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

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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...
Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
Mismatch Repair01:36

Mismatch Repair

Overview
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Viral Mutations00:36

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...

You might also read

Related Articles

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

Sort by
Same author

Targeting Cancer-Specific Mutations with RNA-Triggered Chromatin Shredding.

Nature·2026
Same author

Toward a Random Background for Ligand Optimization.

bioRxiv : the preprint server for biology·2026
Same author

Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding.

bioRxiv : the preprint server for biology·2026
Same author

Two decades of PARP inhibitor synthetic lethality in cancer.

Nature·2026
Same author

Comparative sequence analysis of the mouse pseudoautosomal region from three inbred strains reveals it to be the most rapidly evolving 'chromosome'.

Proceedings of the Japan Academy. Series B, Physical and biological sciences·2026
Same author

Correction to: Elevated APOBEC3B expression drives a kataegic-like mutation signature and replication stress-related therapeutic vulnerabilities in p53-defective cells.

British journal of cancer·2026
Same journal

CDK2 Inhibition Exerts RB-Independent Antitumor Activity in CDK4/6 Inhibitor-Resistant HR+/HER2- Breast Cancer.

Cancer research·2026
Same journal

A Clinically Integrated Pediatric Patient-Derived Xenograft Program Enables Evaluation of Cohort and Patient-Specific Biology and Therapeutic Strategies.

Cancer research·2026
Same journal

Editor's Note: Heterodimerization of Insulin-like Growth Factor Receptor/Epidermal Growth Factor Receptor and Induction of Survivin Expression Counteract the Antitumor Action of Erlotinib.

Cancer research·2026
Same journal

Editor's Note: Deguelin Analogue SH-1242 Inhibits Hsp90 Activity and Exerts Potent Anticancer Efficacy with Limited Neurotoxicity.

Cancer research·2026
Same journal

Retraction: Two Functional Epitopes of Pigment Epithelial-Derived Factor Block Angiogenesis and Induce Differentiation in Prostate Cancer.

Cancer research·2026
Same journal

Editor's Note: Chronic Stress Facilitates Lung Tumorigenesis by Promoting Exocytosis of IGF2 in Lung Epithelial Cells.

Cancer research·2026
See all related articles

Related Experiment Video

Updated: Jun 27, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Drug resistance caused by reversion mutation.

Alan Ashworth1

  • 1The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London, United Kingdom. alan.ashworth@icr.ac.uk

Cancer Research
|December 17, 2008
PubMed
Summary
This summary is machine-generated.

Cells with BRCA mutations are sensitive to PARP inhibitors. Deleting BRCA2 mutations can reverse this sensitivity, leading to resistance. This finding is relevant for ovarian cancer treatment.

More Related Videos

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
09:58

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models

Published on: December 9, 2016

Related Experiment Videos

Last Updated: Jun 27, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
09:58

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models

Published on: December 9, 2016

Area of Science:

  • * Molecular biology
  • * Cancer genetics
  • * DNA repair mechanisms

Background:

  • * Cells with mutated BRCA1 or BRCA2 genes exhibit deficiencies in homologous recombination DNA repair.
  • * This DNA repair defect confers sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors, forming the basis of synthetic lethal cancer therapy.
  • * Understanding resistance mechanisms is crucial for optimizing PARP inhibitor efficacy.

Purpose of the Study:

  • * To investigate the mechanisms underlying acquired resistance to PARP inhibitors in cancer cells with BRCA mutations.
  • * To explore the potential role of BRCA2 mutation deletion in reversing sensitivity to PARP inhibition.
  • * To examine the association between similar mechanisms and carboplatin resistance in BRCA2-mutated ovarian cancer.

Main Methods:

  • * Analysis of DNA repair pathways in cells with BRCA1/BRCA2 mutations.
  • * Investigating the impact of BRCA2 mutation deletion on cellular response to PARP inhibitors.
  • * Clinical data review of BRCA2 mutation carriers with ovarian cancer and their response to carboplatin.

Main Results:

  • * Demonstrated that deletion of a BRCA2 mutation can reverse the sensitivity of cancer cells to PARP inhibitors, leading to acquired resistance.
  • * Identified a potential common mechanism linking BRCA2 mutation status, PARP inhibitor resistance, and carboplatin resistance in ovarian cancer.
  • * Findings suggest that BRCA2 mutation status is a critical factor in therapeutic response.

Conclusions:

  • * Acquired resistance to PARP inhibitors can occur through the deletion of BRCA2 mutations.
  • * This mechanism may also contribute to carboplatin resistance in BRCA2-mutated ovarian cancer.
  • * Targeting DNA repair pathways and understanding resistance mechanisms are key for advancing cancer therapeutics.