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Dermoscopy for malignant melanoma of the nipple and the areola

ing this case have been described. In two cases, including the present case, the skin tumors arose on non-sun-exposed skin without any precursor lesion. While imatinib can exert a therapeutic effect on SCC lesions, in another two cases of SCC, one of lesions was newly developed and another rapidly progressed even during imatinib administration. In head and neck SCC (HNSCC) cells, imatinib mesylate solubilizes membrane-bound heparin-binding epidermal growth factor-like growth factor, resulting in the activation of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase 1/2 and Src kinase. The imatinib-induced activation of the EGFR signaling system upregulates invadopodia-dependent invasion of HNSCC cells via negative regulation of Abl kinase, which is related to worsened prognosis. In addition, STAT3 activation plays a critical role in SCC progression and upregulates PDPN by the EGFR-STAT3 pathway stimulating SCC invasion. We analyzed p-STAT3 and PDPN, and both markers as well as a proliferative marker, Ki-67, were markedly upregulated in the tumor nests of the deep dermis (Fig. 1d–f). This indicates that both invasive and proliferative activities are stimulated possibly by the EGFR signaling pathway. Although imatinib mesylate can be effective for several skin tumors, cutaneous SCC may be more invasive during the imatinib therapy. Dermatologists should be aware of the unique adverse effect, which could be profoundly associated with the keratinocyte tumor biology. CONFLICT OF INTEREST: None declared.