William A. Freed-Pastor

TL;DR: Mechanisms by which Mutant p53 exerts its cellular effects are reviewed, with a particular focus on the burgeoning mutant p53 transcriptome, and the biological and clinical consequences of mutant p 53 gain of function are discussed.

TL;DR: It is found that mutant p53 depletion is sufficient to phenotypically revert breast cancer cells to a more acinar-like morphology, which implicate the mevalonate pathway as a therapeutic target for tumors bearing mutations in p53.

TL;DR: It is demonstrated that repression of the mevalonate pathway is a crucial component of p53-mediated liver tumor suppression and the mechanism by which this occurs is outlined.

TL;DR: It is surmised that mutant p53 impacts transcription of VEGFR2 as well as myriad other genes by promoter remodeling through interaction with and likely regulation of the SWI/SNF chromatin remodeling complex, which means that not only might mutants p53-expressing tumors be susceptible to anti VEGF therapies, impacting SWI-SNF tumor suppressor function in mutant p 53 tumors may also have therapeutic potential.

TL;DR: The results provide several unanticipated and interconnected findings that enable stable formation of p53-DNA complexes to divergent binding sites via DNA-induced conformational changes within the DBD itself.