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PH-SD18

Melanocytic skin tumours

How melanocytes form benign naevi that stop growing, how melanoma escapes those brakes, how its radial and vertical growth phases and clinical subtypes differ, and why Breslow thickness and ulceration are what its staging measures.

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  • 5 steps · 9 questions
  • 3D normal anatomy

By the end, you can

  • Describe where melanocytes lie and how they pass melanin to keratinocytes.
  • Explain how a BRAF-mutant naevus forms, matures with depth and stops growing through oncogene-induced senescence.
  • Distinguish common naevi, dysplastic naevi and melanoma, and name the genetic changes that let melanoma escape senescence.
  • Contrast the radial and vertical growth phases and the four classic clinical subtypes of melanoma.
  • Explain what Breslow thickness, ulceration and nodal spread measure, and relate the ABCDE features to the biology.

What it is

Melanocytic tumours arise from melanocytes, the pigment cells of the epidermal basal layer. Most are benign naevi (moles): clonal growths that stop growing. Melanoma is the malignant tumour; it can arise in a naevus but more often arises in skin without one. Melanomas are described by clinical and microscopic pattern and, in the current WHO classification, by the pathway that produced them, especially how much cumulative sun damage the skin has had.

5 types to tell apart
Common acquired naevi
Junctional, compound and intradermal, by where the nests lie; most carry BRAF V600E and stop growing.
Congenital naevi
Present at birth, usually with NRAS mutations; very large ones carry a higher risk of melanoma.
Dysplastic (atypical) naevi
Irregular junctional nests with cytological atypia, graded low or high; mainly a marker of melanoma risk.
Melanoma in sun-exposed skin
Low cumulative sun damage (superficial spreading, often BRAF) and high cumulative sun damage (lentigo maligna, often NF1 or NRAS).
Melanoma of sun-shielded sites
Acral (palms, soles, nail bed) and mucosal melanomas, with few UV mutations and more copy-number changes and KIT mutations. Uveal melanoma of the eye is a separate disease.

US spelling: tumours → tumors, tumour → tumor, colour → color.

Normal function

Melanocytes: pigment cells of the basal layer

Melanocytes come from the neural crest and migrate into the skin before birth. They sit singly in the , roughly one for every 5 to 10 basal keratinocytes, and reach up between the cells of the with long dendrites. Each supplies melanin to a few dozen keratinocytes, an epidermal melanin unit.

Melanin is made in melanosomes from tyrosine by tyrosinase and handed to keratinocytes, where it forms caps over their nuclei. UV light makes keratinocytes release α-melanocyte-stimulating hormone, which acts on the MC1R receptor of melanocytes and increases dark eumelanin: the tan. Skin colour depends on the amount and type of melanin, not on the number of melanocytes.

Normal melanocytes divide rarely, lie singly rather than in clusters and stay in the basal layer. Melanocytic tumours break these rules one by one.

Point to it on the model