When mutant p53 fires up

Mutant p53 functions as a key molecular element in the inflamed colon tissue joining forces with nuclear factor kappa-B (NF-κB) to prolong and intensify the inflammatory response, leading eventually to a higher risk for colitis associated colorectal cancer (CAC). This phenomenon coincides with the fact that mutations in p53 are an initiating factor of CAC unlike sporadic colorectal cancer (CRC) where they are considered a late event contributing to tumor progression. This research highlight attempts to illuminate the consequences of such a reshuffling in the molecular sequence of events from non-cancerous tissue to invasive carcinoma of the colon. Implications of this different role taken by mutant p53 when inflammation is involved might affect tumorigenesis, pathogenesis, and hierarchical morphogenesis and suggest the reevaluation of current animal models used to study CAC. We also discuss the possible role of mutant p53 in stromal and immune compartments, either in an autonomous or non autonomous manner.