TextbookDermatologyBasal Cell Carcinoma

Basal Cell Carcinoma

The most common skin cancer in the UK, arising from basal keratinocytes. Locally invasive but almost never metastasises. Strongly associated with cumulative UV exposure. Managed per NICE NG12 suspected cancer pathway with 2-week wait referral.

Key Facts

Most common skin cancer: accounts for ~75% of all non-melanoma skin cancers in the UK Incidence: ~150,000 new cases/year in the UK; rising due to UV exposure and ageing population UV radiation: strongest risk factor — cumulative lifetime exposure, sunburn history Nodular BCC: most common subtype (~60%) — pearly, rolled edge, telangiectasia, central ulceration Superficial BCC: flat, scaly, erythematous plaque — often on trunk; may mimic eczema or Bowen's disease Morphoeic (sclerosing) BCC: waxy, scar-like, ill-defined margins — highest recurrence risk Metastasis rate: <0.05% — locally destructive but extremely rarely metastatic NICE NG12: 2-week wait referral for suspected skin cancer — any non-healing skin lesion with typical features

Overview

Key Facts

BCC is the most common malignancy in humans globally. It is slow-growing, locally invasive, and has an excellent prognosis with appropriate treatment. The incidence is rising significantly, particularly in older populations with fair skin.

Epidemiology

  • ~150,000 new cases/year in UK
  • M:F ratio ~1.5:1
  • Incidence increases with age; peak >70 years
  • Most common on sun-exposed sites: head and neck (80%), particularly nose
  • Rare in individuals with Fitzpatrick skin types V–VI
  • Increasing incidence: ~3–5% per year

Aetiology

  • UV radiation: cumulative exposure is the dominant risk factor
  • Fair skin (Fitzpatrick types I–II), red/blonde hair, blue eyes
  • Immunosuppression: organ transplant recipients have 10× increased risk
  • Gorlin syndrome (basal cell naevus syndrome): PTCH1 gene mutation — multiple BCCs from young age
  • Previous BCC: 30–50% risk of further BCC within 5 years
  • Ionising radiation: previous radiotherapy to skin
  • Arsenic exposure: historical occupational risk

Pathophysiology

  • Arises from basal layer keratinocytes or hair follicle stem cells
  • Key pathway: Hedgehog signalling pathway — mutations in PTCH1 (tumour suppressor) or SMO (oncogene)
  • Loss of PTCH1 function → constitutive activation of Hedgehog pathway → uncontrolled proliferation
  • Slow growth, local tissue invasion, rarely metastasises due to stromal dependence

Clinical Presentation

Nodular BCC (60%)

  • Pearly/translucent papule or nodule
  • Rolled, raised border with telangiectasia
  • Central ulceration ('rodent ulcer') — may bleed and crust
  • Most common on face, especially nose

Superficial BCC (25%)

  • Flat, erythematous, scaly plaque with a thin pearly border
  • Often on trunk (back, shoulders)
  • May be multifocal
  • Can mimic eczema, psoriasis, or Bowen's disease

Morphoeic (Sclerosing) BCC (5–10%)

  • Waxy, scar-like, white/yellow plaque
  • Ill-defined margins — often larger than clinically apparent
  • May be depressed relative to surrounding skin
  • Highest recurrence rate after treatment

Pigmented BCC

  • Contains melanin — appears brown/black
  • Can mimic melanoma clinically
  • More common in darker skin types

Red Flags

  • Rapid growth (consider SCC or melanoma)
  • Perineural invasion: pain, paraesthesia, cranial nerve palsies
  • Orbital invasion: visual changes, proptosis
  • Large neglected tumours (>2 cm) on high-risk sites (nose, periorbital, ear)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Squamous cell carcinomaKeratinised, scaly nodule; may be tender; faster growthBiopsy
Melanoma (amelanotic or pigmented BCC)Irregular border, colour variation, ABCDE criteriaExcision biopsy, dermoscopy
Bowen's disease (SCC in situ)Well-demarcated erythematous scaly plaquePunch biopsy
Actinic keratosisRough, scaly patch on sun-exposed skinClinical, biopsy if uncertain
Sebaceous hyperplasiaYellow papule with central dell; no ulcerationClinical
Intradermal naevusDome-shaped, flesh-coloured papule; no ulcerationDermoscopy

Diagnosis / Investigation

Bedside

  • Dermoscopy: arborising (tree-like) vessels, blue-grey ovoid nests, leaf-like areas, ulceration; absence of pigment network
  • Clinical photography: baseline documentation

Biopsy

  • Punch biopsy (3–4 mm): confirms diagnosis and subtype — essential before non-surgical treatment
  • Excision biopsy: small lesions — diagnostic and therapeutic
  • Incisional biopsy: large lesions where subtype determination guides management

Imaging

  • CT/MRI: only if deep tissue invasion suspected (periorbital, perineural)
  • Not routinely required for standard BCC

Special Tests

  • Mohs micrographic surgery mapping: for high-risk sites — complete margin assessment
  • Genetic testing: if Gorlin syndrome suspected (young patient, multiple BCCs)

Management

Non-Pharmacological

  • Sun protection: SPF 30+, protective clothing, avoidance of peak UV hours
  • Patient education: self-examination for new lesions; 30–50% risk of second BCC
  • Surveillance: follow-up for high-risk subtypes and immunosuppressed patients

Surgical (Mainstay of Treatment)

  • Surgical excision: first-line for most BCCs
    • Low-risk: 4 mm peripheral margin
    • High-risk (morphoeic, recurrent, large): wider margins or Mohs
  • Mohs micrographic surgery: gold standard for high-risk sites (periorbital, nasal, periauricular) — complete margin assessment with tissue conservation; cure rate >99%
  • Curettage and cautery: suitable for small, well-defined, low-risk nodular/superficial BCCs on trunk/limbs; not for morphoeic or high-risk sites

Pharmacological

  • Topical imiquimod 5% cream: for superficial BCC — apply 5 nights/week for 6 weeks; stimulates local immune response via TLR7
  • Topical 5-fluorouracil (5-FU) 5% cream: for superficial BCC — apply BD for 3–4 weeks
  • Photodynamic therapy (PDT): methylaminolaevulinate (MAL) cream + red light — for superficial and thin nodular BCC; good cosmetic outcome
  • Vismodegib 150 mg OD (Hedgehog pathway inhibitor): for locally advanced or metastatic BCC not suitable for surgery/radiotherapy — NICE TA489

Radiotherapy

  • Alternative for elderly patients or those unfit for surgery
  • Useful for difficult anatomical sites
  • Not first-line in young patients (risk of secondary malignancy, poor long-term cosmesis)

Referral Criteria

  • NICE NG12: 2-week wait referral for suspected skin cancer
  • All suspected BCCs should be referred to dermatology or plastic surgery
  • Mohs surgery referral: periorbital, periauricular, nasal, morphoeic, recurrent

Prognosis

  • Excellent prognosis overall: 5-year cure rate >95% with appropriate treatment
  • Mohs surgery: >99% cure rate for primary BCC
  • Recurrence rates: excision 2–5%, curettage 5–10%, morphoeic subtype 10–15% higher
  • Metastasis: <0.05% — extremely rare
  • 30–50% risk of developing a further BCC within 5 years
  • Gorlin syndrome: lifelong risk of multiple BCCs
  • Mortality attributable to BCC is very rare — almost exclusively from neglected large tumours with local invasion

Other Relevant Information

BCC Subtype Comparison

SubtypeFrequencyAppearanceRiskTreatment
Nodular60%Pearly papule, telangiectasiaLow–moderateExcision, Mohs
Superficial25%Erythematous plaque, thin borderLowImiquimod, PDT, excision
Morphoeic5–10%Waxy scar-like, ill-definedHighMohs, wide excision
Pigmented<5%Brown/black noduleLow–moderateExcision (exclude melanoma)

Gorlin Syndrome (Basal Cell Naevus Syndrome)

FeatureDetail
GenePTCH1 (chromosome 9q22)
InheritanceAutosomal dominant
Key featuresMultiple BCCs, odontogenic keratocysts, skeletal anomalies, calcified falx cerebri
ManagementLifelong dermatology surveillance, Mohs surgery, vismodegib