You are currently viewing the editor's summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
A p38α-p63 balancing act in skin cancer
Loss of p38α in mice leads to hyperplasia and tumor development in epithelial tissues. Choo et al. analyzed skin tissue and cells from normal donors, patients with premalignant keratosis or squamous cell carcinoma (SCC), and mouse models and found that p38α phosphorylated and consequently induced the degradation of the transcription factor p63, particularly that of its tumor-associated isoform ΔNp63α. Loss of p38α increased p63 abundance in the skin and thereby enhanced the expression of stem cell–associated genes, repressed the expression of a tumor-suppressive metalloprotease, and promoted stem cell outgrowth in the skin. The findings also raise the possibility that p38α inhibitors used to treat other cancers (where p38α is tumor promotive) may cause secondary SCC in patients.
This is an article distributed under the terms of the Science Journals Default License.
