p53, chemokines, and squamous cell carcinoma
David M. Owens
David M. Owens
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Commentary

p53, chemokines, and squamous cell carcinoma

Abstract

The genetic and epigenetic events underlying cutaneous squamous cell carcinoma (SCC) have been actively studied; however, no resulting preventative or therapeutic strategies have successfully targeted this lesion, apart from surgery. In this issue of the JCI, two novel regulators of SCC pathogenesis are introduced, gain-of-function mutations in the p53 gene, reported by Caulin et al., and chemokine sequestration by the D6 receptor, reported by Nibbs et al. (see the related articles beginning on pages 1884 and 1893, respectively). These studies provide new twists and insights into the development of this potentially lethal disease.

Authors

David M. Owens

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Figure 1

Impact of p53 gain-of-function versus null mutations in epidermal carcinogenesis.

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Impact of p53 gain-of-function versus null mutations in epidermal carcin...
In this issue of the JCI, Caulin et al. (7) compare the impact of p53 gain-of-function (G-o-F) versus loss-of-function (L-o-F) mutations in multistage skin carcinogenesis progressing from normal epidermis (i) to initiated epidermis (ii), benign papillomas (iii), malignant SCC (iv), and finally lymph node metastasis (v). p53 gain-of-function mutations effectively stimulate early and late stages of epidermal carcinogenesis, whereas null mutations primarily influence malignant conversion to SCC. Light blue cells, initiated cells containing ras and/or p53 mutations; dark blue cells, metastatic cells; thin arrow, inducer; bold arrow, strong inducer; dotted arrow, little to no effect; asterisk, data previously demonstrated by Kemp et al. (9). PAH, polycyclic aromatic hydrocarbon.