Abstract:The tumor suppressor p53 is mutated in the majority of human cancers, and inactivation of p53 correlates with more aggressive clinical courses and resistance to therapy. Loss of p53 may result in pleiotropic cellular effects such as cell-cycle deregulation, increased survival and aneuploidy. Utilizing the Eµ-myc transgenic mouse as a model system, we previously identified apoptosis as the prime tumor suppressor function of p53 during Myc-driven lymphoma development. However, increasing evidence supports premat… Show more
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