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http://dx.doi.org/10.1111/1346-8138.12825 | DOI Listing |
Indian J Dermatol
October 2024
From the Department of Dermatology, Nowon Eulji Medical Center, Eulji University, Seoul, Korea.
Cureus
September 2024
Oncology, Biokliniki Athinon, Athens, GRC.
Pediatr Dermatol
October 2024
Department of Dermatology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Eruptive melanocytic nevi (EMN) have been reported in the setting of immunosuppression, chemotherapy, and bullous skin disease, including less commonly, Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). This case report presents a 4-year-old girl who developed agminated EMN and nail changes after TEN. A systematic review of the literature supports clinically appropriate follow-up of EMN, as there is no reports of malignancy in EMN following SJS/TEN, nor reports of pediatric melanoma arising within EMN of any etiology.
View Article and Find Full Text PDFJ Am Acad Dermatol
December 2024
Department of Dermatology and Allergy, University Hospital, Ludwig Maximilian University (LMU) Munich, Munich, Germany; Department of Dermatology and Allergy, University Hospital Erlangen, Erlangen, Germany.
Background: Tebentafusp is a novel treatment for patients with metastatic uveal melanoma and often causes cutaneous side effects.
Objectives: The aim of this study was to better characterize these heterogenous cutaneous side effects.
Methods: This prospective cohort study evaluated all patients from a tertiary hospital center who were treated with tebentafusp between January 2019 and June 2023 clinically and assessed skin biopsies histologically.
Case Rep Dermatol
May 2024
Division of Dermatology, David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA, USA.
Introduction: The development of new and changing melanocytic lesions has been increasingly reported as an adverse dermatologic toxicity of BRAF inhibitor therapy. Melanocytic lesions and melanomas induced by BRAF inhibitor therapy that lack V600E expression have been less commonly described. One mechanism that has been proposed for the development of BRAF inhibitor-induced melanocytic lesions, including those lacking V600E expression, is the paradoxical activation of the MAPK signaling pathway in wild-type () cells.
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