Do not scratch that mole!

Abstract

Nevi harbor some of the same oncogene mutations that also drive malign melanoma. Further tumor promoting events are required to unleash their carcinogenic potential. Using zebrafish whose melanocytes overexpress an HRAS-oncogene, a new study reports that injury induces melanoma, possibly through recruitment of neutrophils that trigger proliferation of preneoplastic melanocytes.

Figure 1

Cartoon scheme depicting cytotoxic (N1, red) and trophic (N2, green) neutrophil functions in the context of the innate immune response to infection (right side), and tumor promotion (left side). The trophic activity of neutrophils in part compensates the collateral damage of an antimicrobial innate immune response (e.g., disinfection of wounds). In the absence of microbes or tissue damage, trophic functionality is prevailing, which stimulates (pre-)neoplastic cell proliferation.