Dermoscopic Criteria, Histopathological Correlates and Genetic Findings of Thin Melanoma on Non-Volar Skin

Abstract

Dermoscopy is a non-invasive, in vivo technique that allows the visualization of subsurface skin structures in the epidermis, at the dermoepidermal junction, and in the upper dermis. Dermoscopy brought a new dimension in evaluating melanocytic skin neoplasms (MSN) also representing a link between clinical and pathologic examination of any MSN. However, histopathology remains the gold standard in diagnosing MSN. Dermoscopic-pathologic correlation enhances the level of quality of MSN diagnosis and increases the level of confidence of pathologists. Melanoma is one of the most genetically predisposed among all cancers in humans. The genetic landscape of melanoma has been described in the last years but is still a field in continuous evolution. Melanoma genetic markers play a role not only in melanoma susceptibility, initiation, and progression but also in prognosis and therapeutic decisions. Several studies described the dermoscopic specific criteria and predictors for melanoma and their histopathologic correlates, but only a few studies investigated the correlation among dermoscopy, pathology, and genetic of MSN. The aim of this work is to review the published data about dermoscopic features of melanoma, their histopathological correlates with regards also to genetic alterations. Particularly, this review will focus on low-CSD (cumulative sun damage) melanoma or superficial spreading melanoma, high-CSD melanoma, and nevus-associated melanoma.

Keywords: clinic-pathologic correlation; dermoscopy; genetic; markers; melanoma; pathology.

Figure 1

Superficial spreading melanoma (T1a, Breslow 0.5 mm) on the abdomen of an 82-y old man. This de novo slow-growing melanoma shows on polarized contact dermoscopy (Dermalite ProHR^®, 3Gen, San Juan Capistrano, CA USA) an asymmetric polychromatic multicomponent pattern with atypical pigment network (Panel A: labeled ^), white regression (Panel A: labeled *), structureless blue pigmentation (Panel A: labeled °) and structureless brown-blue bichromatic areas (Panel A: labeled +). The atypical network correlates with the hyperpigmented rete ridges with atypical melanocytes in single units and irregular nests mostly arranged at the DEJ (Panel C: labeled ^); the presence of a heavy lymphohistiocytic infiltrate with melanophages and acanthosis of the epidermis and heavily pigmented atypical nest and melanocytes in the epidermis are responsible for the structureless blue pigmentation (Panel C: labeled °). Panel B shows in the dermis fibrosis with a lymphohistiocytic infiltrate that correlates with the area of regression (Panel B: labeled *) while the atypical melanocytes in single units and irregular nests mostly arranged at the DEJ and the melanophages in the dermis correlate with structureless bichromatic brown-blue areas (Panel B,D: labeled +). (original magnification: Panel B,C: HE, 40×; Panel D: HE, 100×).

Figure 2

Superficial spreading melanoma (T1a, Breslow 0.53 mm) on the left chest of a 44-y old man. Panel A: Polarized contact dermoscopy (Dermaview^®, Tre T Medical, Camposano, NA, Italy) shows asymmetry, multiple colors, pseudopods (labeled *), atypical network, structureless black areas (labeled °), structureless blue areas (labeled ^), irregular globules (labeled +) and dots. Pseudopods correlate with peripheral, confluent, and heavily pigmented atypical junctional nests of melanocytes (Panel B; HE: 100×). Irregular globules correspond to irregularly large atypical nests of melanocytes at the DEJ (Panel C; HE: 100×) while irregular dots to small atypical nests of melanocytes or irregular clumps of melanin in the epidermis (Panel D; HE: 100×). The structureless black and blue areas are related to the heavy band-like lymphohistiocytic infiltrate with melanophages in the dermis.

Figure 3

Melanoma in situ on the left flank of a 62-y old man. This small diameter melanoma showed upon polarized contact dermoscopy (Dermaview^®, Tre T Medical, Camposano, NA, Italy) an asymmetric growth at 1-year digital follow-up (Panel A,B), atypical network, structureless brown areas, and irregular pigmented areas. Histology (Panel C; HE, ×100) shows a proliferation of atypical melanocytes in single units and nest in all layers of the epidermis and a dense lymphohistiocytic infiltrate with melanophages in the dermis. Pagetoid spread is confirmed also by Melan-A staining (Panel E, 200×). The irregular pigmented areas correlate with the clumps of melanin and pigmented parakeratosis (Panel D; 200×); the structureless brown areas correlate with the dense lymphohistiocytic infiltrate with melanophages in the dermis.

Figure 4

Nevus-associated melanoma in a 76-y old woman on the right buttock. Polarized contact dermoscopy (Panel A; Dermalite ProHR^®, 3Gen, San Juan Capistrano, CA, USA) shows an asymmetric lesion with central hypopigmented-brown structureless areas and an atypical network on the right side. Histology shows an asymmetric melanocytic lesion composed on the left side by a dermal proliferation of monomorphous melanocytes with maturation (corresponding to the central hypopigmented-brown-structureless areas) and on the right shoulder elongated rete-ridges with atypical melanocytes in single units and irregular nests in all the epidermal layers, correlating to the atypical network (Panel B; HE: 20×). The Melan-A staining highlights the pagetoid spread (Panel C: ×20; Panel D: 200×).

Figure 5

Lentigo maligna on the left temporal region of a 77-y old man. Panel A: asymmetric, irregularly pigmented macule. Panel B: polarized contact dermoscopy (Dermaview^®, Tre T Medical, Camposano, NA, Italy) shows asymmetry and multiple colors; asymmetric pigmentation of the hair follicles, dots, and annular-granular pattern. Panel C,D: Histology shows atypical melanocytes and irregular nests at the DEJ and in the epidermis with involvement of the hair follicles (correlate with the asymmetric pigmentation of the hair follicles); in the dermis, there is prominent solar elastosis, melanophages (correlate with the dots and annular-granular pattern) and a discrete lymphohistiocytic infiltrate. (Panel C,D: HE, 400×).