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Oliver Dorigo Otoniel Mart´ez-Maza Jonathan S. Berek
The regulation and maintenance of normal tissue requires a balance between cell proliferation and programmed cell death, or apoptosis.
The regulation of ovarian function occurs through autocrine, paracrine, and endocrine mechanisms. Disruption of these autocrine and paracrine intraovarian pathways may be the basis of polycystic ovarian disease, disorders of ovulation, and ovarian neoplastic disease.
Among the genes that participate in control of cell growth and function, protooncogenes and tumor suppressor genes are particularly important.
Growth factors trigger intracellular biochemical signals by binding to cell membrane receptors. In general, these membrane-bound receptors are protein kinases that convert an extracellular signal into an intracellular signal. Many of the proteins that participate in the intracellular signal transduction system are encoded by proto-oncogenes that are divided into subgroups based on their cellular location or enzymatic function.
Oncogenes comprise a family of genes that result from gain of function mutations of their normal counterparts, proto-oncogenes. The normal function of proto-oncogenes is to stimulate proliferation in a controlled context. Activation of oncogenes can lead to stimulation of cell proliferation and development of a malignant phenotype.
Tumor suppressor genes are involved in the development of most cancers and are usually inactivated in a two-step process in which both copies of the tumor suppressor gene are mutated or inactivated by epigenetic mechanisms like methylation. The most commonly mutated tumor suppressor gene in human cancers is p53.