This is known as the cell cycle. Division involves proteins; some tell the cell when to divide, known as proto-oncogenes and some are responsible for making sure DNA is copied accurately. During this cell cycle there are checkpoints that ensure all replication is done accurately and any damage to the DNA is repaired before division occurs. If the damage is irreparable and results in mutations, it is the job of the tumour suppressor genes to stimulate cell death, known as apoptosis (O'Halloran et al 2004).
Damage to any of these proteins involved in cell division can cause cancer. Damage to proto-oncogenes converts them into oncogenes that instead of regulating cell proliferation instruct the cells to continuously divide. Damage to the DNA repair genes mean any damage will remain, and defects to the tumour suppressor genes means that any damaged cell will survive and continue to divide. The most important tumour suppressor gene involved in solid tumour is p.53. The malignant cell behaves in a different way to normal cells. They lose their inhibition and show decreased adhesiveness and attachment. As they grow they can release factors that stimulate growth of new blood supply know as angiogenesis (Souhami & Tobias 2003). Epithelial ovarian cancer arises from a malignant transformation of the ovarian surface epithelium (Neal & Hoskins 2003). Two main hypotheses for this are the incessant ovulation theory first proposed by Fathalla in 1971 and the Gonadotropin theory. Ovulation causes damage to the epithelium of the ovary and the necessary regenerative repairs can lead to genetic instability and mutagenesis (Tung et al. 2005).
Murdoch (2003) demonstrated down regulation of the tumour suppressor gene p.53, led to a failure to repair or remove DNA damage in ovulated follicles. The gonadotropin theory postulates that 'follicle stimulating hormone or luteinizing hormone stimulate cell proliferation and malignant transformation of the ovarian epithelium' (Tung et al.