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Humans engage in aggression when they seek to cause harm or pain to another person. Aggression takes two forms depending on one’s motives: hostile or instrumental. Hostile aggression is motivated by feelings of anger with intent to cause pain; a fight in a bar with a stranger is an example of hostile aggression. In contrast, instrumental aggression is motivated by achieving a goal and does not necessarily involve intent to cause pain (Berkowitz, 1993); a contract killer who murders for...
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Related Experiment Video

Updated: Feb 4, 2026

Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
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Aggressive leukemia driven by MLL-AF9.

Vaia Stavropoulou1, Antoine H F M Peters2,3, Juerg Schwaller1

  • 1Department of Biomedicine and Children's Hospital (UKBB), University of Basel, Switzerland.

Molecular & Cellular Oncology
|September 26, 2018
PubMed
Summary
This summary is machine-generated.

Cellular origin influences acute myeloid leukemia (AML) aggressiveness. MLL-AF9 fusion induction in mice created invasive, chemoresistant AML with genes linked to poor patient survival.

Keywords:
AMLEMTEvi1LT-HSCMLL-AF9

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Area of Science:

  • Hematology
  • Cancer Biology
  • Molecular Biology

Background:

  • Cellular origin is a critical factor influencing the aggressiveness and phenotype of acute myeloid leukemia (AML).
  • Previous research has highlighted the complex interplay between cellular differentiation pathways and leukemia development.

Purpose of the Study:

  • To investigate the impact of specific genetic alterations (MLL-AF9 fusion) on hematopoietic cell compartments.
  • To characterize the resulting acute myeloid leukemia phenotype, including invasiveness and chemoresistance.
  • To identify molecular mechanisms, such as epithelial to mesenchymal transition (EMT)-related genes, contributing to AML aggressiveness.

Main Methods:

  • Utilized a doxycycline-regulated mouse model (iMLL-AF9) for inducible MLL-AF9 fusion expression.
  • Administered doxycycline to activate gene expression in various hematopoietic compartments in vivo.
  • Analyzed the resulting leukemia phenotype, focusing on invasiveness, chemoresistance, and gene expression profiles.

Main Results:

  • Direct induction of the MLL-AF9 fusion resulted in invasive and chemoresistant acute myeloid leukemia.
  • The induced AML exhibited expression of genes associated with epithelial to mesenchymal transition (EMT).
  • These EMT-related genes are implicated in cell migration and invasion, and correlate with poor prognosis in human AML.

Conclusions:

  • The cellular origin and specific genetic drivers significantly shape AML aggressiveness and phenotype.
  • MLL-AF9-driven AML shares molecular pathways (EMT) with solid tumors, contributing to invasive behavior.
  • Targeting EMT pathways may offer novel therapeutic strategies for high-risk AML.