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Reddy and Nguyen present an insightful review on optical coherence tomography (OCT). They explain that OCT is a noninvasive near-infrared imaging technology that can be utilized to diagnose basal cell carcinomas (BCCs) based on specific morphological features. Their aim with this study was to conduct a quantitative review using tumour-level data from published studies in order to assess the in vivo diagnostic accuracy of different OCT systems, and to determine the correlation between OCT features and histopathological diagnosis.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) SnapshotDx Quiz— In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image shown, while additional questions concern the findings reported in a JID article by Sanders et al. (2019) that provides new information about that disease entity (https://doi.org/10.1016/j.jid.2018.07.027).
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Cells to Surgery Quiz— In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image shown, while additional questions concern the findings reported in a JID article by Behar et al. (2018) (https://doi:10.1016/j.jid.2018.05.028).
Mammary Paget’s disease (MPD) and extramammary PD (EMPD) are rare cutaneous intraepithelial malignancies with similar presentations. The histogenesis and underlying mutational landscape of these two entities remain unclear. Using whole-exome sequencing of paired tumor and normal skin samples from 20 MPD and 21 EMPD patients, Zhang and colleagues found recurrent mutations in 6 candidate driver genes with high mutation rates in chromatin-remodeling genes. Furthermore, mutational analyses revealed that MPD likely arises independently from co-occurring underlying breast carcinoma and also that MPD and EMPD exhibit similar genetic origins with recurrent mutations in the same driver genes.
Steve Katz, a beloved colleague, mentor, and friend to many in the investigative dermatology and skin biology communities died suddenly and unexpectedly on Thursday, December 20, 2018, in Bethesda, MD.
Tumor development may be suppressed by the immune system via elimination of cancer cells or via prevention of cancer cell outgrowth. The existence of CD8+CD69+CD103+ tissue resident memory T cells (TRM) and their known role in immune surveillance led Park and colleagues to investigate whether this cell population mediated immunity to epidermis-derived melanoma. Using a mouse model of transplantable melanoma, these investigators demonstrated that tissue-resident TRM established a dynamic melanoma-immune equilibrium in the epidermis, suppressing macroscopic tumor development.
Skin is colonized by microbial communities (microbiota) that participate in immune homeostasis, development and maintenance of barrier function, and protection from pathogens. The past decade has been marked by an increased interest in the skin microbiota and its role in cutaneous health and disease, in part due to advances in next-generation sequencing platforms that enable high-throughput, culture-independent detection of bacteria, fungi, and viruses. Various approaches, including bacterial 16S ribosomal RNA gene sequencing and metagenomic shotgun sequencing, have been applied to profile microbial communities colonizing healthy skin and diseased skin including atopic dermatitis, psoriasis, and acne, among others.
Quantifying the Polygenic Contribution to Cutaneous Squamous Cell Carcinoma Risk
HSP70iQ435A-Encoding DNA Repigments Vitiligo Lesions in Sinclair Swine
The study by Plaquevent et al. strongly supports the recent discovery that the use of gliptins is a risk factor for bullous pemphigoid (BP). However, regarding the phenotype of gliptin-associated BP and the necessity of gliptin withdrawal, clinical data remain scarce. We predict that future studies of gliptin-associated BP will offer valuable information concerning autoimmunity against BP180 and may also shed light on the pathology of autoimmune diseases in general.
Large-giant congenital melanocytic nevi have been well characterized clinically, yet questions remain about the heterogenous phenotypes observed. Martins da Silva et al. (2018) highlight the genotypic diversity between “classic” and “spilus-like” congenital melanocytic nevi by analyzing multiple biopsy sites and matching satellite nevi. This study provides evidence for alternative modes of development beyond the well-established NRAS mutation paradigm.
Almost 150 years have passed since Sir James Paget described the disease that bears his name, but the molecular etiology and cellular origins of Paget’s disease remain poorly understood. Herein, Zhang et al. (2018) bring Paget’s disease into the genomics era, providing evidence for an epidermal origin for Paget’s disease, as well as a high incidence of mutations in genes encoding epigenetic regulators.
Dermal white adipose tissue is a unique layer of adipocytes within the reticular dermis of the skin. Recently, several nonmetabolic activities have been discovered for dWAT and its fibroblast precursors. These functions include antimicrobial defense and roles in hair cycling, wound healing, and thermogenesis. In this review, we discuss recent progress in understanding the role of dermal white adipose tissue in immunity, both as an innate antimicrobial cell type and as an indirect communicator with other cutaneous immunocytes to enhance defense and potentially contribute to inflammatory disease.
Hypoxia-inducible factor-1α (HIF-1α) is constitutively expressed in mouse and human epidermis. It plays a crucial role in skin physiology including the response of keratinocytes to ultraviolet (UV) radiation. However, little information is available about its role in photocarcinogenesis. Using a multistage model of UVB radiation-induced skin cancer, we show that the knockout of Hif-1α in the epidermis prevents tumorigenesis, but at the same time triggers the formation of hyperkeratotic plaques. Our results indicate that the absence of oncogenic transformation in Hif-1α-ablated mice is related to increased DNA repair in keratinocytes, while the formation of hyperkeratotic plaques is caused by an increase in the levels of reactive oxygen species.