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

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
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

5.0K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
5.0K
In-vitro Mutagenesis01:16

In-vitro Mutagenesis

14.1K
To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
14.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.6K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.6K
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
Protein Networks02:26

Protein Networks

4.0K
An organism can have thousands of different proteins, and these proteins must cooperate to ensure the health of an organism. Proteins bind to other proteins and form complexes to carry out their functions. Many proteins interact with multiple other proteins creating a complex network of protein interactions.
These interactions can be represented through maps depicting protein-protein interaction networks, represented as nodes and edges. Nodes are circles that are representative of a protein,...
4.0K

You might also read

Related Articles

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

Sort by
Same author

The PRECISE European initiative for cancer-vulnerability mapping and prediction.

Nature genetics·2026
Same author

Reduced PRC2 function causes asparaginase resistance in T-ALL by decreasing WNT pathway activity.

Blood advances·2026
Same author

Genetic interactions, synthetic lethality and complexity in cancer vulnerability mapping-Insights and perspectives from the 2nd EuroDepMap symposium.

FEBS letters·2026
Same author

nf-core/crisprseq: a versatile pipeline for comprehensive analysis of CRISPR gene editing and screening assays.

NAR genomics and bioinformatics·2026
Same author

Reduced PRC2 function causes asparaginase resistance in T-ALL by decreasing WNT pathway activity.

Blood advances·2025
Same author

Benchmarking genetic interaction scoring methods for identifying synthetic lethality from combinatorial CRISPR screens.

NAR genomics and bioinformatics·2025

Related Experiment Video

Updated: Aug 7, 2025

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions
07:40

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

4.2K

Targeting synthetic lethal paralogs in cancer.

Colm J Ryan1, Ishan Mehta2, Narod Kebabci3

  • 1Conway Institute and School of Computer Science, University College Dublin, Dublin, Ireland; Systems Biology Ireland, University College Dublin, Dublin, Ireland.

Trends in Cancer
|March 8, 2023
PubMed
Summary

Synthetic lethal interactions, involving gene paralogs, offer a promising avenue for targeted cancer therapies. Identifying these interactions aids in developing novel drugs by exploiting shared gene functionalities.

Keywords:
CRISPR screeningparalogssynthetic lethalitytarget identification

More Related Videos

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
07:23

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells

Published on: May 30, 2025

508
Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

1.8K

Related Experiment Videos

Last Updated: Aug 7, 2025

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions
07:40

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

4.2K
Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
07:23

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells

Published on: May 30, 2025

508
Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

1.8K

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Synthetic lethal interactions occur when inhibiting one gene sensitizes cells to the inhibition of another.
  • Duplicate genes (paralogs) are a promising source for synthetic lethal interactions due to shared functions.
  • Targeting gene loss in cancer is a widely applicable therapeutic strategy.

Purpose of the Study:

  • To review methods for identifying synthetic lethal interactions between gene paralogs.
  • To discuss the challenges and potential of exploiting these interactions in cancer drug development.

Main Methods:

  • Review of existing literature on identifying synthetic lethal interactions.
  • Analysis of the role of paralogs in synthetic lethality.
  • Discussion of drug development strategies targeting paralogs.

Main Results:

  • Paralogs represent a rich resource for discovering synthetic lethal interactions.
  • Existing drugs may already leverage synthetic lethality by inhibiting multiple paralogs.
  • Identification of paralog-based synthetic lethality is crucial for advancing targeted cancer therapies.

Conclusions:

  • Exploiting synthetic lethal interactions between paralogs is a key strategy for developing targeted cancer therapeutics.
  • Further research into identifying and exploiting these interactions will inform future drug discovery efforts.