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

The DNA Replication Fork01:02

The DNA Replication Fork

36.5K
An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
36.5K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.8K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.8K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.3K
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...
9.3K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.4K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.4K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.7K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.7K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

5.9K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
5.9K

You might also read

Related Articles

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

Sort by
Same author

A unified catalytic mechanism in bifunctional DNA glycosylases with an evolutionarily conserved aspartate-lysine dyad.

Nature communications·2026
Same author

Avutometinib, Abemaciclib, and Fulvestrant in Patients with HR+/HER2- Metastatic Breast Cancer Previously Treated with CDK4/6 Inhibitor: A Single-Arm Phase I Trial.

Clinical cancer research : an official journal of the American Association for Cancer Research·2026
Same author

PTEN deficiency confers sensitivity to ATR inhibitor-based treatment in high-grade serous ovarian cancer.

The Journal of clinical investigation·2026
Same author

Patient-reported outcomes in castration-resistant prostate cancer with bone metastases treated with radium-223 with or without olaparib.

Cancer·2026
Same author

Fibroblast growth factor receptor inhibition for succinate dehydrogenase-deficient gastrointestinal stromal tumors: a phase 2 trial.

Nature medicine·2026
Same author

Multicenter, Randomized, Phase II Trial of Olaparib Plus Radium-223 Versus Radium-223 in Men With Castration-Resistant Prostate Cancer With Bone Metastases (COMRADE).

Journal of clinical oncology : official journal of the American Society of Clinical Oncology·2026

Related Experiment Video

Updated: Aug 26, 2025

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.1K

Targeting replication stress in cancer therapy.

Alexandre André B A da Costa1, Dipanjan Chowdhury1, Geoffrey I Shapiro2

  • 1Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Nature Reviews. Drug Discovery
|October 6, 2022
PubMed
Summary

Targeting cancer

More Related Videos

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
08:32

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

400
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

8.8K

Related Experiment Videos

Last Updated: Aug 26, 2025

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.1K
Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
08:32

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

400
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

8.8K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Replication stress drives genomic instability and is a key vulnerability in cancer cells.
  • Checkpoint kinases like ATR, CHK1, WEE1, and MYT1 regulate the DNA damage response and cell cycle.
  • Inhibiting these kinases can trigger innate immune responses via cytoplasmic DNA fragments.

Purpose of the Study:

  • To review current and emerging strategies for targeting replication stress in cancer.
  • To discuss the therapeutic potential of inhibiting DNA damage response kinases.
  • To explore combinations of replication stress inhibitors with other cancer therapies.

Main Methods:

  • Review of preclinical research on replication stress targeting.
  • Analysis of clinical trial data for ATR, CHK1, WEE1, and MYT1 inhibitors.
  • Examination of biomarker development for patient stratification.

Main Results:

  • Multiple inhibitors targeting ATR, CHK1, WEE1, and MYT1 are in clinical trials.
  • Combinations with chemotherapy, PARP inhibitors, and immune checkpoint inhibitors are being evaluated.
  • Targeting replication stress aims to exploit cancer vulnerabilities and enhance anti-tumor immunity.

Conclusions:

  • Targeting replication stress is a promising therapeutic avenue in oncology.
  • Combination therapies hold potential for overcoming resistance and improving treatment efficacy.
  • Further research and clinical evaluation are crucial for optimizing these strategies.