Background: Apoptosis is important for maintenance of tissue homeostasis and often dysregulated in cutaneous neoplasms. The apoptosis inhibitor survivin is expressed in melanoma and non-melanoma skin cancers and benign keratinocytic lesions. Its expression has not been studied in melanocytic nevi.
Objective: We determined the expression pattern of survivin in benign melanocytic nevi in comparison to markers of proliferation and apoptosis.
Methods: Six cases of each of the following melanocytic nevi were retrieved from a dermatopathology archive: compound dysplastic nevus, intradermal nevus, compound nevus, neurotized intradermal nevus, and Spitz nevus. Survivin expression was evaluated by in situ hybridization. Apoptotic and proliferation indices were calculated by counting immunoreactive cells in terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling and proliferating cell nuclear antigen immunostained sections, respectively.
Results: All nevi, regardless of histologic type, expressed survivin. Compound melanocytic lesions expressed survivin in both epidermal and dermal compartments. The apoptotic rate was low for dysplastic, compound, and Spitz nevi, and apoptotic cells were not identified in any neurotized nevus. The proliferative index was highest for Spitz nevi, while all other nevi demonstrated rare positive cells.
Conclusions: Survivin is consistently expressed in benign melanocytic lesions, while apoptotic cells are rarely identified, suggesting the dysregulation of apoptotic pathways with the accumulation of cells in these neoplasms.
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http://dx.doi.org/10.1111/j.0303-6987.2005.00242.x | DOI Listing |
Cancers (Basel)
December 2024
Soft-Tissue, Peritoneum and Melanoma Surgical Oncology Unit, Veneto Institute of Oncology IOV-IRCCS, 35128 Padua, Italy.
Diagnosis of nevoid melanoma (NeM) is often difficult because NeM closely resembles a common nevus clinically and histologically. A retrospective study was conducted on 110 patients diagnosed with and/or treated for primary nevoid melanoma at the Veneto Institute of Oncology and at the University Hospital of Padua from August 1999. Mean Breslow thickness was of 1.
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December 2024
65+ Outpatient Clinic, Amalia Fleming General Hospital, 14, 25th Martiou Str., 15127 Melissia, Greece.
: Melanoma, an aggressive form of skin cancer, accounts for a significant proportion of skin-cancer-related deaths worldwide. Early and accurate differentiation between melanoma and benign melanocytic nevi is critical for improving survival rates but remains challenging because of diagnostic variability. Convolutional neural networks (CNNs) have shown promise in automating melanoma detection with accuracy comparable to expert dermatologists.
View Article and Find Full Text PDFSci Rep
January 2025
Laboratory of Veterinary Embryology and Biotechnology (VETEMBIO), Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea.
Mod Pathol
January 2025
Department of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, IL. Electronic address:
Deep penetrating nevi (DPNs) are characterized by activating mutations in the MAP kinase and Wnt/beta-catenin pathways that result in large melanocytes with increased nuclear atypia, cytoplasmic pigmentation, and often mitotic activity. Together with a lack of maturation, this constellation of findings creates challenges for pathologists to distinguish deep penetrating nevus (DPN) from DPN-like melanoma. To assess the utility of next generation sequencing (NGS) in resolving this diagnostic dilemma, we performed NGS studies on 35 lesions including 24 DPNs and 11 DPN-like melanomas to characterize the specific genomic differences between the two groups and elucidate the genetic events involved in malignant transformation of DPNs.
View Article and Find Full Text PDFAm J Dermatopathol
December 2024
Department of Cellular Pathology, Hospital El Bierzo, Ponferrada, Spain.
Introduction: The current WHO classification of melanocytic tumors distinguishes 9 pathogenic routes. This classification is based on the conceptual interpretation that melanocytic tumors evolve from benign counterparts, accumulating mutations, eventually developing into melanomas with metastatic and potentially lethal capacity. In this article, we present a molecular study of 2 melanocytic tumors that suggest a "leap" from pathogenic routes IV to I.
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