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 language | English |
|---|---|
| Title of host publication | Encyclopedia of Cancer |
| Publisher | Elsevier |
| Pages | 483-495 |
| Number of pages | 13 |
| Volume | 1 |
| Edition | 3rd |
| ISBN (Electronic) | 9780128124857 |
| ISBN (Print) | 9780128124840 |
| DOIs | |
| Publication status | Published - 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)
UN SDGs
This output contributes to the following Sustainable Development Goal(s)
