Are p53 and inflammatory chemokines linked?
Collectively, these studies (7, 17) give critical insight into two apparently distinct therapeutic approaches to potentially target cutaneous SCC. However, the induction of late-stage metastases common to both p53 and D6 transgenic mouse models is normally a rare event in experimental mouse skin carcinogenesis and therefore raises the question as to whether there is a more direct relationship between certain proinflammatory signals and p53 gain-of-function mutations as they relate to SCC pathogenesis. For example, can a heightened inflammatory chemokine response critically influence the p53 status in otherwise normal epidermal cells and/or pre-neoplastic epidermal cells that have sustained additional genetic insults? This concept fits well with the UV carcinogenesis model in human skin, in which small clusters of p53 mutant cells exist prior to actinic keratosis (AK) and SCC development (6) and may be selected for clonal expansion by a chronic inflammatory stimulus (13). In addition, A
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