ΔNp63α levels correlate with clinical tumor response to cisplatin

Rachel Zangen, Edward Ratovitski, David Sidransky

Research output: Contribution to journalShort survey

Abstract

After exposure to damaging agents, the p53 tumor suppressor is stabilized mediating cell cycle arrest and apoptosis. p53 family member, ΔNp63 promotes cell proliferation and accelerates tumor growth. We previously found that the genotoxic stress agents induced a decrease of ΔNp63α. We further observed that genotoxic stress mediated phosphorylation of ΔNp63α targeting it into proteasome degradation. Here, we found that high ΔNp63 protein levels in primary tumors accurately predicted response to platinum based chemotherapy and a favorable outcome in head and neck cancer patients. Our data suggest that degradation of ΔNp63α is part of the cellular response to DNA damage in head and neck cancers. The findings may have implications for the rational use of DNA damaging agents in human cancer.

Original languageEnglish (US)
Pages (from-to)1313-1315
Number of pages3
JournalCell Cycle
Volume4
Issue number10
DOIs
StatePublished - Oct 2005

Keywords

  • Chemotherapy
  • Cisplatin
  • DNA damage
  • Genetic marker
  • Head and neck cancer
  • Patient outcome
  • Squamous cell carcinomas
  • p53
  • p63
  • p73

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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