TP53

Simon McDade, Martin Fischer

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Abstract

The p53 transcription factor is mutated or inactivated in most cancers to circumvent its diverse tumor suppressive functions. p53 becomes activated downstream of a range of cellular stresses to induce diverse transcriptional programs. Canonically activation of acute DNA damage results in growth suppression by inducing cell cycle arrest to enable DNA repair or if damage is insurmountable induces senescence or cell death. Genomic and transcriptomic analyses are rapidly advancing our understanding of the diverse signaling network regulated directly and indirectly downstream of p53, their relative contribution to tumor suppression and how we might exploit p53 deregulation to treat cancer.

Original languageEnglish
Title of host publicationEncyclopedia of Cancer
PublisherElsevier
Pages483-495
Number of pages13
Volume1
Edition3rd
ISBN (Electronic)9780128124857
ISBN (Print)9780128124840
DOIs
Publication statusPublished - 26 Jan 2018

Keywords

  • Apoptosis
  • Cancer
  • Cell cycle arrest
  • DNA damage
  • DREAM complex
  • MDM2
  • Mutation
  • TP53
  • Transcription factor
  • Tumor suppressor

ASJC Scopus subject areas

  • Medicine(all)

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