Melanocytic nevi excised during B-Raf proto-oncogene (BRAF) inhibitor therapy: A study of 19 lesions from 10 patients  

Oleh:

Mochel, Mark C. ; Hammond, Marc R. ; Frederick, Dennie T. ; Alora-Palli, Maria B.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JAAD: Journal of the American Academy of Dermatology (keterangan: ada di ClinicalKey) vol. 73 no. 03 (Sep. 2015), page 491–499.
Topik: B-Raf proto-oncogene inhibition; CD4; CD8; melanocytic nevi; phosphorylated extracellular signal-regulated kinase; phosphorylated protein kinase B

Ketersediaan

Perpustakaan FK Nomor Panggil: J15.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background There are limited descriptions of histopathology and immune profiles of new or changing melanocytic nevi in the setting of B-Raf proto-oncogene (BRAF) inhibitor therapy. Objective We sought to identify their distinctive features. Methods Clinical charts and histologic review, neuroblastoma RAS viral (v-ras) oncogene homolog genotyping, and immunohistochemistry for HMB-45, BRAFV600E, phosphorylated extracellular signal-regulated kinase (pERK), phosphorylated protein kinase B, CD4, and CD8 were performed on 19 melanocytic nevi from 10 patients and 23 control nevi. Results BRAF inhibitors were administered for metastatic melanoma (7), colonic adenocarcinoma (2), and papillary thyroid carcinoma (1). The average duration of BRAF inhibition before lesion excision was 8 months. Frequently associated histologic features included pigmentation of the stratum corneum, hyperpigmented keratinocytes, dermal melanophages, and deep HMB-45 expression. The lesions were BRAFV600E and neuroblastoma RAS viral (v-ras) oncogene homolog wild-type, expressed diffuse weak-moderate pERK, and possessed a predominance of CD8+ in comparison with CD4+ T lymphocytes within the dermal infiltrates. Limitation This is a retrospective study of a small and heterogeneous group. Conclusion The nevi associated with BRAF inhibitor therapy invariably lack BRAFV600E mutation. BRAF inhibition appears to cause an increased cytotoxic T-cell response and increased mitogen-activated protein kinase activity in BRAF wild-type lesions, supported by pERK expression, possibly resulting in an activated phenotype characterized by increased melanin pigmentation and deep HMB-45 expression.

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