Superficial spreading melanoma (SSM) or “low-CSD melanoma” is the most common subtype of cutaneous melanoma, accounting for over two-thirds of all melanoma cases. It mostly occurs in young to middle-aged fair-skinned individuals, affecting both genders equally. SSM usually arises on sites intermittently exposed to the sun, most frequently on legs in females and backs in males. It is etiologically linked to intermittent sun exposure (UV radiation). The other strong risk factors are the number of nevi, including dysplastic nevi, fair skin, blue eyes, family history, and genetic susceptibility. SSM is the prototypic subtype in which the ABCDE rule is helpful in early detection. Clinically, it presents as an irregularly outlined, colored macule that progresses to become an elevated plaque or nodule and ulcerate eventually. The most common dermoscopic features are atypical reticular pattern, blue veils, irregular dots, irregular pigmentation, and asymmetry. The dermoscopic features most specific to the SSM subtype are atypical pigment network, irregular streaks, irregular blotches, and peripheral brown structureless areas. Histopathologically, SSM is characterized by asymmetric, poorly circumscribed, large, atypical compound melanocytic proliferation, with confluent lentiginous spread, prominent nesting, pagetoid scatter, and intraepidermal extension of melanoma cells at least three rete ridges beyond any dermal invasive component. There is consumption of the epidermis with clefting or “zipper effect” and expansile growth in the dermis alongside low to moderate solar elastosis. Immunohistochemical staining in some challenging cases for PRAME, HMB45, p16, and Ki-67 helps in differentiating dysplastic nevus, and sometimes, BRAF immunostain helps in the distinction of Spitz nevus. FISH, CGH, NGS, and other molecular techniques are rarely needed for very challenging cases. The BRAF V600E mutation is the most common alteration in SSM and is the earliest oncogenic mutation. Most banal nevi also harbor the same mutation. The melanomagenesis from a normal melanocyte to the development of invasive melanoma and metastasis involves progressive accumulation of mutations related to the mutagenic effects of UV radiation. The progression sequence resulting in the development of SSM molecularly includes BRAF mutation, TERT promoter mutation, biallelic inactivation of CDKN2A, SWI/SNF, PTEN, and TP53 mutation. Besides, copy-number alterations and other chromosomal abnormalities are also common in SSM.

Superficial Spreading (Low-CSD Melanoma) Melanoma

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发表日期：

2026年

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Dinesh Pradhan

摘要

Superficial spreading melanoma (SSM) or “low-CSD melanoma” is the most common subtype of cutaneous melanoma, accounting for over two-thirds of all melanoma cases. It mostly occurs in young to middle-aged fair-skinned individuals, affecting both genders equally. SSM usually arises on sites intermittently exposed to the sun, most frequently on legs in females and backs in males. It is etiologically linked to intermittent sun exposure (UV radiation). The other strong risk factors are the number of nevi, including dysplastic nevi, fair skin, blue eyes, family history, and genetic susceptibility. SSM is the prototypic subtype in which the ABCDE rule is helpful in early detection. Clinically, it presents as an irregularly outlined, colored macule that progresses to become an elevated plaque or nodule and ulcerate eventually. The most common dermoscopic features are atypical reticular pattern, blue veils, irregular dots, irregular pigmentation, and asymmetry. The dermoscopic features most specific to the SSM subtype are atypical pigment network, irregular streaks, irregular blotches, and peripheral brown structureless areas. Histopathologically, SSM is characterized by asymmetric, poorly circumscribed, large, atypical compound melanocytic proliferation, with confluent lentiginous spread, prominent nesting, pagetoid scatter, and intraepidermal extension of melanoma cells at least three rete ridges beyond any dermal invasive component. There is consumption of the epidermis with clefting or “zipper effect” and expansile growth in the dermis alongside low to moderate solar elastosis. Immunohistochemical staining in some challenging cases for PRAME, HMB45, p16, and Ki-67 helps in differentiating dysplastic nevus, and sometimes, BRAF immunostain helps in the distinction of Spitz nevus. FISH, CGH, NGS, and other molecular techniques are rarely needed for very challenging cases. The BRAF V600E mutation is the most common alteration in SSM and is the earliest oncogenic mutation. Most banal nevi also harbor the same mutation. The melanomagenesis from a normal melanocyte to the development of invasive melanoma and metastasis involves progressive accumulation of mutations related to the mutagenic effects of UV radiation. The progression sequence resulting in the development of SSM molecularly includes BRAF mutation, TERT promoter mutation, biallelic inactivation of CDKN2A, SWI/SNF, PTEN, and TP53 mutation. Besides, copy-number alterations and other chromosomal abnormalities are also common in SSM.