Basal cell carcinoma

Meet the patient

A 68-year-old farmer has had a "pimple" on the side of his nose for a year. It never quite heals, bleeds every time he shaves, and lately the centre has ulcerated while the edge has grown pearly and raised with tiny blood vessels running across it. He has spent his life outdoors, burns easily, and has the weathered, wrinkled skin of chronic sun damage.^[1]

That single lesion contains every question a fellowship examiner will ask about BCC: what is it (the pearly papule with arborising telangiectases), where is it (the nose is the heart of the high-risk H-zone), and what do you do about it (the answer is Mohs, not a 4 mm excision). Hold those three questions and the whole topic organises itself.^[1]

The numbers you meet this cancer by

^[1]

BCC is the commonest cancer we make. In fair-skinned populations it accounts for roughly one in two of all cancers; the Australian lifetime risk approaches one in three. The one number examiners love to trap you with is the metastasis rate — under 0.1 percent — which is why BCC is a disease of local destruction, not distant spread.^[1][5]

What BCC is — a local destroyer, almost never a spreader

BCC is a malignant epidermal tumour of basal keratinocytes (or follicular outer-root-sheath cells) — locally invasive and destructive, but rarely metastasising. The morbidity is not from distant disease; it is from the tumour burrowing into the eye, nose or ear of an elderly patient over years of neglect. And it is the prototype of pathway-defined oncogenesis — the first human cancer in which a developmental signalling cascade (Hedgehog) was drugged to clinical effect.^[1][4]

Subtype drives behaviour and management — learn the growth patterns because the histology report, not the clinical photograph, decides whether you excise or send for Mohs:^[2][4]

The face-off that earns marks — split every BCC into low-risk versus high-risk at the bedside, because the fork decides the operation:^[2][4]

^[1]

How common, who, and why the sun

Cumulative ultraviolet damage on fair skin is the engine of BCC. Incidence keeps rising as populations age and accumulate UV; men slightly outnumber women and the median age at diagnosis is around 65, though BCC is increasingly seen under 50 — particularly women, a legacy of indoor tanning.^[1][5]

The risk-factor list, grouped so it stays:^[4]

• Fair skin / Fitzpatrick I–II, red or blonde hair, blue or green eyes, freckling — the strongest host factor; phototype V–VI skin carries about a tenth of the incidence.
• Cumulative UV — chronic and intermittent (childhood sunburn), plus PUVA for psoriasis; UV-B drives the TP53 signature mutation and chronic UV-A leaves the PTCH1 footprint.
• Outdoor occupation and latitude — equator, elevation, farming and sailing all add risk.
• Indoor tanning — beds before age 35 raise risk by roughly 70 percent.
• Prior skin cancer — one BCC predicts about a 50 percent chance of a second within five years.
• Chronic arsenic — well water, smelting, pesticides; multiple BCCs on sun-exposed and sun-protected skin.
• Ionising radiation — childhood tinea-capitis radiotherapy, atomic-bomb survivors, radiographers.
• Immunosuppression — transplant recipients (3–10 times the baseline BCC risk), chronic lymphocytic leukaemia, HIV, long-term azathioprine or ciclosporin.
• Inherited syndromes — Gorlin (germline PTCH1), xeroderma pigmentosum, oculocutaneous albinism, Rombo, Bazex-Dupré-Christol, cartilage-hair hypoplasia, Muir-Torre.
• Chronic ulcers, burn scars, vaccination scars, trauma — rare substrates for BCC. ^[1]

The classic trap: everyone remembers that SCC dominates in transplant recipients, and so concludes BCC is not their problem. It is — the SCC:BCC ratio inverts, but the absolute BCC burden is still high. Examine the whole skin and treat each tumour on its own risk profile.^[4][5]

Morbidity is local, not metastatic. Metastasis is virtually confined to long-neglected tumours over 10 cm or the basosquamous subtype; node, then lung, then bone. The real harm is local invasion — periorbital disease ending in exenteration, alar destruction, auricular cartilage loss.^[5]

The Hedgehog pathway — the one mechanism worth a paragraph

BCC is the paradigm of a single druggable pathway. In normal skin the PTCH1 receptor holds SMO (Smoothened) in check; Hedgehog ligand lifts that brake. In BCC the brake is cut — PTCH1 loss in about 70 percent, or an activating SMO mutation in 10 percent — so SMO fires without ligand, driving GLI1 and GLI2 transcription factors into the nucleus and switching on basaloid proliferation.^[4][5]

The rest of the molecular story sits on top of that one pathway:^[4][5]

• TP53 in about 50 percent, carrying the UV-signature C to T (or CC to TT) transition at dipyrimidine sites — the footprint of UV-B and a founding lesion of UV-driven skin cancer.
• Secondary drivers — MYCN, CDKN2A, NOTCH1/2, PTPN14, KMT2D, TP63 shape behaviour in aggressive subtypes; MMPs and PDGFRα sustain the desmoplastic stroma of morpheaform disease.
• Field cancerisation — chronic UV seeds multiple TP53/PTCH1 clones across clinically normal skin, which is why one BCC heralds many.
• The pathway is the drug target — vismodegib and sonidegib block SMO for locally advanced or metastatic disease, and shrink tumour burden in Gorlin syndrome.^[5]

^[1]

Somatic versus germline: most BCCs are sporadic somatic PTCH1 loss on a UV-damaged background. A small but vital minority carry germline PTCH1 (Gorlin) or SUFU — hundreds of BCCs from childhood. The pathway is identical; only the inheritance shifts the burden from a sporadic tumour to an autosomal-dominant syndrome.^[1]

Etymology for viva gold: the rodent ulcer earned its name in the nineteenth century because it looks as though a rat has been gnawing at the skin — central destruction, raised rolled edge, relentless local erosion. The image outlived the rat.^[4]

Meet the subtypes — recognise the face, predict the behaviour

The clinical picture is governed by subtype, site and chronicity. Walk through each face in turn.^[1]

Nodular BCC (about 60 percent — the one you will see weekly) is a pearly, translucent papule with a rolled, well-defined border, prominent arborising telangiectases crossing the surface, and a central crust or ulcer — the rodent ulcer, Jacob's ulcer when on the eyelid. It sits on the nose, nasolabial fold, cheek, lower eyelid, ear or temple, grows over months to years, and bleeds with minor trauma.^[2]

Superficial BCC (15–30 percent) is a flat, scaly, well-demarcated erythematous patch with a thread-like pearly border and focal erosions, on trunk and limbs. The trap: it mimics eczema, psoriasis or Bowen's disease, but it does not respond to topical steroids and its border is sharper than eczema ever is.^[1]

Morpheaform or sclerosing BCC (5–10 percent) is the deceiver — an ill-defined white or skin-coloured scar-like indurated plaque with subtle telangiectases, on the central face. Clinically quiet, histologically infiltrative, it is the highest-recurrence subtype and is repeatedly under-treated because no one appreciated the true margins.^[1]

Pigmented BCC is a pearly nodule carrying dark brown or black pigment — a near-perfect mimic of nodular melanoma until the dermatoscope separates them.^[1]

Basosquamous (metatypical) BCC shows both BCC and SCC features — keratinisation, intercellular bridges — ulcerates early, behaves aggressively, and carries the highest metastatic potential of all the subtypes.^[1]

Micronodular and infiltrative BCC are clinically subtle and often missed; histology shows small nests (under 0.15 mm) or thin strands with little palisading. Both confer high recurrence and mandate Mohs.^[1]

The H-zone — Mohs territory: periocular, perinasal and nasal ala, periauricular, ear, scalp and temple — the central mask area of the face where recurrence after standard excision runs three to five times the trunk rate.^[1]

Natural history. BCC is asymptomatic or non-tender, slow-growing over months to years, occasionally bleeds on shaving (the first clue in many an elderly man), and rarely hurts unless perineural involvement is present — a red flag in morpheaform or infiltrative H-zone disease.^[1]

The mimics — and the one discriminator that separates each

The discriminator line: arborising telangiectases plus a pearly rolled border is BCC until dermoscopy or biopsy says otherwise. Sebaceous hyperplasia is the closest nodular mimic — but its telangiectasia sits in a central umbilication, where BCC's vessels arborise across the surface.^[1]

Dermoscopy — the bedside diagnostic workhorse

In experienced hands dermoscopy is over 95 percent accurate for nodular BCC and about 85 percent for superficial BCC — and it maps the clinical margins before you ever cut. The presence of any one classic feature is highly suggestive:^[3]

• Arborising (tree-like) telangiectases — sharply focused, branching, large-calibre vessels crossing the lesion; the single most specific sign.
• Blue-grey ovoid nests — large well-circumscribed bluish-grey ovals, tumour nests in the dermis.
• Multiple blue-grey globules — smaller, round, well-circumscribed.
• Leaf-like areas — maple-leaf peripheral pigment of pigmented tumour nests.
• Spoke-wheel areas — radial pigment around a central hub; highly specific.
• Blue-white-veil-like areas — overlap with melanoma; absence of a true pigment network plus arborising vessels favours BCC.
• Ulceration — non-pigmented epidermal loss with adherent crust.
• Shiny white-red structureless areas — collagen and tumour stroma.
• Short fine telangiectases — the superficial-BCC variant. ^[1]

Subtype-specific patterns. Nodular: arborising vessels plus ovoid nests plus ulceration. Superficial: shiny white-red structureless zones, erosions, short fine telangiectases and surface scale — its overlap with Bowen's and psoriasis is the principal pitfall, and the absence of glomerular vessels helps exclude SCC in situ. Pigmented: combined pigment plus the BCC-specific vascular and ulceration features — separation from melanoma rests on arborising vessels, leaf-like and spoke-wheel areas rather than atypical network and blue-white veil. Morpheaform: scarce specific features, fibrosis, white structureless areas — dermoscopy under-reads the margins, and Mohs is justified by histology.^[1]

Histopathology — the report that drives the risk label

Histology is the diagnostic gold standard and the basis of the high-risk label. The cardinal architecture is basaloid tumour islands of small hyperchromatic cells with scant cytoplasm, anchored by three features:^[4][5]

• Peripheral palisading — columnar nuclei aligned like fence posts at the edge of each island, the diagnostic architecture.
• Retraction artefact (clefting) — a cleft between island and stroma holding basophilic mucin; a fixation artefact that helps the pathologist.
• Stromal-epithelial interaction — fibromyxoid mucinous stroma, turning desmoplastic in morpheaform disease.
• Mitoses and apoptotic bodies are common, but bizarre pleomorphism is unusual — one feature separating BCC from SCC. ^[1]

Aggressive-subtype histology — the basis of the high-risk BCC label:^[4]

• Infiltrative — narrow, angulated strands and cords with little palisading.
• Micronodular — small nests (under 0.15 mm) dispersed in fibrous stroma.
• Morpheaform / sclerosing — compressed nests and cords in dense desmoplastic stroma; the most clinically deceptive.
• Basosquamous (metatypical) — keratinisation and SCC-like architecture within basaloid nests; behaves like SCC. ^[1]

Immunohistochemistry sorts the difficult case: BerEP4 positive in BCC and negative in SCC and trichoepithelioma; EMA negative in BCC, often positive in SCC; Bcl-2 diffusely positive; CD10 stromal. PHLDA1 and CK20 (Merkel cells) separate trichoepithelioma (preserved Merkel cells, PHLDA1 positive) from BCC (lost Merkel cells, PHLDA1 negative).^[1]

Perineural invasion — tumour tracking along small nerves — is a high-risk feature demanding Mohs with or without adjuvant radiotherapy.^[1]

The bedside round — map the lesion to the H-zone

Examination has two jobs: confirm the lesion and decide whether it is high-risk. Run it in this order:^[1]

• Full skin examination — BCC patients carry a high rate of second primaries; never biopsy one spot and miss three others.
• Dermoscopy of every suspect lesion, then measure and photograph before biopsy.
• Map the lesion relative to the H-zone — periocular, perinasal, periauricular, ear, scalp, temple — because that single observation drives the Mohs decision.
• Palpate for induration, tethering, fixation and regional nodes (nodal disease is rare but must be sought).
• Assess for high-risk features at the bedside.
• Take a focused history — duration, growth rate, prior treatment, immunosuppression, syndromic features, prior radiotherapy, occupational exposures. ^[1]

Investigations — biopsy to confirm, image only when advanced

• Biopsy is the diagnostic standard. A shave into mid-reticular dermis suffices for most nodular or superficial BCC on trunk and limbs; a 2–4 mm punch is preferred for H-zone or morpheaform lesions to catch deep infiltration; an excisional biopsy can be both diagnostic and therapeutic for a small primary. Partial biopsies under-call morpheaform or infiltrative foci — a reason to re-biopsy if the clinical picture and the histology disagree.^[2]
• Imaging — CT or MRI is reserved for advanced disease with deep invasion, perineural involvement, or staging of locally advanced BCC being considered for a Hedgehog inhibitor; nodal ultrasound for clinically involved nodes.
• Genetic testing — germline PTCH1 or SUFU sequencing when Gorlin syndrome is suspected (multiple childhood BCCs, jaw keratocysts, palmar or plantar pits, falx calcification, family history).
• Gene-expression profiling (40-GEP, Castle Biosciences) — an adjunct for an ambiguous periocular lesion with conflicting histology. ^[1]

High-risk features and staging — the list that picks Mohs

BCC rarely needs formal AJCC staging, but the high-risk feature set is the cornerstone of risk-stratified care — it decides Mohs and predicts recurrence.^[1][4]

Consensus high-risk clinical features:^[1]

• High-risk site (the H-zone): central face, periocular, perinasal, nasal ala, periauricular, ear, scalp, temple; periorbital skin, vermilion border and genitalia are added in many guidelines.
• Size: over 2 cm on trunk or limbs, over 1 cm on the face or H-zone.
• Aggressive histology: morpheaform or sclerosing, infiltrative, micronodular, basosquamous.
• Recurrent tumour or prior incomplete excision.
• Immunosuppression — transplant, leukaemia, HIV, long-term immunosuppressants.
• Prior radiotherapy at the site — altered lymphatics and wound-healing.
• Ill-defined clinical margins — morpheaform and infiltrative subtypes extend invisibly.
• Perineural invasion — clinical (paraesthesia, formication, facial nerve palsy) or histologic.
• Patient factors — young age at first BCC (greater lifetime burden), inability to tolerate surgery, comorbidity precluding excision. ^[1]

AJCC 8th edition (for the record): T1 is under 2 cm with fewer than two high-risk features; T2 is under 2 cm with two or more, or 2 cm and over with fewer than two; T3 adds size over 4 cm, minor bone erosion or perineural invasion; T4 is cortical bone, marrow or skull-base invasion. Stages I–II are localised; III–IV are locally advanced; distant nodal, bone or lung disease is stage IV — rare, and the indication for a Hedgehog inhibitor or immunotherapy.^[1]

Surgery — first-line and definitive in over 95 percent

Surgery is first-line and cures over 95 percent of primary BCCs. The operation is chosen entirely from the risk profile.^[1][2]

• Standard excision with 4-5 mm clinical margins for low-risk nodular BCC on trunk or limbs (extend to 6–10 mm for larger or less-defined lesions); histology confirms complete excision and the 5-year cure exceeds 95 percent.
• Mohs micrographic surgery — the gold standard for high-risk BCC — for the H-zone, morpheaform, infiltrative, micronodular and basosquamous subtypes, recurrent BCC, lesions over 2 cm, immunosuppressed patients, ill-defined margins, perineural invasion, and young patients needing tissue conservation (eyelid, digit, genital). Mohs maps 100 percent of the margin in horizontal frozen sections and re-excises tumour-positive areas layer by layer, achieving 97–99 percent 5-year cure with maximal tissue conservation.
• Curettage and electrodessication (EDC) for selected low-risk nodular BCC under 1 cm on trunk or limbs in low-risk patients — three cycles, accepting a 5–15 percent recurrence and inferior cosmesis; not for terminal-hair-bearing areas (BCC tracks down follicles) or the H-zone.
• Positive or involved margins — re-excise (or Mohs if H-zone or high-risk histology); adjuvant radiotherapy where re-excision is impractical.
• Sentinel lymph node biopsy is not routine; reserve it for advanced disease with nodal suspicion. ^[1]

The classic trap: a 4-5 mm excision on the central face. The H-zone is Mohs territory precisely because the standard margin under-cuts the invisible infiltrative edge — you trade a smaller scar today for a recurrence next year.^[1]

Topical, photodynamic and physical therapy — for the low-risk superficial lesion

For low-risk superficial BCC (and selected small nodular BCC in low-risk patients), tissue-sparing options are first-line:^[1]

• Topical imiquimod 5 percent — five applications a week for six weeks; a TLR7 agonist; 75–85 percent 5-year clearance for superficial BCC. Expect inflammation; not first-line for nodular, infiltrative or H-zone disease.
• Topical 5-fluorouracil (5-FU) 5 percent — twice daily for 2–4 weeks; about 60–70 percent clearance for superficial BCC.
• Photodynamic therapy (PDT) — aminolaevulinic acid (ALA) or methyl aminolaevulinate (MAL) with red-light activation; 75–85 percent clearance, ideal for multiple superficial lesions and large field disease where cosmesis matters.
• Cryotherapy — single or double freeze-thaw for small superficial BCC in low-risk sites; hypopigmentation is the cosmetic cost.
• Combination or sequential therapy — PDT plus imiquimod, or curettage plus imiquimod, improves clearance; field therapy of actinic damage adds value. ^[1]

Radiotherapy — when surgery cannot or must not

• Primary radiotherapy for patients unfit for or refusing surgery — particularly the elderly with large or inoperable facial tumours where surgery would be mutilating.^[2]
• Adjuvant radiotherapy for high-risk, incompletely excised BCC where re-excision is not feasible; 5-year local control approaches 90 percent with thorough debulking.
• Absolute contraindication — Gorlin syndrome and xeroderma pigmentosum: ionising radiation induces new BCCs along the field portal. Never irradiate a DNA-repair-deficient patient.^[5] Young patients (under 60) carry an unfavourable lifetime second-cancer risk, and re-irradiation is limited by cumulative dose.
• Modalities — orthovoltage, megavoltage electrons (preferred for superficial lesions), or interstitial brachytherapy for selected periocular or nasal lesions. ^[1]

Advanced and systemic disease — Hedgehog inhibitors first, then anti-PD-1

Hedgehog pathway (SMO) inhibitors are the first systemic option for locally advanced, unresectable or metastatic BCC:^[5]

• Vismodegib (Erivedge) — 150 mg orally once daily.^[7] In the ERIVANCE study, independent-review objective response was 43 percent for locally advanced and 30 percent for metastatic BCC; the final update reported investigator-assessed response of 60.3 percent (locally advanced) and 48.5 percent (metastatic), median duration of response 26.2 and 14.8 months.^[8] In the real-world STEVIE trial (1215 patients), median treatment duration was 8.6 months; muscle spasm, alopecia, dysgeusia and weight loss are the class signature, and serious adverse events occurred in 23.8 percent.^[7]
• Sonidegib (Odomzo) — 200 mg orally once daily.^[9] In the 42-month BOLT analysis, central-review objective response was 56 percent in locally advanced and 8 percent in metastatic BCC; muscle spasm, alopecia and dysgeusia are the shared class toxicity, and the drug is teratogenic.^[9]
• Mechanism and resistance — both block SMO and prevent GLI activation.^[5] Resistance runs through acquired SMO mutations (the D473H guard-serine change is the canonical example), GLI2 amplification or parallel-pathway upregulation; intrinsic resistance to vismodegib was 6.1 percent in one laBCC cohort, with HIPPO-YAP and WNT hyperactivation in the resistant tumours.^[10] Intermittent schedules achieve similar efficacy with better tolerability, so they are a practical answer to class toxicity.^[1][6]

Immunotherapy — anti-PD-1:^[1]

• Cemiplimab (Libtayo) — approved (2021) for locally advanced or metastatic BCC progressing on, or intolerant of, a Hedgehog inhibitor. In the phase 2 trial after HHI therapy, independent-review objective response was 31 percent (95 percent CI 21–42) of 84 patients, with five complete responses.^[11]
• Pembrolizumab — promising activity; combined with vismodegib under study. ^[1]

Tumour reduction before surgery — neoadjuvant HHI therapy followed by surgery is under active study; the aim is less complex surgery and more tissue preservation when upfront excision would be mutilating. Phase I/II trials are ongoing, so this stays an investigational sequence.^[12]

Special populations — Gorlin is the one you must never miss

Gorlin (nevoid basal cell carcinoma) syndrome (NBCCS) is autosomal-dominant germline PTCH1 (chromosome 9q22.3) — or rarely SUFU — producing hundreds of BCCs from childhood. The associated features are the syndrome's signature: odontogenic keratocysts of the jaw, palmar and plantar pits, bifid or fused ribs, calcification of the falx cerebri, macrocephaly with frontal bossing, childhood medulloblastoma (desmoplastic subtype), and ovarian or cardiac fibromas. Diagnosis is clinical (Evans criteria), confirmed by PTCH1 sequencing. Management is aggressive sun protection from infancy, field therapy of actinic damage, excision of symptomatic BCCs, absolute avoidance of radiotherapy, and consideration of vismodegib for tumour-burden reduction within a multidisciplinary team.^[5]

^[1]

Xeroderma pigmentosum (autosomal-recessive nucleotide-excision-repair defect) brings BCC, SCC and melanoma within the first decade of life — management is rigorous sun avoidance, field treatment of actinic keratoses with 5-FU or imiquimod, excision of individual tumours (Mohs for recurrent or high-risk sites), and oral isotretinoin or acitretin chemoprevention when the tumour load demands it.^[13] Oculocutaneous albinism lacks melanin photoprotection; BCC and SCC arrive in early adulthood.^[1] In kidney-transplant recipients with prior nonmelanoma skin cancer, a randomised trial found conversion from a calcineurin inhibitor to sirolimus lowered the rate of new lesions (1.31 versus 2.48 per patient-year), while a systematic review of transplant prevention strategies overall concluded that evidence remains limited.^[14] In pregnancy BCC is uncommon but should be excised under local anaesthesia; imiquimod and PDT are avoided and radiotherapy is not used.^[1]

Prognosis and surveillance — excellent locally, lifelong for new primaries

• Low-risk BCC has an excellent prognosis — surgical cure over 95 percent at 5 years; Mohs approaches 99 percent for high-risk disease.^[1]
• Local recurrence is the principal concern, highest in H-zone, morpheaform, infiltrative, micronodular, basosquamous, recurrent, over-2 cm, immunosuppressed and incompletely excised lesions.
• Metastasis is rare (under 0.1 percent): node, then lung, then bone; basosquamous carries the highest metastatic potential, and metastatic disease remains guarded despite SMO inhibitors and cemiplimab.
• Lifelong surveillance — one BCC predicts about a 50 percent risk of another within 5 years. Annual full-skin examination (more often if syndromic or immunosuppressed), sun protection, field therapy of actinic damage, and education to re-present urgently for bleeding, ulceration, growth or new lesions. ^[1]

Evidence, guidelines and the regional differences

The European interdisciplinary consensus-based guideline 2023 (Peris) is the most current multiprofessional document and integrates the Hedgehog-inhibitor indications.^[1] North American practice is anchored by the NCCN and AAD, UK by the BAD, and the very high Australian incidence by Cancer Council Australia.^[4][5]

Controversies to name calmly: Mohs versus standard excision for high-risk primary BCC — micrographically controlled surgery is guideline-recommended for high-risk and recurrent lesions, but head-to-head survival data are lacking.^[1] The optimal duration and dosing of Hedgehog inhibitors are unsettled; intermittent schedules are one answer under study.^[6] Cemiplimab sits second-line after HHI failure or intolerance.^[11] And chemoprevention: oral nicotinamide 500 mg twice daily reduced new nonmelanoma skin cancers by 23 percent over 12 months in high-risk adults (ONTRAC); the separate BCC reduction of 20 percent had a confidence interval crossing unity, and trial evidence in transplant recipients shows no certain benefit.^[15][14]

Prevention — sun, field, and self-examination

• Sun protection — broad-spectrum SPF 30-plus, UPF-rated clothing, wide-brimmed hat, sunglasses, shade from 10 am to 4 pm; avoid indoor tanning.^[4]
• Field therapy of actinic damage — imiquimod, 5-FU or PDT to sun-damaged skin to cut the burden of future keratinocyte cancers; in a cohort study, topical 5-FU for actinic keratoses was associated with a lower risk of subsequent keratinocyte carcinoma than imiquimod, and field treatment is the primary preventive strategy in transplant recipients.^[17][14]
• Gorlin, XP and albinism — regular dermatologic examination and strict sun protection from early childhood, radiation avoidance, and HHI for heavy tumour burden.^[16][13]
• Chemoprevention — nicotinamide 500 mg twice daily reduced new skin cancers over 12 months in high-risk immunocompetent adults (ONTRAC); in transplant recipients the evidence is uncertain and no clear benefit is established.^[15][14]
• Self-examination education — teach ABCDE for melanoma and the pearly, scaly, bleeding, non-healing features for BCC, with urgent re-presentation thresholds. ^[1]

The mantra

The mantra: pearly papule, arborising vessels, rolled border — biopsy it, and if it is on the H-zone or an aggressive subtype, send it to Mohs; never irradiate Gorlin.^[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the farmer's nose (answer)ShowHide

The 68-year-old farmer with a pearly, ulcerated, telangiectatic papule on the side of his nose that bleeds on shaving. What is it, and what is the management? Model: This is classic nodular BCC — the pearly papule, rolled border, arborising telangiectases and central ulceration (rodent ulcer) on a sun-exposed site. Confirm with dermoscopy and a biopsy that captures subtype. The nose is the heart of the H-zone, so the management is Mohs micrographic surgery, not a 4-5 mm excision — Mohs gives 97–99 percent 5-year cure with maximal tissue conservation where standard margins would under-cut the invisible infiltrative edge and risk recurrence.^[1]

Stem 2 — the scaly patch that won't clear (answer)ShowHide

A 72-year-old woman has had a scaly pink patch on her back treated as eczema with a topical steroid for three months. It has not improved and the border is unusually sharp. What is the diagnosis and the trap? Model: This is superficial BCC — the flat scaly erythematous patch with a thread-like pearly border on the trunk. The trap is treating it as eczema: superficial BCC does not respond to topical steroids, and its border is sharper than eczema ever is. Confirm with dermoscopy (shiny white-red structureless zones, erosions, short fine telangiectases, and no glomerular vessels to suggest Bowen's) and biopsy. Because it is low-risk, superficial and on the trunk, it is a candidate for topical imiquimod, 5-FU or PDT rather than excision.^[1]

Stem 3 — the child with hundreds of BCCs (answer)ShowHide

A 14-year-old is referred with dozens of BCCs since age 8, a cystic swelling of the jaw, and tiny pits on the palms. What syndrome is this, what is the gene, and what treatment is absolutely contraindicated? Model: This is Gorlin (nevoid basal cell carcinoma) syndrome — autosomal-dominant germline PTCH1 (or rarely SUFU) loss, producing hundreds of BCCs from childhood alongside odontogenic jaw keratocysts, palmar and plantar pits, bifid ribs and falx calcification. The absolute contraindication is radiotherapy — ionising radiation induces new BCCs along the field portal in a DNA-repair-deficient patient. Manage with aggressive sun protection, excision of symptomatic lesions, field therapy, and a Hedgehog inhibitor (vismodegib) for tumour-burden reduction within an MDT.^[5]

^[1]

References17ShowHide

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3. [3]Reiter O, Mimouni I, Dusza S, et al. Dermoscopic features of basal cell carcinoma and its subtypes: A systematic review J Am Acad Dermatol, 2021.PMID 31706938
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7. [7]Basset-Séguin N, Hauschild A, Kunstfeld R, et al. Vismodegib in patients with advanced basal cell carcinoma: Primary analysis of STEVIE, an international, open-label trial Eur J Cancer, 2017.PMID 29073584
8. [8]Sekulic A, Migden MR, Basset-Seguin N, et al. Long-term safety and efficacy of vismodegib in patients with advanced basal cell carcinoma: final update of the pivotal ERIVANCE BCC study BMC Cancer, 2017.PMID 28511673
9. [9]Dummer R, Guminksi A, Gutzmer R, et al. Long-term efficacy and safety of sonidegib in patients with advanced basal cell carcinoma: 42-month analysis of the phase II randomized, double-blind BOLT study Br J Dermatol, 2020.PMID 31545507
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11. [11]Stratigos AJ, Sekulic A, Peris K, et al. Cemiplimab in locally advanced basal cell carcinoma after hedgehog inhibitor therapy: an open-label, multi-centre, single-arm, phase 2 trial Lancet Oncol, 2021.PMID 34000246
12. [12]Paradisi A, Mannino M, Brunetti F, et al. Advanced Basal Cell Carcinoma: A Narrative Review on Current Systemic Treatments and the Neoadjuvant Approach J Pers Med, 2025.PMID 40559089
13. [13]Kraemer KH, DiGiovanna JJ, Tamura D Xeroderma Pigmentosum GeneReviews, 1993.PMID 20301571
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