Abstract
The disregulated growth of cancer cells is associated with the hyperphosphorylation of the retinoblastoma gene product, Rb. In the majority of tumors, loss of Rb function is associated with the alteration of expression of CDK inhibitors, such as p16INKa and p21Waf1, but not the loss of Rb itself. Therefore, we have focused our efforts on regaining control of Rb function by the introduction of p16INK4a and p21Waf1 in tumor cells, maintaing Rb in the active, growth-inhibiting form.
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