Dermoscopy is a widely used non-invasive technique for diagnosing skin tumors. In melanocytic tumors, e.g., melanoma and basal cell carcinoma (BCC), the effectiveness of dermoscopic examination has been fully established over the past two decades. Moreover, dermoscopy has been used to diagnose non-melanocytic tumors. Here, we review novel findings from recent reports concerning dermoscopy of melanoma and non-melanoma skin cancers including BCC, sebaceous carcinoma, actinic keratosis, Bowen's disease, squamous cell carcinoma (SCC), Merkel cell carcinoma (MCC), extramammary Paget's disease (EMPD), and angiosarcoma.

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Some studies showed that clinical response to immune check point inhibitors is lower in acral and mucosal melanoma than in cutaneous melanoma. Although the synergistic effect of radiotherapy (RT) and ipilimumab has been reported in patients with brain metastasis, the efficacy of combined RT and anti‐programmed death 1 (PD‐1) therapy for acral and mucosal melanoma is unclear. The present study aimed to evaluate the efficacy of combined RT and anti‐PD‐1 therapy for acral and mucosal melanoma. We retrospectively analyzed patients with acral or mucosal melanoma who were treated with anti‐PD‐1 and RT at Sapporo Medical University Hospital. In 10 patients (acral, 3; mucosal, 7), the response rate (RR) and the disease control rate (DCR) were 40% and 60%, respectively. As regards mucosal melanoma, four of the seven patients had achieved complete response + partial response, and three had progressive disease (RR = 57.1%). Meanwhile, two of the three patients with acral melanoma had stable disease and one had progressive disease (RR and DCR were 0% and 66.6%, respectively). Except for the patients treated with palliative RT for bone metastasis in the present study, the RR was 50% (4/8 patients), and the DCR was 75% (6/8 patients). Vitiligo developed after RT in five (50%) patients at a median duration of 2 months after RT. The clinical response and the high occurrence of vitiligo suggest that the combination of RT and anti‐PD‐1 therapy could be effective in some patients with mucosal melanoma.

Poroma and trichoblastoma are rare adnexal skin neoplasms that occur sporadically or secondary to a sebaceous nevus (SN).Postzygotic mosaic mutations in HRAS and KRAS genes cause SN, 1 and these RAS-activating mutations have been detected in tumors including sporadic poroma and trichoblastoma. 2,3 Sebaceous nevi are congenital, and the risk of secondary tumors increases with age, suggesting that additional gene mutations may contribute to the tumorigenesis. The genetic landscape of the secondary tumors is still largely unexplored. Herein, we describe the case of a patient with a secondary poroma and a trichoblastoma arising in an SN with an HRAS p.G13R mutation. We investigated additional gene aberrations of the poroma and trichoblastoma in the SN with panel sequencing that was developed for skin cancers.

Background Barrier disruption and an excessive immune response in keratinocytes are now considered to have important roles in the pathophysiology of atopic dermatitis (AD). Furthermore, disturbed keratinocyte differentiation is considered to underlie AD. ΔNp63, a p53‐like transcription factor, is a major regulator of keratinocyte differentiation. However, the functional significance of ΔNp63 in AD has not been clarified. Objective In this study, we aimed to investigate the influence of the type 2 inflammatory environment on ΔNp63 expression and AD‐associated molecules regulated by ΔNp63 in keratinocytes. Methods The immunohistochemical expression profiles of ΔNp63 and AD‐related molecules were evaluated in human skin tissue. The function of ΔNp63 in the regulation of AD‐related molecules and the influence of the type 2 inflammatory environment on ΔNp63 expression were investigated using human primary keratinocytes. Expression of ΔNp63 was manipulated using the RNA interfering method. Results In healthy skin tissue, we observed an inverse expression pattern between ∆Np63 and some barrier‐related proteins including filaggrin, caspase‐14, claudin‐1, and claudin‐4. ΔNp63 regulated expression of these genes and proteins. In addition, production of IL‐1β and IL‐33, pro‐inflammatory cytokines, was modulated by ΔNp63. Furthermore, prolonged IL‐13 exposure increased the thickness of the three‐dimensional culture of keratinocytes. IL‐13 interfered with ΔNp63 downregulation during calcium‐induced keratinocyte differentiation. IL‐13 modulated some barrier‐related and inflammation‐related molecules, which were regulated by ΔNp63. Conclusions We have shown that ΔNp63 modulated AD‐related barrier and inflammatory molecules. In addition, ΔNp63 expression was affected by IL‐4/IL‐13. IL‐13–ΔNp63 axis would integrate two major factors of AD pathogenesis: dysregulated barrier and inflammation.