Death Response to DNA Damage.

Jean Y J Wang1

  • 1Department of Cellular & Molecular Medicine, University of California, San Diego, CA.

The Yale Journal of Biology and Medicine
|December 24, 2019
PubMed
Summary
This summary is machine-generated.

DNA damaging agents (DDA) treat cancer but resistance emerges. The DNA damage response (DDR) can both protect cells and trigger death, offering new therapeutic strategies against resistant cancers.

Keywords:
apoptosiscancerchemotherapymitochondriamitotic catastrophenecroptosisradiation therapy

More Related Videos

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

9.5K
Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry
08:21

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

14.0K

Related Experiment Videos

Last Updated: Jan 1, 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

4.0K
Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

9.5K
Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry
08:21

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

14.0K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • DNA damaging agents (DDA) are crucial in cancer therapy, yet their efficacy is limited by the development of DDA-resistant cancer cells.
  • The DNA damage response (DDR) network comprises genes, proteins, and pathways that protect the genome but can paradoxically induce cell death.

Purpose of the Study:

  • To review the dual role of DDR in protecting the genome and initiating cell death.
  • To explore how DDR determines the timing and location of cell death execution.
  • To discuss exploiting cancer-specific DDR defects for novel therapeutic strategies.

Main Methods:

  • Review of existing literature on DDA and DDR mechanisms.
  • Analysis of clinical outcomes from DDA cancer treatments.
  • Hypothesizing DDR's role in cell death regulation.

Main Results:

  • DDA can cure some cancers, but resistance frequently develops due to DDR.
  • DDR activation can lead to either genome protection or programmed cell death.
  • Cancer cells often possess DDR defects, contributing to initial DDA sensitivity.

Conclusions:

  • Understanding DDR's complex role in cell death is critical for cancer therapy.
  • Targeting cancer-specific DDR defects presents a promising avenue for overcoming DDA resistance.
  • Future therapies may involve inducing death-inducing DNA lesions without DDA to eliminate resistant tumors.