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Activated BRAF induces gliomas in mice when combined with Ink4a/Arf loss or Akt activation

J P Robinson1, M W VanBrocklin, A R Guilbeault

  • 1Drug Development Department, Nevada Cancer Institute, Las Vegas, NV 89135, USA.

Oncogene
|October 27, 2009
PubMed

Insights

BRAF activation contributes to glioma development. Combining activated BRAF with Akt or Ink4a/Arf loss promotes glioma formation, suggesting BRAF as a potential therapeutic target for these brain tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Neuroscience

Background:

  • Receptor tyrosine kinase (RTK) pathway mutations are common in high-grade gliomas, activating MAPK and PI(3)K/Akt signaling.
  • BRAF mutations are prevalent in low-grade gliomas and elevated in high-grade gliomas, but its specific role in glioma formation is unclear.

Purpose of the Study:

  • To investigate the role of activated BRAF in glioma development.
  • To determine if BRAF activation, alone or in combination with other oncogenic pathways, can induce glioma formation in vivo.

Main Methods:

  • Utilized the RCAS/TVA system to deliver genes encoding activated BRAF, KRas, Akt, or Cre into neural progenitor cells in Ink4a/Arf(lox/lox) mice.
  • Assessed tumor formation and characterized glioma phenotypes resulting from genetic manipulations.

Main Results:

  • Activated BRAF alone was insufficient for tumorigenesis.
  • Co-expression of activated BRAF with Akt or loss of Ink4a/Arf induced glioma formation.
  • BRAF-induced gliomas showed similarities to KRas-induced gliomas when combined with Akt, but not with Ink4a/Arf loss.

Conclusions:

  • BRAF activation plays a significant role in glioma development.
  • BRAF signaling pathways are potential therapeutic targets for glioma treatment.

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