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[tigers14]

My cell biology professor said in class that in transformed cells, there is a protein called p14ARF that is expressed at abnormally high levels that can bind to MDM2 and prevent it from interacting with p53, which creates a large pool of stable p53. Why would this be beneficial to a tumor cell? To my understanding, stabilized p53 goes on to induce synthesis of p21 cip, which binds to cyclin-CDK complexes and halts the cell cycle. Wouldn't a tumor cell want less stabilized p53 and a more continuous cell cycle?

[bob1]

Normally you would be correct, but p53 is known to be upregulated in a range of cancers.  I can't remember the exact reason, but I think it has to do with cell survival where p53 activates cellular repair mechanisms that would otherwise cause cell death.