Skin Cancer

Basal Cell Carcinoma

Basal cell carcinoma (BCC) is the commonest human malignancy and the most frequent keratinocyte cancer. It is a locally invasive, slow-growing tumour derived from basal keratinocytes or follicular germinative cells. Metastasis is exceptionally rare, reported in approximately 0.0028–0.55% of cases, but morbidity arises from destructive local invasion, particularly on the face, periorbital region, nose, ear and scalp. For MRCP, BCC is best conceptualised as a tumour of cumulative ultraviolet exposure, impaired DNA repair and Hedgehog pathway activation.

Pathogenesis and Risk Factors

Ultraviolet B radiation induces characteristic C→T and CC→TT pyrimidine dimer mutations, particularly in tumour suppressor genes. The central molecular abnormality is constitutive activation of the Sonic Hedgehog pathway. Inactivating mutations in PTCH1 release inhibition of SMO, leading to GLI-mediated transcription and proliferation. PTCH1 mutations occur in most sporadic BCCs; activating SMO mutations are also recognised. Germline PTCH1 mutation causes Gorlin–Goltz syndrome with multiple early-onset BCCs, odontogenic keratocysts, palmar pits, falx calcification and skeletal anomalies.

• Major risk factors: fair skin, red/blond hair, blue eyes, inability to tan, chronic or intermittent intense UV exposure, sunbed use, increasing age, male sex and previous BCC.
• Iatrogenic risks: immunosuppression after solid-organ transplantation, prior radiotherapy, PUVA therapy and long-term arsenic exposure.
• Genodermatoses: Gorlin syndrome, xeroderma pigmentosum, Bazex–Dupré–Christol syndrome and albinism.

Clinical Subtypes

Subtype	Typical appearance	Clinical significance
Nodular BCC	Pearly papule or nodule with rolled translucent edge, surface telangiectasia and possible central ulceration	Commonest subtype; classically on head and neck
Superficial BCC	Well-demarcated erythematous scaly plaque, often multiple, commonly trunk/limbs	May mimic eczema, psoriasis or Bowen disease; suitable for topical therapy if low risk
Morphoeic/infiltrative BCC	Scar-like, waxy, indurated plaque with poorly defined margins	High-risk; subclinical extension common; Mohs surgery often preferred
Pigmented BCC	Brown/black papule or plaque with pearly edge/telangiectasia	Important melanoma mimic; dermoscopy aids diagnosis
Basosquamous carcinoma	Features of BCC and SCC	More aggressive; higher recurrence and metastatic potential than conventional BCC

Histology and Diagnosis

Histology shows nests of basaloid cells with peripheral palisading, stromal retraction artefact and mucinous stroma. Aggressive histological patterns include infiltrative, micronodular, morphoeic and basosquamous subtypes. Diagnosis is usually clinical plus dermoscopic, confirmed by biopsy when morphology is atypical, lesion is high risk, nonsurgical therapy is planned, or diagnosis is uncertain. Dermoscopy typically demonstrates arborising vessels, blue-grey ovoid nests, maple-leaf-like areas, spoke-wheel structures and ulceration; pigment network is absent, helping distinguish pigmented BCC from melanocytic lesions.

Risk Stratification and Staging Concepts

Formal AJCC staging is rarely clinically useful because nodal and distant spread are exceptional. Management is driven by risk of incomplete excision and recurrence. UK and European guidance stratify lesions by site, size, borders, histology, recurrence and host factors.

Low-risk BCC	High-risk BCC
Primary, well-defined, nodular or superficial lesion	Recurrent tumour or incompletely excised tumour
Trunk/limbs, generally <2 cm	High-risk sites: central face, eyelids, nose, lips, ears, scalp, genitalia, hands/feet
Non-aggressive histology	Morphoeic, infiltrative, micronodular or basosquamous histology
Immunocompetent patient	Immunosuppression, prior radiotherapy, genetic cancer syndrome
Clearly defined clinical margins	Poorly defined margins, perineural invasion, large size, deep fixation

Management

Treatment aims for histological clearance with optimal functional and cosmetic outcome. Surgical excision is standard for most BCCs. For low-risk lesions, a 4 mm clinical margin achieves approximately 95% complete excision. High-risk lesions usually require wider margins, commonly ≥5 mm, or Mohs micrographic surgery, particularly on the “H-zone” of the face or for recurrent, morphoeic or poorly defined tumours. Mohs provides complete peripheral and deep margin assessment and has the lowest recurrence rates; 5-year recurrence is typically ~1% for primary BCC and ~5–6% for recurrent BCC, lower than standard excision in high-risk facial disease.

Treatment	Typical use	Key points
Curettage and cautery	Small, low-risk, well-defined BCCs on trunk/limbs	Operator-dependent; avoid high-risk facial sites and aggressive histology
Topical imiquimod 5%	Superficial BCC, selected small low-risk lesions	Applied usually 5 times weekly for 6 weeks; immune response modifier via TLR7; inflammation predicts response
Topical 5-fluorouracil 5%	Superficial BCC only	Usually twice daily for 3–6 weeks; thymidylate synthase inhibition; less effective for nodular disease
Photodynamic therapy	Superficial and thin nodular BCC	Methyl aminolevulinate or aminolevulinic acid plus red light; good cosmesis but higher recurrence than surgery
Radiotherapy	Older or inoperable patients, difficult surgical sites	Avoid in Gorlin syndrome; risk of chronic radiodermatitis and secondary tumours

Advanced Disease and Hedgehog Inhibitors

For locally advanced or metastatic BCC unsuitable for surgery or radiotherapy, systemic Hedgehog inhibition is indicated. Vismodegib is given 150 mg orally once daily; sonidegib is given 200 mg orally once daily. Both inhibit SMO. Important toxicities include muscle cramps, dysgeusia, alopecia, weight loss, fatigue, nausea and elevated creatine kinase, especially with sonidegib. They are teratogenic; effective contraception is mandatory. In the ERIVANCE BCC study, vismodegib achieved objective response rates of approximately 43% in locally advanced and 30% in metastatic BCC by independent review. Sonidegib demonstrated response rates around 56% in locally advanced BCC in BOLT. Resistance may occur via SMO mutation or downstream pathway activation.

Follow-up and Prognosis

Prognosis is excellent after complete treatment, but patients have a high risk of additional keratinocyte cancers. A previous BCC confers a substantially increased risk of subsequent BCC, especially within the first 3–5 years. Follow-up intensity is tailored to risk: single low-risk completely excised BCC may require discharge with education, whereas multiple, recurrent, high-risk, immunosuppressed or syndromic patients require periodic dermatological surveillance. Examination should include the entire sun-exposed skin surface, assessment of surgical scars for recurrence and reinforcement of ultraviolet avoidance and self-examination.

Squamous Cell Carcinoma

Pathogenesis and epidemiological context

Cutaneous squamous cell carcinoma (cSCC) is a malignant proliferation of epidermal keratinocytes with capacity for local tissue destruction, perineural spread, nodal metastasis and disease-specific mortality. It is the second commonest keratinocyte cancer after basal cell carcinoma, but accounts for most non-melanoma skin cancer deaths. Pathogenesis is dominated by cumulative ultraviolet exposure, particularly UVB-induced cyclobutane pyrimidine dimers producing characteristic TP53 mutations; additional recurrent alterations include NOTCH1/2, CDKN2A, RAS and TERT promoter mutations. Important non-UV drivers include ionising radiation, chronic inflammation, scars and ulcers, arsenic exposure, HPV-associated anogenital/digital SCC, and profound immunosuppression.

Solid-organ transplant recipients have an approximately 65–250-fold increased risk of cSCC, with more aggressive behaviour, multiplicity and a reversal of the usual BCC:SCC ratio. Azathioprine promotes UVA photosensitisation; calcineurin inhibitors impair tumour immune surveillance, whereas sirolimus/everolimus may reduce subsequent cSCC burden in selected transplant recipients, albeit with tolerability limitations.

Clinical phenotypes and precursor lesions

Typical cSCC presents as a rapidly enlarging, indurated, hyperkeratotic papule, plaque, nodule or ulcer on chronically sun-exposed skin, especially scalp, face, dorsal hands, forearms, lower lip and pinna. Pain, paraesthesia, fixation, bleeding, recurrent crusting or ulceration are concerning. Keratoacanthoma is a crateriform, rapidly growing, well-differentiated SCC-like tumour; because distinction from invasive SCC is unreliable clinically and histologically on partial sampling, it is usually excised.

• Actinic keratosis: intraepidermal atypia on sun-damaged skin; per-lesion annual progression risk is low, often quoted around 0.025–0.6%, but field cancerisation confers cumulative risk.
• Bowen disease: SCC in situ, sharply demarcated erythematous scaly plaque; progression to invasive SCC is approximately 3–5%.
• Erythroplasia of Queyrat: penile mucosal SCC in situ with a higher invasive potential than typical extragenital Bowen disease.

Histology, staging and prognostic stratification

Diagnosis requires histological confirmation, ideally by excision biopsy for small lesions or deep punch/incisional biopsy including dermis and subcutis for larger lesions. Superficial shave biopsy may underestimate invasion, differentiation and perineural invasion. Histology assesses degree of differentiation, depth/thickness, desmoplasia, lymphovascular invasion, perineural invasion and margin status.

High-risk feature	Exam-relevant significance
Diameter ≥2 cm, or ≥1 cm on cheek/forehead/scalp/neck/pretibia, or ≥6 mm on mask areas, genitalia, hands/feet	Higher recurrence and nodal metastasis; influences excision margin and referral urgency
Depth >6 mm or invasion beyond subcutaneous fat	Key AJCC8/BWH adverse criterion
Poor differentiation, desmoplastic or acantholytic subtype	Increased metastatic risk
Perineural invasion, especially nerve calibre ≥0.1 mm, named nerve or clinical neurological symptoms	Indication for imaging discussion and often adjuvant radiotherapy
Ear, lip, genitalia; recurrent tumour; immunosuppression; chronic scar/ulcer	Disproportionately aggressive biology

Overall metastatic risk for primary cSCC is approximately 2–5%, but exceeds 10–20% in high-risk groups, particularly lower lip, ear, immunosuppressed patients and tumours with perineural invasion. AJCC 8th edition applies mainly to head and neck cSCC: T1 <2 cm; T2 2–4 cm; T3 ≥4 cm, minor bone erosion, perineural invasion or deep invasion; T4 denotes gross cortical/marrow bone or skull base/axial skeleton involvement. The Brigham and Women’s Hospital system is often more prognostic: risk factors are diameter ≥2 cm, poor differentiation, perineural invasion and invasion beyond subcutaneous fat; T1 has 0, T2a has 1, T2b has 2–3, and T3 has 4 risk factors or bone invasion.

Management

Definitive treatment is surgical where feasible. Low-risk invasive cSCC is treated by standard excision with 4–6 mm clinical margins to the level of subcutaneous fat, aiming for complete histological clearance. High-risk tumours generally require wider margins, commonly 6–10 mm or more, or margin-controlled surgery. Mohs micrographic surgery is preferred for high-risk facial sites, recurrent tumours, poorly defined borders, perineural invasion risk, tissue-sparing indications and immunosuppressed patients. Clinically suspicious nodes require ultrasound-guided fine-needle aspiration or core biopsy; routine sentinel lymph node biopsy is not universally recommended because evidence of survival benefit is lacking.

Radiotherapy is appropriate for non-surgical candidates, selected anatomically difficult tumours, positive margins not amenable to re-excision, extensive perineural invasion, or nodal disease after lymphadenectomy. Typical definitive schedules are around 55 Gy in 20 fractions or 60–66 Gy in 30–33 fractions, adapted to site, size and patient fitness. Adjuvant radiotherapy is considered for involved margins, named-nerve perineural invasion, recurrent high-risk disease and extracapsular nodal extension.

Setting	Treatment options
SCC in situ/Bowen disease	Excision, curettage and cautery, cryotherapy, photodynamic therapy; topical 5-fluorouracil 5% once or twice daily for about 4 weeks, or imiquimod 5% typically 3–5 times weekly for 6–16 weeks depending on regimen
Localised invasive low-risk cSCC	Excision with 4–6 mm margins; curettage alone generally avoided for invasive or high-risk lesions
High-risk/recurrent cSCC	Mohs or wide excision; consider imaging, nodal assessment and multidisciplinary review
Locally advanced/metastatic unresectable cSCC	PD-1 blockade: cemiplimab 350 mg IV every 3 weeks; pembrolizumab 200 mg IV every 3 weeks or 400 mg every 6 weeks

PD-1 inhibitors are now central for unresectable locally advanced or metastatic cSCC. In EMPOWER-CSCC-1, cemiplimab produced objective response rates of approximately 44–50%, with durable responses in many responders. Pembrolizumab showed response rates around 34–50% in KEYNOTE-629 cohorts. Immune-related toxicities include colitis, pneumonitis, hepatitis, endocrinopathies and nephritis; transplant recipients risk graft rejection, making decisions highly individualised. EGFR inhibition, such as cetuximab, is a less preferred option when immunotherapy is contraindicated.

Melanoma

Cutaneous melanoma is a malignant tumour of melanocytes with disproportionate mortality relative to incidence because of early lymphovascular and haematogenous dissemination. The key exam concept is that Breslow thickness, ulceration and nodal status dominate prognosis; surface diameter or cosmetic appearance is less important than vertical invasion.

Pathogenesis and risk factors

Melanoma arises through accumulated ultraviolet-induced DNA damage, particularly intermittent intense exposure and blistering childhood sunburn. UVB causes cyclobutane pyrimidine dimers; UVA contributes oxidative DNA injury. High-risk phenotypes include Fitzpatrick I–II skin, red/blond hair, freckling, numerous common naevi, atypical naevi, prior melanoma, family history, immunosuppression and inherited syndromes such as CDKN2A mutation. Molecularly, common driver alterations include BRAF V600E/K mutations in approximately 40–50% of cutaneous melanomas, NRAS mutations in 15–25%, and KIT mutations particularly in acral and mucosal melanoma.

Clinical subtypes

Subtype	Typical features	Exam points
Superficial spreading melanoma	Most common; irregular pigmented macule/plaque with radial growth	Often associated with intermittent sun exposure and pre-existing naevus
Nodular melanoma	Rapidly enlarging blue-black, pink or amelanotic nodule; early vertical growth	May not satisfy ABCDE; remember “EFG”: elevated, firm, growing
Lentigo maligna melanoma	Chronically sun-damaged elderly face; irregular macule evolving over years	In situ phase is lentigo maligna; invasive disease once dermal invasion occurs
Acral lentiginous melanoma	Palms, soles, subungual sites; more common in darker skin	Subungual melanoma may cause longitudinal melanonychia, Hutchinson sign
Amelanotic melanoma	Pink/red lesion, often vascular or ulcerated	Diagnostic delay common; consider in any changing non-healing lesion

Assessment and diagnosis

Suspicious lesions are assessed using the ABCDE criteria: asymmetry, border irregularity, colour variegation, diameter usually >6 mm, and evolution. “Evolution” is the most sensitive clinical discriminator. Dermoscopy may show atypical pigment network, irregular streaks, blue-white veil, regression structures, atypical dots/globules and polymorphous vessels. In the UK, the NICE 7-point checklist scores major features—change in size, irregular shape, irregular colour—as 2 points each, and minor features—diameter ≥7 mm, inflammation, oozing/crusting, altered sensation—as 1 point each; a score ≥3 warrants urgent suspected cancer referral.

The diagnostic procedure is complete excision biopsy with a narrow 1–3 mm clinical margin, oriented to permit subsequent definitive excision. Incisional or punch biopsy is reserved for very large lesions or cosmetically sensitive sites when complete excision is impractical, but partial sampling risks underestimating Breslow thickness. Histology reports must include Breslow thickness in mm, ulceration, mitotic rate, margin status, microsatellites, lymphovascular invasion and regression where relevant. Clark level is now largely historical except occasionally for very thin lesions when Breslow data are limited.

Staging and prognosis

AJCC 8th edition staging is based on tumour thickness and ulceration, nodal disease and metastases. T1 is ≤1.0 mm; T1a is <0.8 mm without ulceration, while T1b is 0.8–1.0 mm or <0.8 mm with ulceration. T2 is 1.01–2.0 mm, T3 2.01–4.0 mm and T4 >4.0 mm, each subdivided by ulceration. Sentinel lymph node biopsy is generally discussed for melanomas >1.0 mm and considered for 0.8–1.0 mm or thinner ulcerated/high-risk tumours; it is primarily prognostic, although it refines eligibility for adjuvant systemic therapy. Five-year melanoma-specific survival is approximately >95% for stage IA, 80–90% for stage II, 40–75% for stage III depending on nodal burden, and historically <25% for stage IV, though modern immunotherapy has substantially improved outcomes.

Definitive management

Breslow thickness	Recommended wide local excision margin
Melanoma in situ	5 mm clinical margin, often wider for lentigo maligna if margins indistinct
≤1.0 mm	1 cm
1.01–2.0 mm	1–2 cm depending on site and MDT decision
>2.0 mm	2 cm

Routine elective lymph node dissection is not indicated after a positive sentinel node in many patients. The MSLT-II trial showed no melanoma-specific survival benefit from immediate completion lymph node dissection compared with ultrasound surveillance, although regional control improved. Imaging is stage-dependent: early thin melanoma does not require routine CT/PET, whereas stage IIB–IV disease often undergoes cross-sectional staging and brain imaging according to local protocols.

Systemic therapy

Immune checkpoint inhibition and targeted therapy are central in advanced or high-risk resected melanoma. Anti-PD-1 therapy with nivolumab 240 mg IV every 2 weeks or 480 mg every 4 weeks, or pembrolizumab 200 mg IV every 3 weeks or 400 mg every 6 weeks, improves recurrence-free survival in stage III and selected stage IIB/IIC disease. Toxicities are immune-mediated: dermatitis, colitis, hepatitis, endocrinopathies including hypophysitis and thyroiditis, pneumonitis and nephritis; management ranges from treatment interruption to prednisolone 0.5–1 mg/kg/day for grade ≥2–3 toxicity.

Combination CTLA-4/PD-1 blockade, e.g. ipilimumab 3 mg/kg plus nivolumab 1 mg/kg IV every 3 weeks for 4 doses followed by nivolumab maintenance, yields higher response rates but substantially greater grade 3–4 toxicity. CheckMate 067 demonstrated durable survival benefit in metastatic melanoma, with 6.5-year overall survival around 49% for nivolumab–ipilimumab versus 42% for nivolumab and 23% for ipilimumab alone. For BRAF V600-mutant disease, BRAF/MEK combinations such as dabrafenib 150 mg orally twice daily plus trametinib 2 mg once daily, or encorafenib/binimetinib, produce rapid responses; fever, rash, cardiomyopathy, ocular toxicity and secondary cutaneous neoplasms are relevant adverse effects. The COMBI-AD trial established adjuvant dabrafenib/trametinib benefit in resected stage III BRAF-mutant melanoma.

Follow-up focuses on detection of recurrence and new primary melanoma, as survivors have increased risk of subsequent melanomas. Patients should be counselled on monthly self-examination, sun protection, avoidance of sunbeds and prompt review of evolving lesions.

Benign Pigmented Lesions

Benign pigmented lesions are common mimics of melanoma and are therefore high-yield in MRCP: the key task is to recognise reassuring morphology while identifying lesions requiring urgent assessment. Pigmentation may arise from increased melanocyte number, increased melanin production, melanin incontinence, vascular or keratinocytic lesions containing pigment, or exogenous pigment. Clinical assessment should integrate history of change, patient risk factors, lesion morphology and, where available, dermoscopy. In UK practice, NICE recommends urgent suspected cancer referral for a pigmented lesion with a weighted 7-point checklist score ≥3, or if dermoscopy suggests melanoma.

Melanocytic naevi

Acquired melanocytic naevi are benign clonal proliferations of melanocytes driven commonly by activating mutations in BRAF V600E or NRAS, followed by oncogene-induced senescence mediated through p16INK4A. They typically appear in childhood and adolescence, increase until the third decade, and involute with age. A high naevus count is itself a melanoma risk marker: approximately >50 common naevi or >5 atypical naevi substantially increases risk, and exam questions often use this as a risk-stratification clue rather than as evidence of malignant change in a single lesion.

Lesion	Typical features	Key examination points
Junctional naevus	Flat, uniformly brown macule; melanocytes at dermo-epidermal junction	Common in younger patients; symmetrical pigment network on dermoscopy
Compound naevus	Raised, dome-shaped, brown papule; junctional and dermal nests	May be papillomatous or hair-bearing; symmetry and stability are reassuring
Intradermal naevus	Skin-coloured or lightly pigmented soft papule; dermal melanocytes	Often on face in adults; may lose pigment with age
Blue naevus	Blue-grey papule or nodule due to dermal melanin and Tyndall effect	Usually stable; new or enlarging blue-black nodules require melanoma exclusion
Halo naevus	Naevus surrounded by depigmented halo from immune-mediated melanocyte destruction	Associated with vitiligo; in older adults consider melanoma causing halo phenomenon
Spitz/Reed naevus	Pink, red-brown or black rapidly growing papule, often in children or young adults	Can mimic melanoma histologically; excision is usual in adults or atypical lesions

Congenital melanocytic naevi

Congenital melanocytic naevi are present at birth or arise within the first few months of life and are classified by projected adult size. Small lesions are <1.5 cm, medium 1.5–20 cm, large >20 cm, and giant commonly >40 cm. Melanoma risk correlates with size, axial/paravertebral distribution and multiple satellite naevi. Small and medium congenital naevi carry a low lifetime melanoma risk, often quoted as <1%; large/giant lesions have higher risk, approximately 2–5% in contemporary cohorts, with greatest risk in childhood for very large lesions. Neurocutaneous melanosis is associated with large posterior axial naevi and multiple satellites; MRI brain/spine is considered in high-risk infants, particularly before myelination is complete.

Atypical naevi and dysplastic naevus phenotype

Atypical naevi are benign but clinically irregular lesions, usually >5 mm, with variable pigmentation, indistinct borders and macular components. Histological dysplasia does not equate to melanoma, but atypical naevus burden is a strong risk marker. Familial atypical multiple mole melanoma syndrome is associated with multiple atypical naevi, family history of melanoma and sometimes CDKN2A mutations; pancreatic cancer risk is also increased in some pedigrees. Management is surveillance rather than indiscriminate excision: baseline total body photography and serial digital dermoscopy are used for high-risk patients. A changing solitary lesion should be excised completely with a narrow diagnostic margin rather than sampled by shave biopsy if melanoma is possible.

Lentigines, freckles and other benign pigmented mimics

Ephelides are freckles: small, tan macules induced by ultraviolet exposure, darkening in summer and fading in winter, with increased melanin production but no melanocytic hyperplasia. Solar lentigines are persistent sharply demarcated brown macules on chronically sun-exposed skin, reflecting increased melanocyte number and elongated rete ridges. Lentigo simplex occurs independent of sun exposure and may affect mucosa. Multiple lentigines should prompt syndromic consideration when accompanied by systemic features, for example LEOPARD/Noonan spectrum, Peutz-Jeghers syndrome with perioral lentigines and hamartomatous polyps, or Carney complex.

Seborrhoeic keratoses are benign keratinocytic tumours that may be deeply pigmented and simulate melanoma. Classical features are a “stuck-on”, waxy or verrucous surface, comedo-like openings and milia-like cysts on dermoscopy. Sudden eruption of numerous seborrhoeic keratoses, the Leser-Trélat sign, is classically associated with gastrointestinal adenocarcinoma but has poor specificity and is often overcalled. Dermatofibromas are firm brown papules, commonly on the legs, showing a central dimple when compressed laterally; dermoscopy often shows a central white scar-like area with peripheral pigment network.

Assessment thresholds and management principles

Tool	Criteria	Interpretation
ABCDE	Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolution	Screening heuristic; evolution is the most discriminatory clinical feature
Weighted 7-point checklist	Major: change in size, irregular shape, irregular colour; minor: diameter ≥7 mm, inflammation, oozing/crusting, altered sensation	Major features score 2; minor score 1; urgent referral if total ≥3
Dermoscopy	Benign naevi show symmetry and organised network/globules; melanoma shows atypical network, blue-white veil, irregular dots/globules, pseudopods, atypical vessels	Meta-analyses show dermoscopy improves diagnostic accuracy versus naked-eye examination, with sensitivity commonly around 85–95% in trained users

Benign lesions require reassurance unless symptomatic, cosmetically troublesome, traumatised or diagnostically uncertain. Destructive treatment such as cryotherapy is inappropriate for lesions in which melanoma is in the differential because it prevents histological assessment. Cryotherapy may be used for unequivocal seborrhoeic keratoses or solar lentigines, but pigmented lesions with recent change, asymmetry, irregular pigmentation, bleeding, or a new lesion after age 40 should be assessed with dermoscopy and usually excised or referred. Patient education should emphasise sun protection, self-surveillance every 1–3 months in high-risk individuals, and prompt review of evolving lesions.