Journal article

Targeting Mdmx to treat breast cancers with wild-type p53

S Haupt, D Buckley, J-MB Pang, J Panimaya, PJ Paul, C Gamell, EA Takano, Y Ying Lee, S Hiddingh, T-M Rogers, AFAS Teunisse, MJ Herold, J-C Marine, SB Fox, A Jochemsen, Y Haupt

CELL DEATH & DISEASE | NATURE PUBLISHING GROUP | Published : 2015

Abstract

The function of the tumor suppressor p53 is universally compromised in cancers. It is the most frequently mutated gene in human cancers (reviewed). In cases where p53 is not mutated, alternative regulatory pathways inactivate its tumor suppressive functions. This is primarily achieved through elevation in the expression of the key inhibitors of p53: Mdm2 or Mdmx (also called Mdm4) (reviewed). In breast cancer (BrCa), the frequency of p53 mutations varies markedly between the different subtypes, with basal-like BrCas bearing a high frequency of p53 mutations, whereas luminal BrCas generally express wild-type (wt) p53. Here we show that Mdmx is unexpectedly highly expressed in normal breast ep..

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