Overview of skin cancer
Introduction
Related conditions
The most common malignancy of the skin in fair-skinned adults in the US, Australia, and Europe.[1]
CRUK Cancer incidence statistics
Opens in new window It typically presents as pearly papules and/or plaques; non-healing scabs; small crusts and non-healing wounds; plaques, nodules, and tumours with rolled borders; or papules with associated telangiectasias.[2][3][Figure caption and citation for the preceding image starts]: Nodular basal cell carcinoma on the cheek, on background of diffuse solar damage with marked solar elastosisFrom the collection of Dr Robert A. Schwartz [Citation ends].
Strong risk factors include exposure to UV radiation from sunlight (not tanning beds), previous x-ray surface therapy (e.g., as acne therapy), arsenic exposure (e.g., in contaminated well water),[4] xeroderma pigmentosum, basal cell naevus syndrome (Gorlin-Goltz syndrome), and history of transplantation (particularly solid organ). Metastases and advanced lesions are uncommon.
Treatment is usually surgical, locally destructive (curettage and electrodessication, radiotherapy), and, for selected superficial basal cell carcinomas, cryosurgery or topical therapy with 5-fluorouracil or imiquimod is used.[5] Choice of treatment is dictated by the lesion size, location, number, subtype, depth of invasion, and tissue margin (if biopsied).[6]
Ranges from in situ tumours (Bowen's disease), to invasive tumours, and to metastatic disease. It can present as a non-healing wound, often attributed to trauma by the patient. In situ tumours are typically thin, flesh-coloured to erythematous, scaly plaques, while invasive squamous cell carcinoma (SCC) may present as an exophytic tumour or ulcer.[Figure caption and citation for the preceding image starts]: Squamous cell carcinoma on the ear with surrounding actinic damageFrom the collection of Dr Jessica M. Sheehan and Dr Keyoumars Soltani [Citation ends].
Tumours may be friable and bleed easily and are located mostly on sun-exposed areas of skin, such as the head and neck (84%) and extensor upper extremities (13%).[7]
Strong risk factors include exposure to UV radiation, immunosuppression, genodermatosis (e.g., oculocutaneous albinism), and older age. Key diagnostic factors include a tumour that grows in size over time and older age (>40 years). Older patients have a longer history of sun/UV exposure and also decreased immune surveillance and tumour detection.[8]
The methods used to treat SCC vary depending on tumour type, size and location, patient history, and practitioner. Treatment can be surgical, locally destructive (cryotherapy, electrocautery, photodynamic therapy), or pharmacological.[9] In addition, sunscreens with UV-A and UV-B spectrum coverage or sunblocks should be advised for secondary prevention. Similarly, physical sun protection with clothing and hats, and sun avoidance, should be emphasised.[14][15]
A malignant tumour arising from pigment-producing melanocytes found in the skin, eye, and central nervous system. Several variants exist. Typically presents as a deeply pigmented skin lesion that is new or changing in size, shape, or colour.[16][17][Figure caption and citation for the preceding image starts]: Superficial spreading malignant melanomaFrom the collection of Dr Hobart W. Walling [Citation ends].
Unlike basal cell carcinoma and squamous cell carcinoma, melanoma is most common at body sites that have received intense, intermittent sun/UV exposure.[18] Lesions are more common on the trunk in men and on the legs and feet in women.[19] Tanning beds and sun lamps have been positively correlated with melanoma.[20] The likelihood of metastatic disease as a complication is high, and in young adults melanoma is a common cause of cancer-related death.
Once the diagnosis of primary cutaneous malignant melanoma is established, the standard of care is complete excision of the malignancy with an appropriate margin depending on the Breslow depth. The goals of treatment are to remove the primary tumour and to prevent persistent disease, local recurrence, and, ultimately, metastatic disease. Metastases are treated depending on the site (nodal, in-transit, or systemic).
A low-grade vasoformative neoplasm associated with human herpesvirus-8 (HHV-8) or Kaposi's sarcoma herpesvirus (KSHV) infection.[21] Lesions frequently involve mucocutaneous sites, but may become more extensive to involve the lymph nodes and visceral organs. Skin lesions evolve from an early patch, to a plaque, and later to ulcerating tumour nodules.[Figure caption and citation for the preceding image starts]: Kaposi sarcoma cutaneous purple-brown plaque on the footFrom the collection of Dr Bruce J. Dezube [Citation ends].
There are 4 main subtypes: epidemic AIDS-associated, classic sporadic, iatrogenic and transplant-associated, and African endemic Kaposi's sarcoma. In HIV-positive people, antiretroviral therapy without treatment interruptions may help prevent Kaposi's sarcoma or result in a less-aggressive presentation. Patients with AIDS-related Kaposi's sarcoma should adhere to an effective, uninterrupted antiretroviral regimen in order to avoid disease progression and/or the development of new lesions.
Therapy is given for symptom palliation, to prevent disease progression, and for cosmetic reasons. Treatment is individualised according to prognosis and the desired outcome of therapy. Treatment options are similar for each of the epidemiological forms of Kaposi's sarcoma, but may need to be tailored according to drug availability in resource-poor settings. Supportive care may be necessary in severely ill patients.
Heterogeneous group of uncommon disorders characterised by clonal accumulation of T lymphocytes primarily or exclusively in the skin. Mycosis fungoides and its leukaemic variant, Sézary syndrome, are the most common subtypes. Establishing a diagnosis is often difficult, as the disease can manifest in a number of different ways, including flat patches, raised plaques, large tumours, and/or marked erythroderma (intense and widespread reddening of the skin).[Figure caption and citation for the preceding image starts]: Cutaneous T-cell lymphoma: extensive patch diseaseFrom the collection of the Christie NHS Foundation Trust, Manchester, UK; used with permission [Citation ends].
Diagnosis is based on clinical findings, skin biopsy (specimens should be sent for histology, immunophenotyping, and molecular studies), and laboratory blood tests, and usually requires specialist expertise.[22][23] Early-stage disease is usually managed with skin-directed therapy (topical medications, phototherapy, and localised radiotherapy). If skin disease is extensive or refractory, or the patient presents with advanced disease, systemic therapies are often necessary (chemotherapy, biological or immunological therapy, photopheresis). Clinical trials may be considered in early and advanced disease if the patient is a suitable candidate. The choice of skin-directed therapy or systemic treatment is usually dependent on both doctor and patient preference, as no one treatment option has been shown to be superior to another.[24]
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Lesions are skin-coloured, yellowish or erythematous, ill-defined, irregularly shaped, small scaly macules or plaques localised in sun-exposed areas of the body (e.g., face, lower lip, dorsum of the hands, forearms, bald areas of the scalp, and ears).[Figure caption and citation for the preceding image starts]: Regular actinic keratosisFrom the collection of the Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine [Citation ends].
Typically, they occur in middle-aged or older men with light-coloured skin and a history of chronic sun exposure. It has the potential to progress into an invasive squamous cell carcinoma (SCC). The risk of progression to SCC has been calculated to be between 0.025% and 16% per year.[25][26] Although diagnosed clinically, a biopsy may help to rule out SCC.
As it is very difficult to predict which actinic keratosis (AK) lesion might progress to SCC, the recommendation is to treat all AKs.[27] Treatment options should be chosen depending on variables such as number, size, anatomical location, change in growth pattern, and prior treatment of the lesions. The goal of the treatment is the total destruction of the AKs, to minimise the risk of progression to invasive SCC, while obtaining the best cosmetically acceptable outcome. Treatment consists of destructive methods (e.g., cryotherapy with liquid nitrogen, curettage with or without electrodesiccation, chemical peels, and photodynamic therapy) or topical medication (e.g., topical fluorouracil, imiquimod, diclofenac, or ingenol mebutate). In addition, all patients are advised to wear broad-spectrum sunscreen regardless of treatment.
Sunburn is an acute inflammatory reaction of the skin induced by overexposure to UV radiation. Skin findings include erythema and oedema, with or without vesiculation, followed by desquamation. Symptoms include pain and/or pruritus. Acute sunburn is a self-limiting condition and typically requires only supportive care. Primary prevention via sun avoidance, physical protection, and the appropriate use of sunscreen is key to managing the condition, as cellular damage caused by UV radiation is irreversible and may with time increase the risk of skin cancer. No current treatments can reverse UV-induced DNA damage in the skin.[28]
Contributors
Authors
Editorial Team
BMJ Publishing Group
Disclosures
This overview has been compiled using the information in existing sub-topics.
Evidence
How do interventions affect outcomes in people with mycosis fungoides?
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Skin cancer (melanoma)
Skin cancer (squamous cell)
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