Skin cancer is the most common type of cancer worldwide. Possible risk factors include exposure to sunlight or UV radiation (e.g., tanning beds), viral infection (e.g., HPV), fair skin type, presence of large numbers or certain types of nevi (moles), exposure to arsenic, immunosuppression, certain genetic conditions (e.g., xeroderma pigmentosum), and family history of skin cancer.
The most common malignancy of the skin in fair-skinned adults in the US, Australia, and Europe.  It typically presents as pearly papules and/or plaques; nonhealing scabs; small crusts and nonhealing wounds; plaques, nodules, and tumors with rolled borders; or papules with associated telangiectasias.   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),  xeroderma pigmentosum, basal cell nevus 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, radiation therapy), and, for selected superficial basal cell carcinomas, cryosurgery or topical therapy with 5-fluorouracil or imiquimod is used.  Choice of treatment is dictated by the lesion size, location, number, subtype, depth of invasion, and tissue margin (if biopsied). 
Ranges from in situ tumors (Bowen disease), to invasive tumors, and to metastatic disease. It can present as a nonhealing wound, often attributed to trauma by the patient. In situ tumors are typically thin, flesh-colored to erythematous, scaly plaques, while invasive squamous cell carcinoma (SCC) may present as an exophytic tumor or ulcer. Tumors 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%). 
Strong risk factors include exposure to UV radiation, immunosuppression, genodermatosis (e.g., oculocutaneous albinism), and older age. Key diagnostic factors include a tumor 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 tumor detection. 
The methods used to treat SCC vary depending on tumor type, size and location, patient history, and practitioner. Treatment can be surgical, locally destructive (cryotherapy, electrocautery, photodynamic therapy), or pharmacologic.  In addition, sunscreens with UV-A and UV-B spectrum coverage or sunblocks should be advised for secondary prevention. Evidence B Similarly, physical sun protection with clothing and hats, and sun avoidance, should be emphasized.  
A malignant tumor 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 color.   Unlike basal cell carcinoma and squamous cell carcinoma, melanoma is most common at body sites that have received intense, intermittent sun/UV exposure.  Lesions are more common on the trunk in men and on the legs and feet in women.  Tanning beds and sun lamps have been positively correlated with melanoma.  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 tumor 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 sarcoma herpesvirus (KSHV) infection.  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 tumor nodules. There are 4 main subtypes: epidemic AIDS-associated, classic sporadic, iatrogenic and transplant-associated, and African endemic Kaposi sarcoma. In HIV-positive people, antiretroviral therapy without treatment interruptions may help prevent Kaposi sarcoma or result in a less-aggressive presentation. Patients with AIDS-related Kaposi 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 individualized according to prognosis and the desired outcome of therapy. Treatment options are similar for each of the epidemiologic forms of Kaposi 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 characterized by clonal accumulation of T lymphocytes primarily or exclusively in the skin. Mycosis fungoides and its leukemic 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 tumors, and/or marked erythroderma (intense and widespread reddening of the skin). 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.   Early-stage disease is usually managed with skin-directed therapy (topical medications, phototherapy, and localized radiation therapy). If skin disease is extensive or refractory, or the patient presents with advanced disease, systemic therapies are often necessary (chemotherapy, biologic or immunologic 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.  [ ]
Lesions are skin-colored, yellowish or erythematous, ill-defined, irregularly shaped, small scaly macules or plaques localized in sun-exposed areas of the body (e.g., face, lower lip, dorsum of the hands, forearms, bald areas of the scalp, and ears). Typically, they occur in middle-aged or older men with light-colored 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.   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.  Treatment options should be chosen depending on variables such as number, size, anatomic location, change in growth pattern, and prior treatment of the lesions. The goal of the treatment is the total destruction of the AKs, to minimize 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 edema, with or without vesiculation, followed by desquamation. Symptoms include pain and/or pruritus. Acute sunburn is a self-limited 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. 
BMJ Publishing Group
This overview has been compiled using the information in existing sub-topics.
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