Abstract
The proliferation of normal cells is regulated by a combination of stimulatory and inhibitory factors that can respond to external signals in a coordinated manner (MacLachlan et al. 1995; Grana and Reddy 1995; Paggi et al. 1996). Various mitogens, growth factors, cytokines, and a host of other agents can perturb the cell cycle machinery eliciting proliferation, differentiation, or apoptosis (Reed et al. 1994; Reddy 1994). Any permanent alteration of the cell cycle-regulatory mechanisms can lead to abnormal proliferation, resulting in neoplasia (Blshor 1987, 1991; Morgan 1992). Such a situation can result following the inactivation of various tumor suppressor proteins, such as Rb and its family members and p53 (Marshall 1991; Cobrinik et al. 1992; Hollingsworth et al. 1993; Ewen 1994; Hooper 1994; Picksley and Lane 1994; Weinberg 1995; Giordano and Kaiser 1996), or by the dominant activation of positive-acting components of the cell cycle machinery, such as the cyclins and cyclin-dependent kinases (CDK) or proto-oncogenes (Pines 1995a, b; Kamb 1995; Bates and Peters 1995).
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Chellappan, S.P., Giordano, A., Fisher, P.B. (1998). Role of Cyclin-Dependent Kinases and Their Inhibitors in Cellular Differentiation and Development. In: Vogt, P.K., Reed, S.I. (eds) Cyclin Dependent Kinase (CDK) Inhibitors. Current Topics in Microbiology and Immunology, vol 227. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71941-7_4
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