The p53 mutation "gradient effect" and its clinical implications.
The p53 tumor suppressor-signaling pathway is inactivated in most human cancers. Depending on how p53 is targeted during tumorigenesis impacts whether partial or full tumor suppressor activity is lost. The degree of remaining p53 activity, if any, intuitively impacts the tumor phenotype. This review focuses on recent findings from human cancer studies and genetically engineered mouse models to highlight a p53 functional "gradient effect" and its clinical implications.
Zambetti
Gerard P
GP
Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. gerard.zambetti@stjude.org
D000310:Adrenal Gland Neoplasms / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D016158:Genes, p53; D006801:Humans; D016864:Li-Fraumeni Syndrome / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D011110:Polymorphism, Genetic; D051736:Proto-Oncogene Proteins c-mdm2 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53; D051736:Proto-Oncogene Proteins c-mdm2