OncologyTier 1Disease (DEADMAN)

Cancer - skin

Description

Keratinocyte ("non-melanoma") skin cancer - BCC and SCC, arising from the epidermal keratinocyte lineage, on the same UV-damage continuum as actinic keratosis/Bowen's disease
Collectively the commonest cancer diagnosis in Australia by far - most managed entirely by dermatology/GP surgical excision, but oncology involvement matters for high-risk, locally advanced, or metastatic disease
For clinical morphology, dermoscopy, and standard surgical/topical management of BCC, SCC, and premalignant lesions individually, see basal cell carcinoma and squamous cell carcinoma - this note is the oncology risk-stratification and systemic therapy lens

Australia has among the world's highest incidences of both BCC and SCC, driven by UV exposure
BCC essentially never metastasises; cutaneous SCC metastasises in a small but clinically important minority (~2-5% overall, higher with high-risk features) - this asymmetry is why oncology involvement is almost always SCC-driven, not BCC-driven

Cumulative UV-induced DNA damage - hedgehog pathway (PTCH1) mutation drives BCC; p53 and RAS pathway mutation drives SCC via the AK -> Bowen's -> invasive SCC continuum
Immunosuppression (transplant recipients) - disproportionately raises SCC risk more than BCC (SCC:BCC ratio inverts compared with the general population) and drives more aggressive, higher-metastatic-risk tumours

High-risk SCC features - the trigger for oncology/multidisciplinary involvement

Size >2cm, depth >4mm/invasion beyond subcutaneous fat, poor differentiation, perineural invasion, high-risk site (lip, ear), recurrent tumour, immunosuppression - each raises local recurrence and metastatic risk
AJCC 8th edition staging applies to cutaneous SCC of the head and neck specifically - incorporates size, depth, and high-risk features into T-category
Regional lymph node assessment (clinical +/- imaging) for high-risk SCC given metastatic potential - BCC does not require nodal staging

A. Localised disease - surgical/dermatological (see dedicated BCC/SCC notes)

Excision with margins or Mohs micrographic surgery remains first-line for the great majority of both BCC and SCC

B. Locally advanced or metastatic BCC

Hedgehog pathway inhibitors - vismodegib or sonidegib - for disease not amenable to surgery/radiotherapy
Cemiplimab (anti-PD-1) - option after hedgehog inhibitor failure/intolerance

C. Locally advanced or metastatic cutaneous SCC

Cemiplimab or pembrolizumab (anti-PD-1) - now standard for disease not curable by surgery/radiotherapy, superseding cytotoxic chemotherapy as first-line systemic option
Radiotherapy - adjuvant for high-risk features (positive margins, perineural invasion, nodal disease) or definitive for non-surgical candidates
Regional lymph node dissection +/- adjuvant radiotherapy for nodal metastasis

D. Across both

Multidisciplinary team input (dermatology, plastics, radiation oncology, medical oncology) once disease is locally advanced, recurrent, or metastatic
Lifelong surveillance and aggressive sun protection - risk of further keratinocyte cancers is high once one has occurred

Field cancerisation - actinic keratosis, Bowen's disease, multiple synchronous/metachronous BCC and SCC in the same UV-damaged skin
Immunosuppression (transplant recipients) - markedly increased incidence and aggressiveness, particularly of SCC
Genetic syndromes - Gorlin syndrome (BCC), xeroderma pigmentosum (both)

BCC - excellent prognosis, local tissue destruction the main risk if neglected, metastasis exceptionally rare
High-risk SCC - the entity that drives most oncology involvement; nodal or distant metastasis carries a materially worse prognosis than localised disease
Immune checkpoint inhibitors have transformed outcomes for locally advanced/metastatic SCC and BCC that would previously have had very limited systemic options
A history of one keratinocyte cancer predicts further lesions - ongoing dermatological surveillance is part of long-term management regardless of initial treatment modality

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