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Article Synopsis
  • - A case study discusses a 64-year-old male with metastatic colorectal cancer who developed severe itching and new skin lesions after treatment with encorafenib and panitumumab, medications targeting cancer pathways.
  • - The patient showed a mix of skin lesions, including benign moles and keratoacanthomas, with further evaluation confirming a link between the skin reactions and the use of encorafenib, as validated by the Naranjo scale.
  • - Stopping the medications led to significant improvement in skin lesions, highlighting the importance of ongoing skin assessments for patients on BRAF inhibitors to manage side effects effectively.
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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.

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Clinical and pathological characterization of tebentafusp-associated skin toxicity: A cohort study with 33 patients.

J 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.

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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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