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p53-mediated adaptation to serine starvation is retained by a common tumour-derived mutant.

Timothy J HumptonAndreas K HockOliver D K MaddocksKaren H Vousden
Published in: Cancer & metabolism (2018)
Our work shows that mutant p53s can selectively retain wild-type p53 functions that allow adaptation to serine starvation through the activation of antioxidant defence pathways. Tumours containing this p53 mutation are resistant to serine-limited conditions and less responsive to therapy.
Keyphrases
  • wild type
  • protein kinase
  • oxidative stress
  • cancer therapy
  • anti inflammatory
  • mesenchymal stem cells