title: p53 in the game of transposons.
abstract: Throughout the animal kingdom, p53 genes function to restrain mobile elements and recent observations indicate that transposons become derepressed in human cancers. Together, these emerging lines of evidence suggest that cancers driven by p53 mutations could represent "transpospoathies," i.e. disease states linked to eruptions of mobile elements. The transposopathy hypothesis predicts that p53 acts through conserved mechanisms to contain transposon movement, and in this way, prevents tumor formation. How transposon eruptions provoke neoplasias is not well understood but, from a broader perspective, this hypothesis also provides an attractive framework to explore unrestrained mobile elements as inciters of late-onset idiopathic disease. Also see the video abstract here.
authors.affiliation: Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
authors.forename: Annika
authors.initials: A
authors.lastname: Wylie
authors.affiliation: Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
authors.forename: Amanda E
authors.initials: AE
authors.lastname: Jones
authors.affiliation: Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA. john.abrams@utsouthwestern.edu.
authors.forename: John M
authors.initials: JM
authors.lastname: Abrams
mesh_terms: D000818:Animals; D004251:DNA Transposable Elements; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D004251:DNA Transposable Elements; D016159:Tumor Suppressor Protein p53
keywords: Drosophila; human cancers; mobile elements; mouse cancer models; p53; piRNAs; retrotransposons; zebrafish