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

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 specific...

You might also read

Related Articles

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

Sort by
Same author

Degron-independent recruitment of KAT2A expands the target space of CRBN molecular glues.

Science (New York, N.Y.)·2026
Same author

Menin-MLL inhibitors enhance JUND activity in MLLr leukemic cells contributing to tumorigenesis and therapy resistance.

Blood·2026
Same author

Beckwith-Wiedemann syndrome multiomic analysis of hepatoblastoma uncovers unique tumour heterogeneity and cellular landscapes, including transition cells leading to tumour formation.

BJC reports·2026
Same author

CRISPR base editor screening identifies spectrum of MEN1 mutations impacting menin inhibitors in clinical trials.

Nature communications·2026
Same author

Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.

Blood advances·2026
Same author

Genetic variation reveals a homeotic long noncoding RNA that modulates human hematopoietic stem cells.

Cell·2026

Related Experiment Video

Updated: May 26, 2026

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

Targeting epigenetic programs in MLL-rearranged leukemias.

Kathrin M Bernt1, Scott A Armstrong

  • 1Division of Hematology/Oncology, Children's Hospital, Boston, MA 02215, USA. Scott.Armstrong@childrens.harvard.edu

Hematology. American Society of Hematology. Education Program
|December 14, 2011
PubMed
Summary

Rearrangements of the Mixed-Lineage Leukemia (MLL) gene are common in infant leukemia and confer a poor prognosis. Targeting epigenetic regulators like DOT1L shows promise for treating MLL-rearranged leukemias.

More Related Videos

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
13:21

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

Published on: June 16, 2017

Enhanced Reduced Representation Bisulfite Sequencing for Assessment of DNA Methylation at Base Pair Resolution
13:47

Enhanced Reduced Representation Bisulfite Sequencing for Assessment of DNA Methylation at Base Pair Resolution

Published on: February 24, 2015

Related Experiment Videos

Last Updated: May 26, 2026

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

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
13:21

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

Published on: June 16, 2017

Enhanced Reduced Representation Bisulfite Sequencing for Assessment of DNA Methylation at Base Pair Resolution
13:47

Enhanced Reduced Representation Bisulfite Sequencing for Assessment of DNA Methylation at Base Pair Resolution

Published on: February 24, 2015

Area of Science:

  • Hematologic Malignancies
  • Cancer Epigenetics
  • Molecular Oncology

Background:

  • Mixed-Lineage Leukemia (MLL) gene rearrangements are prevalent in infant leukemia (>70%) and adult acute myeloid leukemia (~10%), often indicating a poor prognosis.
  • Over 60 MLL fusion partners exist, influencing disease phenotype and prognosis, with common fusions leading to aberrant homeotic (Hox) gene expression.

Purpose of the Study:

  • To investigate the role of epigenetic dysregulation in MLL-rearranged leukemias.
  • To highlight the significance of histone methyltransferase DOT1L in MLL-fusion-driven leukemogenesis.
  • To explore the therapeutic potential of targeting epigenetic regulators in MLL-rearranged leukemia.

Main Methods:

  • Analysis of genomic stability in MLL-rearranged leukemias.
  • Review of studies implicating epigenetic regulators (DNA methylation, histone acetylation, histone methylation) in MLL-fusion leukemogenesis.
  • Focus on the role of DOT1L as a key mediator.

Main Results:

  • MLL-rearranged leukemias exhibit significant genomic stability, suggesting epigenetic mechanisms are primary drivers.
  • Epigenetic regulators, including DNA methylation and histone modifications, are implicated in MLL-fusion leukemogenesis.
  • The histone methyltransferase DOT1L is identified as a critical mediator of MLL-fusion-induced leukemic transformation.

Conclusions:

  • Epigenetic dysregulation is a key driver of MLL-rearranged leukemias.
  • DOT1L is a crucial therapeutic target in MLL-fusion-driven leukemogenesis.
  • Targeted inhibition of epigenetic regulators offers a promising therapeutic strategy for MLL-rearranged leukemia.