Loss of the retinoblastoma protein, pRb, appears to have a role in several human tumor types. Mice lacking pRb have been produced as models of human disease, but have a different spectrum of affected tissues. Recent work shows that the tumorigenic effects of pRb may be revealed only after additional genetic alterations, such as loss of p53. New targets/effectors of pRb have been identified recently, and the system of kinases that inactivate pRb is proving to be complex.
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