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

9.0K
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...
9.0K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

9.9K
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...
9.9K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

6.2K
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...
6.2K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

6.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.2K
Lethal Alleles02:41

Lethal Alleles

18.5K
Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
18.5K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.8K
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...
3.8K

You might also read

Related Articles

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

Sort by
Same author

Bridging Simplicity and Depth in Single-Cell Proteomics: A Cost-Effective Workflow and an Expanded Framework for Data Evaluation.

Journal of proteome research·2026
Same author

Single-cell analysis of matched FFPE and frozen tissue samples reveals comparable resolution of intratumoural heterogeneity.

Frontiers in genetics·2026
Same author

Global partnerships in rare disease research.

Disease models & mechanisms·2025
Same author

Synthetic cytotoxicity profiling of cohesin mutants highlights recombination-based dependencies.

DNA repair·2025
Same author

Deep structure-function analysis of the endonuclease Mus81 with dominant mutational scanning.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Mapping of DDX11 genetic interactions defines sister chromatid cohesion as the major dependency.

G3 (Bethesda, Md.)·2024

Related Experiment Video

Updated: Feb 27, 2026

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

4.7K

Synthetic lethality and cancer.

Nigel J O'Neil1, Melanie L Bailey1, Philip Hieter1

  • 1Michael Smith Laboratories, University of British Columbia, 2185 East Mall, Vancouver, British Columbia V6T 1Z4, Canada.

Nature Reviews. Genetics
|June 27, 2017
PubMed
Summary

Synthetic lethality exploits gene pairs lethal only when both are perturbed, offering cancer treatment avenues. Identifying these interactions aids targeted therapies by analyzing tumor mutations and gene expression data.

Area of Science:

  • Genetics
  • Oncology
  • Molecular Biology

Background:

  • Synthetic lethality describes gene pairs where individual gene disruption is viable, but simultaneous disruption is lethal.
  • Exploiting synthetic lethality is crucial for developing novel cancer therapies.
  • Next-generation sequencing technologies facilitate the discovery of numerous tumor-specific mutations and gene expression alterations.

Purpose of the Study:

  • To highlight the importance of identifying and mechanistically characterizing synthetic lethal genetic interactions.
  • To discuss the potential of leveraging tumor-specific mutations and gene expression alterations for targeted cancer therapy.
  • To emphasize the role of integrating genetic interaction data from diverse sources for therapeutic translation.

Main Methods:

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

1.2K
Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.7K

Related Experiment Videos

Last Updated: Feb 27, 2026

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

4.7K
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

1.2K
Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.7K
  • Review of advances in next-generation sequencing for identifying genetic interactions.
  • Synthesis of genetic interaction data from model organisms, tumor genomes, and human cell lines.
  • Focus on mechanistic characterization of identified synthetic lethal interactions.
  • Main Results:

    • Identification of numerous potential synthetic lethal targets through next-generation sequencing.
    • Demonstration of the feasibility of targeting tumor-specific alterations via synthetic lethality.
    • Integration of data from multiple sources to build a comprehensive understanding of synthetic lethal interactions.

    Conclusions:

    • Synthetic lethality presents a promising strategy for targeted cancer therapy.
    • Further research integrating diverse genetic data is essential for clinical translation.
    • Mechanistic understanding of synthetic lethal interactions is key to successful therapeutic application.