Abstract
Normal cells proliferate in response to injury or to replace cells with a limited survival time. This is true for cells in the hematopoietic system and epithelial cells of the skin and bowel. It has been estimated that 1 million cell divisions per second are required for the replacement of lost cells. The proliferation of normal cells is regulated by the action of a number of polypeptide and lipid factors called growth factors [1–8]. These growth factors bind to specific cell surface receptors and transmit activation signals across the cell membrane. These signals initiate a limited number of intracellular biochemical cascades which in turn communicate with the nucleus, eventually leading to cellular proliferation [5–8]. In addition to positive growth signals, a series of proteins is involved in limiting cellular proliferation [9–10]. Several of these, such as p53 and the product of the retinoblastoma gene (RB), are more commonly known as tumor suppressor genes [9,10]. Finally, some activated cells are sensitized to a physiological process Known as programmed cell death or apoptosis [11–13]. Both the products of tumor suppressor genes and the products of the genes involved in programmed cell death must be overcome for a cell to divide.
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Xu, Y., Mills, G.B. (1995). Activation of human ovarian cancer cells: role of lipid factors in ascitic fluid. In: Sharp, F., Mason, P., Blackett, T., Berek, J. (eds) Ovarian Cancer 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0136-4_13
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DOI: https://doi.org/10.1007/978-1-4757-0136-4_13
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