title: MEK'ing the most of p53 reactivation therapy in melanoma.
abstract: Melanoma is one of the few tumor types in which p53 is functionally repressed without extraneous mutations. With the number of kinase-based drug targets rapidly declining, p53 represents a relatively untapped resource for therapeutic intervention. Studies in other tumor types have demonstrated that reactivation of p53 is a viable strategy to initiate sustained tumor regression; combining p53 reactivation while inhibiting traditional genetic targets, such as mitogen-activated protein kinase/extracellular signal-related kinase kinase (MEK), holds therapeutic promise.
authors.affiliation: Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
authors.forename: John T
authors.initials: JT
authors.lastname: Lee
authors.forename: Meenhard
authors.initials: M
authors.lastname: Herlyn
mesh_terms: D006801:Humans; D008545:Melanoma / Q000188:drug therapy*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000037:antagonists & inhibitors*; D051736:Proto-Oncogene Proteins c-mdm2 / Q000037:antagonists & inhibitors*; D012878:Skin Neoplasms / Q000188:drug therapy*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
chemical_list: C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C497206:MDM2 protein, human; D051736:Proto-Oncogene Proteins c-mdm2; D020929:Mitogen-Activated Protein Kinase Kinases