Understand the spots and changes on your skin

Melanoma is one of Australia’s most commonly diagnosed cancers. Risk rises with age, but it can occur in younger adults.

UV exposure—especially episodes of sunburn—is the major preventable risk. Fair skin, many or atypical moles, family or personal history, and immune suppression also increase risk. Melanoma can occur on skin with little sun exposure.

Superficial spreading melanoma commonly enlarges across the skin before invading more deeply. Nodular melanoma often presents as a firm, rapidly enlarging lump and may not satisfy the ABCDE rule. Lentigo maligna melanoma usually develops on chronically sun-damaged facial skin in older adults. Acral lentiginous melanoma occurs on palms, soles or beneath nails and is relatively more important in darker skin types. Amelanotic melanoma may be pink, red or skin-coloured.

Melanoma in situ (Stage 0 melanoma) means abnormal melanocytes are confined to the epidermis—the outer layer of skin—and have not invaded the dermis. It often appears as a slowly enlarging, irregular flat patch with uneven colour; lentigo maligna is an in-situ subtype usually found on chronically sun-damaged facial skin. Pathology confirms the diagnosis. Because there is no dermal invasion, Breslow thickness is not assigned and the lesion itself cannot spread to lymph nodes or distant organs. Complete surgical removal is usually curative, commonly with a further margin after the diagnostic biopsy. Large or poorly defined facial lesions may need staged margin-controlled surgery. Untreated lesions can enlarge and some eventually develop an invasive focus, so treatment and ongoing skin surveillance remain important.

Desmoplastic melanoma is a rare invasive melanoma in which malignant spindle-shaped melanocytes lie within dense fibrous tissue. It usually affects older, fair-skinned people on chronically sun-damaged head or neck skin and may arise beneath lentigo maligna. It may look like a firm, pale, pink or scar-like thickening rather than a dark mole, making recognition and partial-biopsy diagnosis difficult. Involvement of small nerves (neurotropism) can cause pain, tingling or numbness and increases concern for local recurrence. Diagnosis requires an adequately deep biopsy and specialist dermatopathology. Wide surgical excision is the main treatment; margin-controlled surgery, radiotherapy and staging investigations are considered according to site, thickness, margins, neurotropism and whether pathology describes a pure or mixed subtype. Management should be planned by an experienced melanoma team.

Melanoma may be a new lesion or a changing existing mole. Warning patterns include asymmetry, an irregular edge, uneven colour, evolution, or a spot unlike the person’s other lesions. Men more often develop melanoma on the trunk and women on the legs, but it can arise anywhere—including scalp, nails, soles, genital skin and rarely the eye or mucosa.

A trained clinician may see an atypical or broadened pigment network, irregular dots or globules, streaks, blue-white structures, regression, asymmetrical structureless areas or atypical blood vessels. No single feature proves melanoma; the complete pattern and clinical history matter.

Atypical or irritated moles, seborrhoeic keratosis, pigmented BCC, dermatofibroma, a blood blister and benign nail pigmentation may resemble melanoma. Conversely, melanoma can look deceptively harmless, so persistent change should be examined rather than matched to photographs.

Assessment includes history, examination of the lesion and surrounding skin, comparison with other moles and usually dermoscopy. When feasible, the entire suspicious lesion is removed with a narrow margin for pathology. The report records features such as melanoma thickness and ulceration. A wider excision is then planned; sentinel lymph-node biopsy and scans are considered only for selected stages.

Surgery is the main treatment for localised melanoma: diagnostic excision is followed by a wider excision based on pathology. Selected patients may be offered sentinel-node biopsy. Higher-risk or advanced melanoma may require specialist immunotherapy, targeted therapy when an actionable mutation is present, radiotherapy in selected situations, or a combination planned by a multidisciplinary team.

Outlook is excellent for many thin, early melanomas. It becomes less favourable once melanoma is thicker or has spread, which is why prompt assessment of change matters.

Follow-up is individualised according to stage and personal risk. It commonly includes scar and lymph-node review, full-skin examinations, self-check education and lifelong sun protection. A previous melanoma increases the chance of another melanoma and other skin cancers.

BCC is the most common skin cancer. It is particularly frequent in Australia and becomes more likely with cumulative UV exposure and age.

Long-term and intermittent UV exposure are major contributors. Fair skin, previous BCC, outdoor work, radiation exposure, immune suppression and some inherited syndromes increase risk.

Nodular BCC is often a pearly or shiny papule with fine surface vessels and may ulcerate. Superficial BCC resembles a slowly enlarging red scaly patch, commonly on the trunk. Infiltrative and morphoeic BCC may be subtle, firm or scar-like with poorly defined extensions. Micronodular and basosquamous patterns can behave more aggressively. Pigmented BCC contains brown, blue or black colour and may mimic melanoma.

BCC commonly develops on the head, neck and other sun-exposed skin, but superficial BCC often occurs on the trunk. It may bleed after minor contact, crust, appear to heal and then return, or slowly enlarge over months or years. Borders can extend beyond what is visible, particularly with infiltrative subtypes.

Typical clues include branching ‘tree-like’ vessels, shiny white-red areas, small erosions or ulceration, blue-grey ovoid nests and leaf-like or spoke-wheel pigmented structures. Superficial lesions may show many fine short vessels. These features guide assessment but pathology confirms the diagnosis when required.

Dermatitis, psoriasis, an irritated seborrhoeic keratosis, scar tissue, a benign mole, sebaceous hyperplasia and melanoma can resemble BCC. A persistent solitary patch or sore deserves assessment even when it causes no symptoms.

A clinician assesses the border, site, size, recurrence status and dermoscopic pattern. A shave, punch or excision biopsy may be used depending on the lesion and proposed treatment. Pathology identifies the subtype and whether tumour reaches the specimen edges; these details help classify the lesion as lower or higher risk.

Choice depends on subtype, size, anatomical site, border definition, whether it has recurred, patient health and the desired balance between cure, function and appearance. Facial ‘H-zone’ lesions, aggressive histology, nerve symptoms, recurrence and poorly defined borders generally require more margin-controlled planning.

Standard excision is common. Mohs micrographic surgery offers staged margin examination for selected high-risk, recurrent or tissue-critical lesions. Curettage with cautery may suit selected low-risk lesions. Topical imiquimod or 5-fluorouracil, photodynamic therapy or cryotherapy may be considered for selected superficial disease; radiotherapy can be useful when surgery is unsuitable. Locally advanced or metastatic BCC needs specialist systemic treatment.

Most BCCs are cured, especially when treated early. Recurrence risk depends on subtype, site, size, borders and previous treatment. People who develop one BCC have a higher chance of developing another.

The wound and pathology result should be reviewed, including whether margins are clear. Ongoing skin checks and self-examination are important because both recurrence and new primary skin cancers can occur. A changing scar, new lump, ulcer or persistent numbness near the site should be reported.

SCC is the second most common skin cancer. It is common on sun-exposed skin in older adults, but risk is strongly influenced by cumulative UV exposure and immune status.

Cumulative UV damage is the leading cause. Actinic keratoses, immune suppression, chronic wounds or scars, previous radiation, and some chemical or viral exposures can increase risk.

SCC in situ (Bowen disease) remains within the epidermis and usually appears as a persistent scaly plaque. Invasive SCC extends into the dermis and may be keratotic, ulcerated or tender. Keratoacanthoma-type SCC can form a rapidly growing crater-like nodule. Less common variants include acantholytic, spindle-cell and desmoplastic SCC, which require pathology assessment.

SCC usually occurs on chronically sun-exposed areas such as the face, bald scalp, ears, lower lip, forearms and backs of the hands. It may appear as a firm tender lump, thick scaly plaque, cutaneous horn, rapidly growing crater or non-healing ulcer. SCC may also develop in a chronic wound, burn scar, genital skin or an area of previous radiation.

Possible clues include surface scale or keratin, white circles, white structureless areas, blood spots, ulceration and irregular coiled, dotted, hairpin or polymorphous vessels. Bowen disease often shows clustered glomerular vessels. Dermoscopy cannot reliably determine invasion depth, so adequate biopsy is important.

Actinic keratosis, inflamed seborrhoeic keratosis, wart, eczema, psoriasis, keratoacanthoma, BCC and amelanotic melanoma can look similar. Pain or tenderness, rapid growth, increasing thickness and persistent ulceration raise concern but are not diagnostic by themselves.

Assessment includes lesion size and depth, anatomical site, growth rate, nerve symptoms, lymph nodes and immune status. A biopsy must be sufficiently deep to distinguish in-situ from invasive disease and to identify differentiation, thickness, perineural invasion and other high-risk features. Imaging or lymph-node investigation is reserved for selected high-risk disease.

In-situ and invasive SCC are treated differently. For invasive disease, clinicians consider tumour diameter and thickness, differentiation, site, recurrence, immune suppression, nerve involvement and whether the lesion arose in a scar or chronic wound. High-risk lesions merit specialist or multidisciplinary planning.

Excision is the usual treatment for invasive SCC. Mohs surgery may be appropriate for selected high-risk, recurrent or anatomically critical tumours. Curettage and cautery, cryotherapy, topical treatment or photodynamic therapy may suit selected SCC in situ or carefully chosen low-risk lesions, but are not interchangeable with treatment of higher-risk invasive SCC. Radiotherapy may be primary or additional treatment; nodal or advanced disease may require surgery, radiotherapy and/or immunotherapy.

Most SCCs are successfully treated. Risk of recurrence or spread is higher for thick, large, rapidly growing, recurrent or poorly differentiated tumours and those on certain sites or in immunosuppressed patients.

Follow-up frequency depends on tumour risk and patient factors. Reviews may include the scar, surrounding skin and regional lymph nodes as well as a total-skin examination. New pain, numbness, a lump near the scar or in nearby lymph-node areas, or rapid local change should prompt review.