R4.5a: Self Sufficiency In Growth Signals

Oncogenes are genes that provide an autonomous source of growth stimulus for a cell. Many human genes are proto-oncogenes that require mutation or chromosomal abnormalities to become an oncogene.
Proto-oncogenes are categorised into several categories:

  • Growth factors (such as TGFA or HST)
  • Growth factor receptors (such as ERBB1/2, or FLT3)
  • Signal transduction proteins (such as RAS, RAF downstream, or non-receptor tyrosine kinase)
  • Nuclear regulatory proteins (such as MYC)
  • Cell cycle regulators (such as cyclins or CDKs)

Transformation into oncogenes can occur through:

  • Amplification occurs when a normal gene is copied numerous times within the genome (eg: ERBB2). Overexpression occurs due to the large number of gene copies within the nucleus.
  • A point mutation replaces one of the bases in the chromosome with an incorrect base (eg: RAS proteins). This can lead to a conformal change in the protein product, which may then be always ‘switched on’ and immune to regulation.
  • A translocation may place a normal gene next to an incorrect promoter region (eg: CCND / cyclin D). This can lead to increased production of that normal gene product.

Other oncogenes

Some viruses, such as HPV, introduce extra genes into the human genome. These genes typically disable essential parts of the cell cycle and behave as oncogenes. For the example of HPV, proteins are produced that inhibit the function of RB1 and TP53, two essential cell cycle control genes.


1. Hanahan, D., & Weinberg, R. A. (2000). The hallmarks of cancer. Cell, 100(1), 57–70.
2. Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of Cancer: The Next Generation. Cell, 144(5), 646–674. doi:10.1016/j.cell.2011.02.013