PMC6381421_01
The pigmented lesion with a peripheral halo of hypopigmentation. Within the previous year prior to referral, it had started to enlarge and thicken centrally with no associated pruritus or pain.
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It later developed as a 6 mm brown papule, which was diagnosed as a nevus, with a peripheral halo of hypopigmentation and central thickening (Figure 1).
Hematoxylin and eosin stain of the biopsy. Low power 20x magnification (a) revealed a compound melanocytic proliferation involving the base of the epidermis and superficial dermis. The melanocytic proliferation was symmetrical. An inflammatory response was not identified. At 40x magnification, (b) most of the epidermal melanocytes were confined to the epidermal base. There was only focal intra-epidermal ascent of the melanocytes identified. At 100x magnification, (c) there was no intra-epidermal ascent of melanocytes identified in this photograph. The dermal melanocytes showed maturation to the base of the lesions. At 400x, (d) some of the melanocytes were multinucleate and exhibited pleomorphism of nuclear size variation (>4x variation). Occasional nucleoli and mitoses were identified.
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In the epidermis, melanocytes were distributed primarily as nests at the tips and sides of the rete ridges with some clefting from the overlying epidermis and discohesion among melanocytes within the nests (Figure 2(a)). Nests appeared to predominate over single cells, without a significant upwards scatter (Figure 2(b) and (c)). The dermal component also revealed prominent nuclear atypia with scattered mitotic figures (Figure 2(d)).
(a) aCGH analysis of the lesion. There was a gain in chromosome 7p (B), (b) subthreshold gain in chromosome 7q, (c) subthreshold loss in 8p, and (d) loss in chromosome 9.
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Due to the atypical features, the specimen was sent out for further molecular investigations. aCGH demonstrated gain in chromosome 7p, subthreshold gain in chromosome 7q, loss in chromosome 9, and subthreshold loss in 8p (Figure 3). The loss of chromosome 9 was the most prominent molecular result and directly correlated with the loss of p16 expression demonstrated by immunohistochemistry (Figure 3(d)).