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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Fungal Group Zygomycota01:29

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Related Experiment Video

Updated: May 10, 2026

Sexual Crosses with the Mucoromycete Phycomyces blakesleeanus
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Notching up MYC gives a LIC.

David Levens1, Peter D Aplan

  • 1Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-9760, USA. levensd@mail.nih.gov

Cell Stem Cell
|July 6, 2013
PubMed
Summary

Mutations in FBXW7 increase MYC protein, expanding leukemia-initiating cells in T-ALL. Inhibiting MYC eradicates these cells, offering potential new therapies for T-cell acute lymphoblastic leukemia.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Notch1 signaling is crucial in T-cell acute lymphoblastic leukemia (T-ALL) development.
  • The ubiquitin ligase FBXW7 normally regulates protein degradation, including MYC.
  • Leukemia-initiating cells (LICs) drive T-ALL progression and are therapeutic targets.

Purpose of the Study:

  • To investigate the role of FBXW7 mutations in T-ALL pathogenesis.
  • To determine the impact of FBXW7 loss on MYC levels and LIC activity.
  • To explore therapeutic strategies targeting MYC in T-ALL.

Main Methods:

  • Utilized a mouse model of Notch1-induced T-ALL.
  • Assessed FBXW7 mutations and their effect on MYC protein stability.
  • Quantified leukemia-initiating cell populations.

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  • Employed genetic and pharmacological inhibition of MYC.

    • Main Results:

    • FBXW7 mutations were found to stabilize MYC protein, leading to its accumulation.
    • Increased MYC levels correlated with an expansion of leukemia-initiating cells in T-ALL.
    • Targeted inhibition of MYC effectively eliminated LIC activity in this model.

    Conclusions:

    • FBXW7 acts as a tumor suppressor in T-ALL by limiting MYC levels.
    • MYC is a critical driver of leukemia-initiating cell function in T-ALL.
    • Targeting MYC presents a promising therapeutic avenue for T-ALL treatment.