Basal Cell Carcinoma (BCC)
Summary
Basal Cell Carcinoma (BCC) is the most common skin cancer and the most common malignancy in humans overall. It arises from basal keratinocytes in the epidermis and is almost always caused by cumulative UV sun exposure. BCC is locally invasive but, crucially, almost NEVER metastasises (<0.1%). This makes it highly curable if detected and treated appropriately. However, if neglected, BCC can cause significant local destruction ("rodent ulcer"), particularly on the face. Management depends on subtype, location, and patient factors, ranging from simple excision to Mohs micrographic surgery for high-risk lesions.
Key Facts
- Commonest Cancer: ~75% of all skin cancers. ~150,000/year in UK.
- Metastasis Rate: <0.1%. Cure is the norm.
- Cause: Cumulative UV exposure (UVB primarily).
- Classic Appearance: Pearly/translucent nodule with rolled edge, telangiectasia. +/- Central ulceration (Rodent Ulcer).
- Subtypes: Nodular (most common), Superficial, Morphoeic/Infiltrative (aggressive).
- Treatment: Surgical excision (4mm margin standard). Mohs surgery for high-risk sites. Topical/ablative for superficial.
- Key Guideline: NICE CSG8 / BAD Guidelines on Skin Cancer.
Clinical Pearls
"The H-Zone": The central face (around Eyes, Nose, Lips, Ears, Temples) is high-risk. BCCs here require careful management (often Mohs) due to complex anatomy and risk of incomplete excision.
"If it bleeds, crusts, and never heals": This is the classic patient description of a BCC. Any skin lesion that repeatedly crusts and bleeds without fully healing should raise suspicion.
Morphoeic = Malignant Scar: The morphoeic subtype looks like a scar (flat, white, waxy). It has indistinct borders and is often much larger subclinically than it appears. Always think of it if a "scar" appears without a history of trauma.
Hedgehog Pathway: BCC is driven by aberrant activation of the Hedgehog signalling pathway (PTCH1, SMO genes). This is the target for oral drugs like Vismodegib in advanced BCC.
Why This Matters Clinically
While BCC is rarely life-threatening, it is incredibly common. Every clinician will encounter it. Recognising the subtypes and understanding which lesions need specialist referral (vs. GP excision) is essential. Inappropriate management of morphoeic or H-zone BCCs can lead to incomplete excision and recurrence, requiring more complex surgery later.
Incidence & Prevalence
- UK Incidence: ~150,000 new cases per year.
- Australia: Highest incidence globally (>1000 per 100,000).
- Lifetime Risk (UK): ~1 in 5-6 for fair-skinned individuals.
- Trend: Incidence is rising (ageing population, sun exposure habits).
Demographics
| Factor | Association |
|---|---|
| Age | Risk increases with age. Peak 60-80 years. Can occur younger in sun-seekers. |
| Sex | Historically Male > Female (occupational exposure). Now equalising. |
| Skin Type | Fitzpatrick I-II (Fair skin, burns easily) highest risk. Rare in dark skin. |
| Location | Sun-Exposed Sites: Face (80%), especially nose. Trunk (Superficial BCC). |
Risk Factors
| Risk Factor | Notes |
|---|---|
| Cumulative UV Exposure (UVB) | Primary cause. Lifelong sun exposure. |
| Sunburn History | Especially childhood burns. |
| Fair Skin (Fitzpatrick I-II) | Poor melanin protection. |
| Immunosuppression | Organ transplant recipients: 10-16x increased risk. |
| Previous BCC | 30-50% chance of another BCC within 5 years. |
| Genetic Syndromes | Gorlin Syndrome (Naevoid BCC Syndrome) – PTCH1 mutation. Multiple BCCs. |
| Ionising Radiation | History of radiotherapy. |
| Arsenic Exposure | Historical risk (drinking water). |
UV Damage & Hedgehog Pathway
The molecular driver of BCC.
- UVB Radiation: Causes direct DNA damage (pyrimidine dimers).
- Failed Repair: Accumulated mutations in tumour suppressor genes.
- PTCH1 Mutation: PTCH1 normally inhibits SMO (Smoothened) in the Hedgehog (Hh) pathway.
- Inactivating mutation in PTCH1 -> SMO is constitutively active.
- Activated Hh pathway -> Uncontrolled basal cell proliferation.
- p53 Mutation: Common. Contributes to tumour progression.
Key Genes
| Gene | Role |
|---|---|
| PTCH1 | Tumour suppressor. Gatekeeper of Hedgehog pathway. Mutated in ~90% of sporadic BCCs. |
| SMO (Smoothened) | Oncogene when activated. Target for Vismodegib. |
| p53 | Tumour suppressor. Mutated in >0% of BCCs. |
| GLI1/GLI2 | Transcription factors activated downstream. Drive proliferation. |
Gorlin Syndrome (Naevoid BCC Syndrome)
Autosomal Dominant. PTCH1 germline mutation.
- Features:
- Multiple BCCs (often >100 by adulthood).
- Odontogenic Keratocysts (jaw cysts).
- Palmar/Plantar Pits.
- Skeletal abnormalities (Rib bifurcation, macrocephaly).
- Calcification of Falx Cerebri.
- Medulloblastoma risk.
- Management: Careful sun avoidance. Regular skin surveillance. Vismodegib may be needed.
Classic BCC Appearance
"The Pearly Pink Pimple that never heals."
| Feature | Description |
|---|---|
| Translucent/Pearly Surface | Hallmark. Shiny, waxy appearance. |
| Rolled Edge | Raised, rounded border. |
| Telangiectasia | Fine, branching blood vessels visible on surface. |
| Central Ulceration | "Rodent Ulcer". Crusted, bleeding. |
| Slow Growth | Months to years. |
BCC Subtypes
| Subtype | Prevalence | Appearance | Behaviour |
|---|---|---|---|
| Nodular | ~60% | Classic pearly nodule. Telangiectasia. Central ulceration. | Most common. Well-defined. |
| Superficial | ~25% | Flat, red, scaly plaque. Often on trunk. Thin, pink, erosion. | Least aggressive. Often multiple. |
| Morphoeic / Infiltrative | ~10% | Pale, waxy, scar-like. Indistinct borders. Firm. | Most Aggressive. Subclinical spread. Difficult to excise. |
| Pigmented | <5% | Nodular or superficial with brown/black pigment. | Can mimic Melanoma. |
| Basosquamous | Rare | Mixed BCC and SCC features. | Higher recurrence/metastasis risk. |
High-Risk Features
| Feature | Why High-Risk |
|---|---|
| Location in H-Zone | Central face – complex anatomy, cosmetic importance, higher recurrence. |
| Size >cm | Indicates longer duration, higher recurrence risk. |
| Morphoeic/Infiltrative Subtype | Indistinct borders, subclinical spread. |
| Recurrent BCC | Previous incomplete excision. More aggressive behaviour. |
| Perineural Invasion | On histology. Risk of spread along nerves. |
| Immunosuppression | More aggressive BCCs in transplant patients. |
Dermoscopy Findings
| Feature | Description |
|---|---|
| Arborising (Tree-like) Vessels | Branching telangiectasia. Highly specific for BCC. |
| Leaf-Like Structures | Brown/grey pigment. In pigmented BCC. |
| Blue-Grey Ovoid Nests | Pigment clusters. |
| Spoke-Wheel Areas | Pigment spokes radiating from centre. |
| Ulceration | Surface disruption. |
| Shiny White Structures / Blotches | Seen with polarised dermoscopy. |
| Absence of Pigment Network | Differentiates from benign naevi and Melanoma (which have a network). |
Differential Diagnosis
| Condition | Distinguishing Feature |
|---|---|
| Intradermal Naevus | Flesh-coloured papule. Softer. No telangiectasia/ulceration. |
| Sebaceous Hyperplasia | Yellow papules. Central dell. No rolled edge. |
| Molluscum Contagiosum | Multiple, umbilicated. Paediatric. |
| Keratoacanthoma | Rapid growth. Central keratin plug. May regress. |
| SCC | More keratinised, crusty. Faster growing. Tender. |
| Melanoma (Nodular) | For pigmented BCC. Dermoscopy differentiates. |
| Fibrous Papule (Nose) | Small, firm, dome-shaped. No telangiectasia. |
BCC is a clinical and histological diagnosis.
Diagnosis
| Investigation | Purpose |
|---|---|
| Clinical Examination | Standard. Dermoscopy aids accuracy. |
| Dermoscopy | Increases diagnostic accuracy. Identifies subtype features. |
| Biopsy | Confirms diagnosis. Identifies subtype. Punch or Shave. |
| Excision Biopsy | Diagnostic AND therapeutic for small, well-defined lesions. |
Imaging (Rarely Needed)
| Indication | Investigation |
|---|---|
| Suspected Perineural Invasion | MRI |
| Suspected Bone Invasion | CT |
| Gorlin Syndrome Workup | CT Brain (Falx calcification), OPG (Jaw cysts). |
Management Algorithm (NICE / BAD)
┌─────────────────────────────────────────────────────────────────────┐
│ BCC DIAGNOSED │
├─────────────────────────────────────────────────────────────────────┤
│ │
│ STEP 1: Assess Risk │
│ ├── Low Risk: Small (<2cm), Non-H-Zone, Nodular/Superficial. │
│ └── High Risk: H-Zone, Morphoeic, Recurrent, >2cm, Immunosuppr. │
│ │
│ STEP 2: Select Treatment │
│ │
│ LOW RISK (Nodular): │
│ └── Standard Surgical Excision (4mm margin). │
│ │
│ LOW RISK (Superficial): │
│ ├── Curettage & Cautery (C&C). │
│ ├── Topical Imiquimod (5 days/week x 6 weeks). │
│ ├── Topical 5-FU (Fluorouracil). │
│ ├── Photodynamic Therapy (PDT). │
│ └── Cryotherapy. │
│ │
│ HIGH RISK: │
│ ├── Refer to Specialist (Dermatology / Plastics). │
│ ├── Mohs Micrographic Surgery (H-Zone, Morphoeic, Recurrent). │
│ └── Excision with Wider Margins (if Mohs not available). │
│ │
│ LOCALLY ADVANCED / INOPERABLE: │
│ ├── Radiotherapy. │
│ └── Hedgehog Inhibitors (Vismodegib / Sonidegib). │
│ │
└─────────────────────────────────────────────────────────────────────┘
After excising the BCC, we are left with a defect. The "Reconstructive Ladder" applies.
- Secondary Intention (Heal by itself). Good for concave surfaces (inner canthus, conchal bowl). Poor for convex surfaces (nose tip).
- Direct Closure. Ellipse. Orientation along Relaxed Skin Tension Lines (RSTLs).
- Skin Graft. Full Thickness (FTSG) preferred for face (better colour match). Donor: Pre/Post-auricular, Supraclavicular.
- Local Flaps. The workhorse of facial reconstruction.
Common Facial Flaps
- Transposition Flaps: The Bilobed Flap (Zitelli).
- Indication: Distal nose defect <1.5cm.
- Concept: Borrow skin from the lax upper nose to fill the tight lower nose.
- Advancement Flaps: The cheek advancement.
- Indication: Large cheek defects.
- Rotation Flaps: The Rieger Flap (Dorsal Nasal Flap).
- Indication: Large dorsal nasal defects.
- Interpolation Flaps: The Paramedian Forehead Flap.
- Indication: Large defects of the nasal tip/ala (>1.5cm).
- Concept: Forehead skin is the best match for nose skin. Requires 2 stages (pedicle division at 3 weeks).
The H-Zone Danger
- Reconstruction vs Surveillance:
- Using a flap hides the deep margin.
- If your excision wasn't complete, you have buried the tumour under a flap.
- Rule: Never put a flap over a high-risk tumour unless margins are confirmed clear (Frozen section or Mohs).
- If no frozen section available, use a Skin Graft or Secondary Intention first.
Mohs Micrographic Surgery (The Process)
- Debulking: Visible tumour removed.
- Layer 1: A thin disc of tissue (1-2mm) is removed including the whole margin.
- Mapping: Tissue is cut into quadrants, colour-coded, and mapped to a diagram.
- Freezing: Tissue froze and sectioned horizontally (en face).
- Microscopy: Surgeon examines 100% of the peripheral and deep margin.
- Targeted Re-excision: If tumour found at "3 o'clock", surgeon goes back ONLY to 3 o'clock.
- Reconstruction: Once clear, the hole is repaired.
Surgical Excision
| Feature | Standard Excision |
|---|---|
| Margin | 4mm peripheral margin. Clear deep margin to fat/fascia. |
| Cure Rate | ~95% for primary, well-defined BCC. |
| Indication | Most nodular BCCs outside H-Zone. |
Mohs Micrographic Surgery
The gold standard for high-risk BCC.
| Feature | Details |
|---|---|
| Principle | Excise in thin layers. Map and examine 100% of the margin intraoperatively. Continue until margins clear. |
| Advantage | Tissue-sparing. Highest cure rate (99%). |
| Indication | H-Zone (Nose, Eyes, Ears, Lips). Morphoeic. Recurrent. Large BCCs. Where tissue preservation is critical. |
| Availability | Specialist centres. Not universally available. |
Topical Treatments (Superficial BCC only)
| Treatment | Regimen | Notes |
|---|---|---|
| Imiquimod 5% (Aldara) | 5 times per week x 6 weeks. | Immune modulator. Inflammatory response – warn patient. |
| 5-Fluorouracil (5-FU / Efudix) | Twice daily x 4-6 weeks. | Anti-metabolite. Erosion, crusting expected. |
| Photodynamic Therapy (PDT) | In-clinic. Photosensitiser + Light. | Good cosmesis. Lower cure rate than excision. |
Curettage & Cautery (C&C)
- Indication: Small, low-risk, superficial or nodular BCCs.
- Technique: Scrape tumour with curette, cauterise base. Repeat 2-3 times.
- Cure Rate: ~90% for appropriate lesions.
- Cosmesis: Leaves flat, hypopigmented scar.
Hedgehog Pathway Inhibitors
| Drug | Target | Indication |
|---|---|---|
| Vismodegib | SMO Inhibitor | Locally advanced BCC (inoperable). Metastatic BCC (rare). Gorlin Syndrome. |
| Sonidegib | SMO Inhibitor | Second-line. |
| Side Effects | Muscle cramps, alopecia, taste disturbance, weight loss. Often limit tolerability. |
The Hedgehog Pathway (Deep Dive)
The discovery of the Hedgehog (Hh) pathway revolutionised our understanding of BCC.
- Normal State:
- PTCH1 (Patched) is the receptor. It inhibits SMO (Smoothened).
- With SMO inhibited, the pathway is OFF. No cell division.
- Ligand Binding:
- Sonic Hedgehog (SHH) ligand binds to PTCH1.
- Binding stops PTCH1 from inhibiting SMO.
- SMO becomes active -> Activates GLI transcription factors -> Cell Division.
- In BCC:
- Mutation: PTCH1 is broken (loss of function).
- It cannot inhibit SMO.
- SMO is permanently ON.
- Cell divides uncontrollably.
- Treatment: Vismodegib binds to SMO and turns it off. It is a "SMO Inhibitor".
Adnexal Tumours (The Mimics)
BCC arises from the "folliculo-sebaceous-apocrine germ". Many benign tumours also arrive here and look like BCCs.
- Trichoepithelioma: Benign hair follicle tumour. Flesh coloured papules on nasolabial folds. Multiple in "Brooke-Spiegler Syndrome". Can look exactly like BCC histologically (but no retraction artefact).
- Sebaceous Hyperplasia: Yellowish papules with central dell. "Mature" sebocytes. Benign.
- Microcystic Adnexal Carcinoma (MAC): Very dangerous. Looks like a benign lump but invades nerves aggressively. Needs Mohs.
Facial surgery leaves scars. A poor scar can be devastating.
The Process of Maturation
- 0-6 Weeks: Red, lumpy, immature. Sutures out at day 5-7 to prevent "railroading".
- 6 Weeks - 6 Months: Scar remodels. Collagen aligns.
- 12-18 Months: Final maturation (Pale, flat).
Interventions
- Silicone Gel/Sheets: Gold standard. Hydrates the scar, reduces fibroblast activity.
- Massage: Breaking down adhesions. Desensitisation.
- Sun Protection: Fresh scars hyper-pigment permanently if sunburnt. Factor 50 is mandatory for 1 year.
- Steroid Injection (Triamcinolone): For hypertrophic/keloid scars.
The SINS Trial (Surgery vs Imiquimod for Nodular & Superficial)
- Findings: Surgery is superior to Imiquimod.
- Recurrence: 2% (Surgery) vs 17% (Imiquimod) at 5 years.
- Cosmesis: Better in Imiquimod group.
- Conclusion: Trade-off. If you want a cure -> Surgery. If you want no scar and accept risk -> Cream.
The M-BCC Study (Morphoeic BCC)
- Confirmed that morphoeic BCCs extend subclinically far beyond visible margins.
- Standard 4mm excision often inadequate.
- Mohs recommended.
(As per original - restored)
What is a BCC?
A Basal Cell Carcinoma (BCC) is a type of skin cancer. It's the most common type and is almost always caused by sun damage over many years. The good news is that BCCs almost never spread to other parts of the body. They grow slowly and are very treatable.
What does it look like?
Often a shiny, pearly lump or a sore that won't heal. It may crust, bleed, and then seem to get a bit better, but never fully heals.
How is it treated?
Usually, it is removed with a small operation under local anaesthetic. For BCCs in difficult areas (like around the eyes or nose), a specialist surgery called Mohs can be used to make sure all the cancer is removed while saving as much healthy skin as possible.
Will it come back?
If completely removed, it is unlikely to come back at the same spot. However, having one BCC means you are at higher risk of getting another somewhere else on your skin in the future.
How can I prevent more?
- Sun protection: Sunscreen (SPF 30+), hats, protective clothing.
- Regular skin checks: Check your skin and see your GP if you notice any new or changing spots.
(As per original)
- NICE Improving Outcomes Guidance (CSG8)
- British Association of Dermatologists Guidelines
- Sekulic A, et al. Efficacy and safety of vismodegib. N Engl J Med. 2012.
- Rowe DE, et al. Mohs surgery is the treatment of choice. J Dermatol Surg Oncol. 1989.
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. If you have a skin lesion you are concerned about, please see a healthcare professional.