Aetiology | Medibuddy
14th July 2026

Aetiology

Exposure to UV radiation, history of sunburn during childhood, family history of melanoma, Fitzpatrick type I and II skin (Table 1), genetic syndromes (xeroderma pigmentosum), the proportion of congenital and acquired melanocytic nevi and genetic susceptibility. Melanoma arises from melanocytes. The CDKN2A gene is associated with familial melanoma. The MAPK pathway activates the BRADF and NRAS oncogenes and the CDKN2/RB1 pathway. BRAF mutations are present in around 40 to 50% of melanomas.

Type Characteristics
I Always burns, pale white skin
II Burns easily, tans minimally, white skin
III Burns moderately, tans uniformly, light brown skin
IV Burns minimally, always tans well, moderate brown skin
V Rarely burns, tans profusely, dark brown skin
VI Never burns, deeply pigmented dark brown to black skin

Table 1. Fitzpatrick skin types

Risk factors for metastasis in those with stage I or II:

  • > 55 years of age
  • Head and neck tumour
  • Breslow’s thickness > 4mm 
  • BRAF mutations
  • Vascular invasion 

Diagnosis

Subtypes of melanoma:

  • Superficial spreading (Figure 5): most common, usually found on the torso, incidence increases with age
  • Nodular: second most common, typically associated with a late diagnosis and subsequent poor prognosis
  • Lentigo maligna melanoma: more common in older population and on sun-damaged skin, typically slow growing. Dermoscopy findings include annular granular pigmentation, atypical globules, atypical network, rhomboidal structures, and blue-white veil.
  • Acral lentiginous: ~1-3% of melanomas, most commonly seen in those with Fitzpatrick type V or VI. 
  • Rate variants: amelanotic (non-pigmented), spitzoid, desmoplastic  

Superficial spreading melanoma

Superficial spreading melanoma 

Image Source: Wikimedia Commons (2020), ECG AVNRT, Licenced under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Melanoma_(2).jpg (Accessed: 20 May 2026).

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