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Section Summary: Oncogenes

Oncogenes

  • Oncogenes are the mutated forms of normal cellular genes (proto-oncogenes).
  • The protein products of proto-oncogenes stimulate cell division and/or inhibit cell death.
  • Proto-oncogenes can be likened to the gas pedal in a car.
  • Normally, internal and external signals strictly regulate the activity of the proto-oncogenes, but oncogenes are defective and are 'on' even when they do not receive appropriate signals.
  • Oncogenes also help cells to ignore negative signals that would prevent a healthy cell from dividing.
  • Oncogenes can cause cells to divide continuously even in the absence of any pro-growth signals.
  • The following list describes different cellular roles for a few of the many known oncogenes:
      HER-2/neu
      • HER-2/neu encodes for a cell surface receptor that can stimulate cell division
      • The HER-2/neu gene is amplified in up to 30% of human breast cancers
    • RAS
      • The Ras gene products are involved in kinase signaling pathways that ultimately control transcription of genes, regulating cell growth and differentiation.
      • Overexpression and amplification of RAS can lead to continuous cell proliferation.
    • MYC
      • The Myc protein is a transcription factor and controls expression of several genes.
      • Myc is thought to be involved in avoiding the cell death mechanism.
      • MYC oncogenes may be activated by gene rearrangement or amplification.
    • SRC
      • SRC was the first oncogene ever discovered.
      • The Src protein is a tyrosine kinase which regulates cell activity.
    • hTERT
      • hTERT codes for an enzyme (telomerase) that maintains chromosome ends.
      • In most normal cells telomerase is only present during fetal development.
      • Activation of hTERT in adult cells gives them the ability to divide indefinitely.
    • BCL-2
      • The Bcl-2 protein works to prevent cell death (apoptosis).
      • Overexpression of BCL-2 allows continued division of mutated cells.
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Last Modified: 07/15/2011 Print Email Page Share
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