@article{3087583,
    title = "Mutant p53 Prolongs NF-κB Activation and Promotes Chronic Inflammation and Inflammation-Associated Colorectal Cancer",
    author = "Cooks, T. and Pateras, I. and Tarcic, O. and Solomon, H. and Schetter, A. and Wilder, S. and Lozano, G. and Pikarsky, E. and Forshew, T. and Rozenfeld, N. and Harpaz, N. and Itzkowitz, S. and Harris, C. and Rotter, V. and Gorgoulis, V. and Oren, M.",
    journal = "Cancer Cell",
    year = "2013",
    volume = "23",
    number = "5",
    pages = "634-646",
    publisher = "Cell Press",
    doi = "10.1016/j.ccr.2013.03.022",
    keywords = "dextran sulfate;  immunoglobulin enhancer binding protein;  protein p53, article;  cell culture;  chromatin immunoprecipitation;  chronic inflammation;  colitis;  colorectal cancer;  disease association;  disease severity;  enzyme activation;  human;  human cell;  inflammation;  invasive carcinoma;  mouse;  nonhuman;  nucleotide sequence;  priority journal;  real time polymerase chain reaction;  tissue injury",
    abstract = "The tumor suppressor p53 is frequently mutated in human cancer. Common mutant p53 (mutp53) isoforms can actively promote cancer through gain-of-function (GOF) mechanisms. We report that mutp53 prolongs TNF-α-induced NF-κB activation in cultured cells and intestinal organoid cultures. Remarkably, when exposed to dextran sulfate sodium, mice harboring a germline p53 mutation develop severe chronic inflammation and persistent tissue damage, and are highly prone to inflammation-associated colon cancer. This mutp53 GOF is manifested by rapid onset of flat dysplastic lesions that progress to invasive carcinoma with mutp53 accumulation and augmented NF-κB activation, faithfully recapitulating features frequently observed in human colitis-associated colorectal cancer (CAC). These findings might explain the early appearance of p53 mutations in human CAC. © 2013 Elsevier Inc."
}