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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Awarded by NHMRC
Awarded by CCV grant
Awarded by National Health and Medical Research Council of Australia
Funding Acknowledgements
This work was supported by NHMRC project grants (1026990, 1026988, 1049179 and 1063389) and NHMRC Fellowship to YH (9628426), by the CCV grant (1085154) and by the CASS Foundation. MJH was supported by an NHMRC project grant (APP1049720).