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2. CANCER GENES


  • Protooncogenes - mostly code for proteins involved in cell signalling, cell cycle control. Mutations are dominant - i.e. a change in only one allele is needed to give cells a transformed (potentially tumorigenic) phenotype.

  • Tumour suppressor genes - when acting normally, have a protective effect; e.g. p53 delays the cell cycle and allows DNA repair to take place, or directs severely damaged cells to apoptosis. The RB1 gene (the name comes from retinoblastoma) normally prevents uncontrolled DNA replication and cell proliferation Mutations are recessive - one functioning allele is normally sufficient for the cell to behave normally - see retinoblastoma .


Retinoblastoma is a rare disease of early childhood, caused by a defect in the RB protein. In the non-hereditary form of the disease, a tumour develops in the retina of one eye. In the hereditary form of the disease, there can be multiple tumours in each eye. Given the information you have about tumour suppressor genes, can you explain this difference between the two forms of the disease?


  • Mutator genes - a loss of function of the gene causes mutations to accumulate at a rapid rate in the clone derived from the altered cell. This increases the chance of cancer. DNA repair genes are one example; if less damage is repaired, there will be more to produce mutations.
http://meddev.uio.no/elaring/lcms13/ernaeringslaere/nutr-cancer-biology/illustrations/p53-DNA-complex.jpg