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Transformation by raf and myc oncogenes

U R Rapp1, J L Cleveland, S M Storm

  • 1Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701.

Princess Takamatsu Symposia
|January 1, 1986
PubMed

Insights

RAF oncogenes and MYC collaborate in cell transformation. RAF acts as a protein kinase downstream of RAS, potentially activating MYC, and its targeted vaccination prevented lung tumor promotion in mice.

Area of Science:

  • Oncology
  • Molecular Biology
  • Signal Transduction

Background:

  • RAF oncogenes and MYC are implicated in cellular transformation.
  • MYC acts as a second messenger in growth factor signaling.
  • RAF is a cytosolic serine/threonine-specific protein kinase downstream of RAS.

Purpose of the Study:

  • To elucidate the synergistic roles of RAF and MYC in cell transformation.
  • To investigate the signal transduction pathway involving RAS, RAF, and MYC.
  • To examine the role of RAF in lung tumorigenesis and evaluate RAF protein vaccination.

Main Methods:

  • Antibody microinjection experiments to determine RAF's position in signal transduction.
  • Development of a mouse model for lung tumor induction using ethylnitrosourea and butylated hydroxytoluene.
  • Assessment of RAF protein expression and vaccination efficacy in the mouse model.

Main Results:

  • RAF acts synergistically with MYC, suggesting a downstream role from RAS.
  • RAF's inability to replace competence factors highlights its specific role in growth control.
  • High levels of normal-sized RAF proteins were observed in tumors.
  • RAF protein vaccination effectively eliminated the promoted phase of lung tumor induction.

Conclusions:

  • RAF functions downstream of RAS and synergizes with MYC, possibly via phosphorylation.
  • RAF plays a critical role in cellular growth control and lung tumorigenesis.
  • RAF protein vaccination demonstrates therapeutic potential against lung cancer promotion.

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