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Naevi and Melanoma - Skin Neoplasia

Naevi = hamartoma of the skin. With respect to melanocytes, a benign neoplasm

Skin Neoplasia


Naevi and Melanoma


·        Naevi = hamartoma of the skin.  With respect to melanocytes, a benign neoplasm


Melanocytic Naevi


·        Normal skin: epidermal cells, plus melanocytes, Langerhans cells (Antigen Presenting Cells –APC), prickle cells and merkel cells (sensory receptors)

·        Benign melanocytic naevi: 

o   Junctional: epidermis only, early active growth to <0.5 cm. Can be non-pigmented. Overgrowth of melanocytes in nests along the junction of the dermis and epidermis. 

o   Compound: epidermis and dermis, older active growth (moles on palms, soles and genitalia stay junctional) 

o   Intradermal: stopped growing, loss of tyrosinase ® small and pale. Don‟t have contact with the epidermal junction (ie are deep). Don‟t become malignant – must have junctional activity to do this 

·        Dysplastic melanocytic naevi (Atypical Mole Syndrome): 

o   Uncontrolled proliferation without malignancy (> 100 with at least one Dysplastic more or a mole > 0.5 cm)

o   Mostly benign with possibility of malignancy

o   If have > 100 moles, 100 to 200 times normal risk

o   Risk of melanoma proportional to the number of moles, plus family history and degree of atypia

o   Management:

·        Self checking each month

·        Annual doctor check (to make sure they‟re self checking)

·        Most moles that change aren‟t melanoma, but if suspicious need to remove it 

·         Halo naevi: Fairly common, especially in kids. Depigmented symmetrical halo around the mole, but the mole is normal (cf depigmented melanoma where pigmented lesion is not normal and not central)

·        Pathogenesis: ?Somatic mutation

·        Differential:

o   Melanoma

o   Dermatofibroma: feels firm

o   Seborrheic keratosis: altered texture




·        Host Risk Factors: Skin colour, Naevi, Atypical naevi, DNA repair, Immune status


·        Environment Risk Factors: UV light (geography, season, time), behaviour. Risk from sun determined by age 15. After that sunscreen mainly protects against squamous and basal cell carcinomas

·        Epidemiology:

o   1 – 3% of childhood cancers

o   Females 14/100,000, males 9/100,000. Difference is in the distribution on the legs

·        Spotting them:

o   A: asymmetry

o   B: border irregular – e.g. growing a peninsular

o   C: colour – 3 or more, colour not symmetrical, areas of black, variegated 

o   D: dimension > 0.6 cm (although you can get smaller melanomas, and most larger lesions aren‟t melanomas 

o   E: elevated ® ­dermal penetration (but most are initially flat – superficial spreading melanomas)

o   Usually asymptomatic: don‟t bleed until late (ie take bleeding seriously) and don‟t usually itch

·        Watch out for:


o   Changes: but moles can change for lots of reasons. And patients aren‟t good at detecting changes (either miss them or think they‟ve changed when they haven‟t) 

o  Bleeding, itching and halo (although can get two tone moles – OK if symmetrical)

·        Progression: 

o  Radial Growth Phase: initially growth is along the dermo-epidermal junction and within the epidermis 

o  Vertical Growth Phase: Growth into the dermis ® malignant cells in contact with lymphatics and capillaries ® metastasis 

o  Nodular melanoma: bad news

o  Acral Letigenous Melanoma: on palms and soles

·        Differential:

o  Benign mole

o  BCC

o  Seborrheic keratosis: stuck on appearance, monotone and symmetrical, greasy surface, numerous

o  Angiokeratomas

o  Dermatofibroma: firm, round, monotone

o  Any lesion under a nail (usually thumb) is a melanoma or SCC until proven otherwise

·        Pathology:


o  Features of malignant cells: irregular, hyperchromatic, large N:C ratio, mitoses (blackberry nuclei), abnormal number of mitosis

o  Radical/Superficial/Horizontal growth phase: cells in contact with dermis, don‟t metastasise 

o  Vertical growth: mass of atypical melanocytes infiltrating dermis, lymphocytes, not necessarily pigmented, metastasises 

o  Will always have junctional activity. If they only exist deeper in the dermis then they‟re not malignant.

·        Prognosis:


o  Breslow tumour thickness (> 0.76 cm bad) or Clarke‟s levels (grade 1- 5, 3 ~ Breslow 0.76, bigger = worse)

o  Ulceration > 3 mm (bad)

o  High mitotic rate (bad)

o  Regression an indication of metastasis (bad)

o  Tumour infiltrating lymphocytes (bad)

·        Treatment: surgical excision


·        Hutchison‟s Freckle: freckly „in-situ‟ melanoma. Usually on face, tan macule that slowly enlarges and develops a geographic shape, multicoloured in time. Malignant change of melanocytes along the epidermis border but no infiltration. Takes years to become invasive. On sun damaged skin. On elderly watch for a while. Now showing up on younger people – excise before they get too big


Other Naevi


·        Epidermal Naevi:

o  Defined according to their predominant cell type

o  Circumscribed distribution over a part of the body surface, usually dermatomal

o  Any size, never cross the midline, uncommon on face and head


·        Sebaceous Naevi: hamartomas of predominantly sebaceous glands. Usually on scalp (lesion is bald). Raised, velvety surface, present at birth, usually small. ­Risk of basal-cell carcinoma, but no longer prophylactically excised


·        Dermal Melanocytic naevus (Mongolian spot): macular blue-grey pigmentation present at birth, over sacral area in Mongoloid and some other races. Looks like a large bruise. Rarely persist into adulthood.


·        Congenital naevocellular naevus: Small is < 1.5 cm, intermediate = 1.5 – 20 cm, large is > 20 cm. If over lower sacrum ® ?spinabifida occulta. May arise or darken in puberty. Large ones have ­risk of melanoma


·        Spitz naevus: appears in early childhood as a firm, round red or reddish brown nodule. May bleed and crust. Benign. Local excision.


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