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Superficial Spreading Melanoma


The term superficial spreading melanoma (SSM) is commonly used to refer to melanomas characterized by a combination of clinical and histopathologic findings. They usually occur at intermittently sun-exposed sites, manifest as peripherally spreading surface lesions, and display an intraepidermal growth of melanocytes characterized by the presence of nests and/or pagetoid melanocytes. SSM is the most common melanoma variant among adolescents and young to middle-aged adults. In prepubertal children, nodular melanoma (NM) predominates. In adolescence the ratio of SSM to NM is approximately 2 : 1, and in adults the ratio is closer to 5 : 1, with SSM constituting approximately 60% to 70% of all melanomas in mid adulthood. SSM may occur in all areas of the body but are most frequent on the trunk and extremities. Ultraviolet (UV) light plays a role in the risk for developing an SSM. The odds ratio for developing an SSM is nearly 2 : 1 for individuals with a tendency to burn to those who never burn, when controlled for phototype. The odds ratio is nearly 2 : 1 for patients with their first burn before 15 to those with their first burn after age 15, also controlled for phototype. Another related risk factor for SSM is an elevated total body nevus count.

From a pathomechanistic and epidemiologic perspective descriptive reporting of melanoma growth pattern as SSM versus lentigo maligna or acral melanoma has some value and follows tradition. However, for most clinical purposes this classification is of limited or no relevance. What clinically matters in a melanoma pathology report is the correct diagnosis of a tumor as melanoma and key prognostic parameters for American Joint Committee on Cancer (AJCC) tumor staging. In this textbook, melanoma subclassification mainly serves didactic purposes. The chapter on SSM is an opportunity to discuss diagnostic issues related to nested and pagetoid growth of melanocytes in the epidermis.

Clinical Findings

SSM is the type of melanoma for which the ABCD rule for clinical melanoma diagnosis is most useful. A symmetry, with irregular b order, multiple c olors, and d iameter greater than 6 mm are clinical features that suggest melanoma ( Fig. 13.1 ). Many of the 10 melanoma-specific dermoscopic structures are most relevant to identification of SSM. This includes atypical pigment network, streaks, irregular blotches, and peripheral brown structureless areas ( Table 13.1 ). The other structures such as negative pigment network, chrysalis, atypical dots and globules, blue white structures, and atypical vascular structures may be seen in SSM but are also frequent in other subtypes of melanoma ( Figs. 13.2–13.4 , see also Fig. 13.1 ).

Fig. 13.1, Pigmented Superficial Spreading Melanoma.

TABLE 13.1
Distinguishing Features of Superficial Spreading Melanoma, Dysplastic Nevi, and Spitz Nevi
Dermoscopic Features Histologic Features Molecular Features
Superficial Spreading Melanoma Favors melanoma:

  • Atypical pigment network

  • Asymmetric streaks

  • Irregular blotches

  • Peripheral brown structureless area

  • Atypical vasculature

  • Inverse pigment pattern

  • Chrysalis

  • Blue gray veil

  • Regression structures

  • Atypical dots and globules

  • Often has predominant growth pattern of single cells over nests with lentiginous or pagetoid growth pattern. Lesion maybe poorly circumscribed laterally.

  • Destructive features of the epidermis such as effacement or epidermal consumption favor melanoma, though recurrent or traumatized nevus needs to also be considered

  • Nested patterns should have quite notable nuclear atypia and often closely opposed nests along the rete ridges, which often expand the interretial space.

  • Majority have driver mutations in BRAF, although NRAS driver mutations may also be seen. Subsequent genetic alterations include TERT promoter mutation or amplification, homozygous deletions or mutations of CDKN2A, and/or deletions or mutations in PTEN.

  • FISH positivity such as clonal gains in 6p25, 11q23, 8q24 or homozygous deletions in 9p21 all favor a diagnosis of melanoma.

Dysplastic Nevus

  • May have 1 or 2 of the dermoscopic structures typical of melanoma, such as focal chrysalis or atypical network, irregular dots, or globules.

  • Typically will maintain some symmetry of dermoscopic structures at least in one axis.

  • Typically have a predominantly nested pattern.

  • May have focal upward migration of melanocytes, typically toward the center of the lesion or around follicular units.

  • Some level of lateral circumscription is maintained.

  • May have driver mutations in NRAS or BRAF and can have heterozygous deletions in CDKN2A but lack many of the other mutations typically of fully transformed lesions.

Spitz Nevus

  • Dermoscopic symmetry is a key factor.

  • Frequent patterns include symmetric inverse pigment pattern with or without chrysalis, symmetric starburst pattern, and symmetric tiered globular pattern.

  • Histomorphology can vary depending on the subtype, but generally some level of symmetry at the histologic level, as well as some level of lateral circumscription, should be present.

  • Epidermal hyperplasia is frequent and Kamino bodies are characteristic.

  • Clefted spaces between the epidermis and junctional melanocytes is frequent.

  • Single cells or nests can predominate in the epidermis but again some lateral circumscription should be present. Focal effacement of the epidermis may occur but broad effacement with epidermal consumption would raise concern for melanoma.

  • HRAS mutations and/or HRAS copy number gains or fusions in ALK, NTRK, ROS, BRAF, or RET, NTRK3, and MET.

Fig. 13.2, Superficial Spreading Melanoma.

Fig. 13.3, Amelanotic Superficial Spreading Melanoma.

Fig. 13.4, Melanoma of Small Clinical Diameter.

Most lesions of SSM arise de novo, but approximately 30% to 40% may develop in association with a precursor melanocytic nevus. There is currently no way to determine which nevi are most likely to be associated with a subsequent melanoma. The probability of a melanoma to arise in association with any given nevus, whether a common nevus, dysplastic, or other nevus, is extremely low. There are approximately 90,000 new cases of melanoma in the United States per year, of which 30% may have developed in association with a nevus (0.3 × 90,000 = 27,000 nevus-associated melanomas per year). If one considers 27,000 as the number of nevus-associated melanomas in the numerator of a fraction and the total number of dysplastic nevi in the United States (a number difficult to estimate) in the denominator, it is apparent that the fraction of dysplastic nevi with subsequent development of melanoma per year is a rare event.

Histopathologic Findings

Histopathologically, SSM is distinguished from other melanoma types by the features of its in situ component. In SSM the intraepidermal tumor cells typically form nests and solitary units of atypical epithelioid melanocytes which are seen in the spinous cell layer in a pattern often referred to as “pagetoid” (e.g., similar to what is seen in Paget disease). The proportion of nests and solitary units may vary ( Figs. 13.5–13.10 ). In some lesions, melanoma cells distributed in a pagetoid pattern constitute most of the intraepidermal tumor cell population. In others, nests may predominate. In most lesions, there is a mix of nests and solitary units.

Fig. 13.5, Superficial Spreading Melanoma With Dominant Pagetoid Spread of Single Tumor Cells.

Fig. 13.6, Superficial Spreading Melanoma With Dominant Nested Pattern.

Fig. 13.7, Paucicellular Melanoma In Situ.

Fig. 13.8, Melanoma With Sharp Circumscription and Minor Spitzoid Features.

Fig. 13.9, Melanoma With Nested Growth.

Fig. 13.10, Melanoma With Predominant Nested Growth Pattern.

As with other melanoma variants, its silhouette is often asymmetric and its peripheral margin(s) ill defined. The asymmetry in the distribution of melanocytes may be accompanied by irregular melanization. Often SSMs will have effacement of the epidermis in focal areas. This may be seen in either the center of the lesion or at one lateral edge.

Most lesions measure more than 4 mm in diameter, but on occasion an SSM may present as a small macule (see Fig. 13.4 ). The cell density of most SSMs is high, but some early lesions may be paucicellular (see Fig. 13.7 ). Associated inflammation and/or fibrosis are common stromal changes. Secondary epidermal changes include epidermal hyperplasia, effacement of rete ridges (aka “consumption of the epidermis”), and ulceration. Some lesions of SMM are associated with a nevus remnant. The presence of a banal nevus remnant facilitates recognition of the melanoma because of the contrast in cytology and/or growth pattern.

Differential Diagnosis

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