DermatologyTier 1Disease (DEADMAN)

Cutaneous oncology - premalignant skin lesions

Description

Actinic (solar) keratosis (AK) - the commonest premalignant lesion, a UV-induced field of dysplastic keratinocytes confined to the epidermis - low but real risk of progression to invasive SCC
Bowen's disease (SCC in situ) - full-thickness epidermal dysplasia without dermal invasion - a step further along the same continuum as AK
Field cancerisation - the key concept: chronically sun-damaged skin harbours multiple subclinical/clinical dysplastic lesions across a whole area, not just the visible one - drives field-directed rather than purely lesion-directed treatment

Very common in fair-skinned, chronically sun-exposed Australians - AK prevalence >40-50% in older adults in high-UV regions
Risk rises with cumulative UV exposure, age, fair skin (Fitzpatrick I-II), and immunosuppression (markedly increased incidence and faster progression in transplant recipients)

Cumulative UV-induced DNA damage (particularly UVB) -> p53 mutation -> keratinocyte dysplasia confined initially to the epidermis
Progression pathway: normal skin -> AK -> Bowen's disease (SCC in situ) -> invasive SCC - a continuum, not discrete separate diseases
Immunosuppression (transplant recipients, HIV, chronic corticosteroids) - impairs immune surveillance of dysplastic keratinocytes -> higher lesion burden and faster progression to invasive disease

Clinical

AK: rough, scaly, erythematous macules/papules on chronically sun-exposed skin (face, scalp, forearms, dorsal hands) - easier felt than seen (sandpaper texture)
Bowen's disease: well-demarcated, scaly/crusted erythematous plaque, slow-growing, can mimic psoriasis/eczema (single, persistent, non-responsive plaque is the clue)
Biopsy if: induration, ulceration, rapid growth, bleeding, or failure to respond to field therapy - excludes invasive SCC

Distinguishing features from invasive SCC

Induration/thickening on palpation, ulceration, and rapid growth suggest invasion - biopsy rather than treat empirically as AK/Bowen's

A. Lesion-directed therapy - few, discrete, easily visualised lesions

B. Field-directed therapy - multiple lesions/field cancerisation

Topical 5-fluorouracil - induces visible inflammation in affected/subclinical areas, several-week course
Topical imiquimod - immune-mediated, alternative field agent
Photodynamic therapy (PDT) - photosensitiser applied then light-activated, good cosmetic outcome, useful for facial field disease
Diclofenac gel - milder option, longer course, for thinner AKs
Choice guided by lesion thickness, cosmetic priority, and patient tolerance of the inflammatory reaction

C. Bowen's disease specifically

Cryotherapy, curettage and cautery, PDT, or topical 5-FU/imiquimod - all options depending on site/size; excision if diagnostic uncertainty or failure of destructive/topical methods

D. Prevention - applies to all

Daily broad-spectrum sunscreen, sun avoidance/protective clothing - reduces new lesion formation
Regular skin surveillance, particularly in immunosuppressed/transplant patients - more frequent review given accelerated progression risk

Chronic UV exposure/photoageing, fair skin
Immunosuppression (organ transplant recipients especially) - higher lesion burden, faster and more frequent progression to invasive SCC
Field cancerisation - coexisting BCC/SCC risk in the same sun-damaged area
HPV - relevant to genital/perianal Bowen's disease specifically (different aetiology to UV-driven cutaneous disease)

Individual AK - low absolute risk of progression to invasive SCC per lesion per year (~<1%), but cumulative risk across a field of many lesions over years is clinically significant
Some AKs spontaneously regress, particularly with sun protection - not all require treatment, but surveillance is needed
Untreated Bowen's disease - progresses to invasive SCC in a minority but with unpredictable timing - treatment reduces this risk
Immunosuppressed patients - the natural history is compressed (faster progression, more aggressive resultant SCC) - justifies closer surveillance intervals

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