With all the growth-promoting and -inhibiting signals that are integrated into the core cell-cycle controllers, it is surprising that the majority of cancers, although arising from mutations in many different genes, result from the improper activation or inactivation of relatively few pathways. Recent research in cell culture systems coupled with genetic analysis has shown that human cells acquire changes to as few as five distinct pathways, mainly controlling protein phosphatase 2A (PP2A) function, telomere maintenance, RAS activation, the pRb pathway, and the p53 pathway.1 Currently the contribution of PP2A inactivation to cancer is unknown, although it has been suggested that only the inactivation of a particular subtype of PP2A complexes is required for transformation of human cells. However, significantly more is known about telomere maintenance, RAS activation, the pRb pathway, and p53 pathway in human cancer.
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