Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Genetic Screens

Genetic Screens

Genetic screens are tools used to identify genes and mutations responsible for phenotypes of interest. Genetic screens help identify individuals or a group of people at risk of developing genetic diseases and help them with early intervention, targeted therapy, and reproductive options.
Forward genetic screens
Forward or “classical” genetic screens involve creating random mutations in an organism’s DNA using radiation, mutagens, or insertion of additional bases, which...

You might also read

Related Articles

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

Sort by

Same author

Unraveling cellular and molecular mechanisms of relapse in CD19/CD22 dual-targeting chimeric antigen receptor T-cell therapy for B-cell acute lymphoblastic leukemia.

Leukemia·2026

Same author

Clinical Characteristics, Treatment Patterns, and Prognosis of Central Nervous System Involvement in Multiple Myeloma: A Multicenter Retrospective Study From China.

Cancer medicine·2026

Same author

Valosin-Containing Protein Contributes to Plexiform Neurofibroma Formation and Represents a Novel Therapeutic Target.

Cells·2026

Same author

Low- vs standard-dose regimens as induction for pediatric AML: a multicenter, randomized noninferiority trial.

Blood·2026

Same author

ZNF711 promotes enzalutamide resistance through transcriptional and epigenetic modification of the androgen receptor signaling pathway.

Cellular and molecular life sciences : CMLS·2026

Same author

Phf6 truncating mutation drives leukemogenesis via disrupted epigenetic regulation in mice.

Leukemia·2026

Same journal

Real-time Targeted Enrichment in Single-cell Long-read Sequencing.

Genomics, proteomics & bioinformatics·2026

Same journal

Decoding RNA N6-Methyladenosine Methylome of Wheat Using Machine Learning and Nanopore Direct RNA Sequencing.

Genomics, proteomics & bioinformatics·2026

Same journal

Tranquillyzer: A Neural Network Framework for Long-read Annotation and Demultiplexing.

Genomics, proteomics & bioinformatics·2026

Same journal

Advancing Functional Transcriptomics in Zebrafish with High-accuracy Full-length RNA Sequencing.

Genomics, proteomics & bioinformatics·2026

Same journal

NanoRAPID: A Deep Learning-based Framework for Single-molecule RNA Structure Analysis Using Nanopore Direct RNA Sequencing.

Genomics, proteomics & bioinformatics·2026

Same journal

Single-cell Multiomic and Spatiotemporal Dissection of the Liver Circadian Clock.

Genomics, proteomics & bioinformatics·2026

See all related articles

Search research articles

Related Experiment Video

Updated: May 9, 2025

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

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

Published on: June 17, 2022

Integrated Computational and Functional Screening Identifies G9a Inhibitors for SETD2-mutant Leukemia.

Ya Zhang^1,2,3, Mengfang Xia^1,2,3, Zhenyi Yi^1,2,3

¹China National Center for Bioinformation, Beijing 100101, China.

Genomics, Proteomics & Bioinformatics

|April 29, 2025

Summary

This summary is machine-generated.

G9a inhibitors show promise for treating SETD2-mutant leukemia by downregulating Myc. This epigenetic therapy reverses gene expression changes and selectively targets cancer cells, offering a new therapeutic strategy.

Keywords:

SETD2-mutant leukemia G9a inhibitor L1000 MYC let-7a

More Related Videos

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

A Rapid Screening Workflow to Identify Potential Combination Therapy for GBM using Patient-Derived Glioma Stem Cells

A Rapid Screening Workflow to Identify Potential Combination Therapy for GBM using Patient-Derived Glioma Stem Cells

Published on: March 28, 2021

Related Experiment Videos

Last Updated: May 9, 2025

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

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

Published on: June 17, 2022

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

A Rapid Screening Workflow to Identify Potential Combination Therapy for GBM using Patient-Derived Glioma Stem Cells

A Rapid Screening Workflow to Identify Potential Combination Therapy for GBM using Patient-Derived Glioma Stem Cells

Published on: March 28, 2021

Area of Science:

Epigenetics
Cancer Biology
Pharmacology

Background:

SETD2 is a tumor suppressor frequently mutated in acute leukemia, linked to chemotherapy resistance and poor prognosis.
Targeting epigenetic alterations in SETD2-mutant leukemia is crucial for developing novel therapeutics.

Purpose of the Study:

To identify potential therapeutics for SETD2-mutant leukemia.
To investigate the mechanism of action for identified drug candidates.

Main Methods:

Integrated computational prediction and epigenetic compound library screening.
RNA-sequencing and chromatin immunoprecipitation sequencing (ChIP-seq) analyses.
Correlation analysis between computational predictions and phenotypic outcomes.

Main Results:

G9a inhibitors were identified as promising candidates, selectively inhibiting SETD2-deficient cells.
G9a inhibition downregulated Myc and Myc-regulated genes in SETD2-mutant leukemia cells.
G9a inhibition led to upregulation of let-7a-2 microRNA, contributing to MYC suppression.

Conclusions:

G9a inhibitors represent a potential therapeutic strategy for SETD2-mutant leukemia.
The MYC signature is a key predictor of drug efficacy in this context.
This study provides insights into refining drug prediction strategies for epigenetic therapies.