Code for proteins that stimulate the cellcycle, promoting celldivision
Mutations in a proto-oncogene:
Proto-oncogene -> oncogene
Consequently, gene is permanently active
Receptor protein effect:
receptor proteins (that some proto-oncogenes normally code for) to growthfactors of cell cycle are permanently activated, even in the absence of growth factors
-> uncontrolled cell division
Growth factor effect:
Excessive growth factor production -> uncontrolled cell division
Oestrogen & breast cancer
Oestrogen production falls in the ovaries but fatcells in breast tissue produce more even after menopause
Oestrogen PROMOTES transcription -> hyperpromote proto-oncogene expression -> become oncogenes
The Two Hit Hypothesis:
A mutation of one allele of proto-oncogene is sufficient to induce cancer
A mutation of both alleles is required to deactivatetumour suppressor genes
Gain-of-function mutations that convert proto-oncogenes act dominantly (i.e mutation in only one of the two alleles is sufficient for inducing cancer)
Mutations in tumoursuppressor genes act recessively so two recessive alleles required (to induce cancer)