title: Does control of mutant p53 by Mdm2 complicate cancer therapy?
abstract: Missense mutant forms of p53 are expressed at high levels in some human cancers and may contribute to oncogenesis. In this issue of Genes & Development, Terzian and colleagues (pp. 1337-1344) describe a mutant p53 knock-in mouse in which normal tissues and some tumors have low levels of mutant p53 protein unless Mdm2 or p16(INK4A) are absent. Once stabilized, mutant p53 promotes metastasis. Therefore, therapies that release p53 from Mdm2 might have unwanted consequences when cells have sustained a mutation in p53.
authors.affiliation: Department of Biological Sciences, Columbia University, New York, New York 10027, USA.
authors.forename: Carol
authors.initials: C
authors.lastname: Prives
authors.forename: Eileen
authors.initials: E
authors.lastname: White
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy* / Q000235:genetics; D051736:Proto-Oncogene Proteins c-mdm2 / Q000502:physiology*
chemical_list: D000970:Antineoplastic Agents; D051736:Proto-Oncogene Proteins c-mdm2