The ultraviolet radiation from tanning beds increases the risk of melanoma. The International Agency for Research on Cancer finds that tanning beds are "carcinogenic to humans" and that people who begin using tanning devices before the age of thirty years are 75% more likely to develop melanoma.

Those who work in airplanes also appear to have an increased risk, believed to be due to greater exposure to UV.

Ultraviolet UVB light (wavelengths between 315 – 280 nm) from the sun is absorbed by skin cell DNA and results in a type of direct DNA damage called cyclobutane pyrimidine dimers (CPDs). Thymine-thymine, cytosine-cytosine or cytosine-thymine dimers are formed by the joining of two adjacent pyrimidine bases within a DNA strand. Somewhat similarly to UVB, UVA light (longer wavelengths between 400 – 315 nm) from the sun or from tanning beds can also be directly absorbed by skin DNA (at about 100 to 1000 fold lower efficiency than UVB is absorbed).

Studies suggest that exposure to ultraviolet radiation (UVA and UVB) is one of the major contributors to the development of melanoma. Occasional extreme sun exposure (resulting in "sunburn") is causally related to melanoma. Melanoma is most common on the back in men and on legs in women (areas of intermittent sun exposure). The risk appears to be strongly influenced by socio-economic conditions rather than indoor versus outdoor occupations; it is more common in professional and administrative workers than unskilled workers. Other factors are mutations in or total loss of tumor suppressor genes. Use of sunbeds (with deeply penetrating UVA rays) has been linked to the development of skin cancers, including melanoma.

Possible significant elements in determining risk include the intensity and duration of sun exposure, the age at which sun exposure occurs, and the degree of skin pigmentation. Melanoma rates tend to be highest in countries settled by migrants from northern Europe that have a large amount of direct, intense sunlight that the skin of the settlers is not adapted to, most notably Australia. Exposure during childhood is a more important risk factor than exposure in adulthood. This is seen in migration studies in Australia.

Having multiple severe sunburns increases the likelihood that future sunburns develop into melanoma due to cumulative damage. The sun and tanning beds are the main sources of UV radiation that increase the risk for melanoma and living close to the equator increases exposure to UV radiation.

Melanomas are usually caused by DNA damage resulting from exposure to ultraviolet light from the sun. Genetics also plays a role.

Having more than fifty moles indicates an increased risk melanoma might arise. A weakened immune system makes it easier for cancer to arise due to the body’s weakened ability to fight cancer cells.

Lymphoma is the most common type of blood-related cancer in horses and while it can affect horses of all ages, it typically occurs in horses aged 4–11 years.

Ultraviolet radiation from sun exposure is the primary environmental cause of skin cancer. Other risk factors that play a role include:

- Smoking tobacco

- HPV infections increase the risk of squamous-cell skin cancer.

- Some genetic syndromes including congenital melanocytic nevi syndrome which is characterized by the presence of nevi (birthmarks or moles) of varying size which are either present at birth, or appear within 6 months of birth. Nevi larger than 20 mm (3/4") in size are at higher risk for becoming cancerous.

- Chronic non-healing wounds. These are called Marjolin's ulcers based on their appearance, and can develop into squamous-cell skin cancer.

- Ionizing radiation such as X-rays, environmental carcinogens, artificial UV radiation (e.g. tanning beds), aging, and light skin color. It is believed that tanning beds are the cause of hundreds of thousands of basal and squamous-cell skin cancer. The World Health Organization now places people who use artificial tanning beds in its highest risk category for skin cancer. Alcohol consumption, specifically excessive drinking increase the risk of sunburns.

- The use of many immunosuppressive medications increases the risk of skin cancer. Cyclosporin A, a calcineurin inhibitor for example increases the risk approximately 200 times, and azathioprine about 60 times.

Skin cancers result in 80,000 deaths a year as of 2010, 49,000 of which are due to melanoma and 31,000 of which are due to non-melanoma skin cancers. This is up from 51,000 in 1990.

More than 3.5 million cases of skin cancer are diagnosed annually in the United States, which makes it the most common form of cancer in that country. One in five Americans will develop skin cancer at some point of their lives. The most common form of skin cancer is basal-cell carcinoma, followed by squamous cell carcinoma. Unlike for other cancers, there exists no basal and squamous cell skin cancers registry in the United States.

This type of cancer occurs most often in Caucasians between 60 and 80 years of age, and its rate of incidence is about twice as high in males as in females. There are roughly 1,500 new cases of MCC diagnosed each year in the United States, as compared to around 60,000 new cases of melanoma and over 1 million new cases of nonmelanoma skin cancer. MCC is sometimes mistaken for other histological types of cancer, including basal cell carcinoma, squamous cell carcinoma, malignant melanoma, lymphoma, and small cell carcinoma, or as a benign cyst. Researchers believe that exposure to sunlight or ultraviolet light (such as in a tanning bed) may increase the risk of developing this disease. Similar to melanoma, the incidence of MCC in the US is increasing rapidly.

Immunosuppression can profoundly increase the odds of developing Merkel-cell carcinoma. Merkel-cell carcinoma occurs 30 times more often in people with chronic lymphocytic leukemia and 13.4 times more often in people with advanced HIV as compared to the general population; solid organ transplant recipients have a 10-fold increased risk compared to the general population.

Tumors related to squamous-cell carcinoma (SCC) can appear anywhere on the body, but they are most often located in non-pigmented skin near mucocutaneous junctions (where skin meets mucous membranes) such as on the eyelids, around the nostrils, lips, vulva, prepuce, penis or anus. The tumors are raised, fleshy, often ulcerated or infected and may have an irregular surface. Rarely, primary SCC develops in the esophagus, stomach (non-glandular portion), nasal passages and sinuses, the hard palate, gums, guttural pouches and lung. The eyelid is the most common site, accounting for 40-50% of cases, followed by male (25-10% of cases) and female (10% of cases) genitalia. Horses with lightly pigmented skin, such as those with a gray hair coat or white faces, are especially prone to developing SCC, and some breeds, such as Clydesdales, may have a genetic predisposition. Exposure of light-colored skin to UV light has often been cited as a predisposing factor, but lesions can occur in dark skin and in areas that are not usually exposed to sunlight, such as around the anus. Buildup of smegma ("the bean" in horseman's terms) on the penis is also linked to SCC and is thought to be a carcinogen through penile irritation. Pony geldings and work horses are more prone to developing SCC on the penis, due to less frequent penile washing when compared to stallions. Equine papillomavirus-2 has also been found within penile SCCs, but has not been determined to cause SCC.

Benign melanocytic tumors of the choroid, such as choroidal freckles and nevi, are very common and pose no health risks, unless they show signs of malignancy, in which case they are considered melanomas. Uveal melanoma is distinct from most skin melanomas associated with ultraviolet exposure; however, it shares several similarities with non-sun-exposed melanomas, such as acral melanomas and mucosal melanomas. BRAF mutations are extremely rare in posterior uveal melanomas; instead, uveal melanomas frequently harbor GNAQ/GNA11 mutations, a trait shared with blue nevi, Nevus of Ota, and Ocular melanosis. As seen in BRAF, mutations in GNAQ/GNA11 are early events in tumorigenesis and are not prognostic for tumor stage or later metastatic spread. In contrast, mutations in the gene BAP1 are strongly linked to metastatic spread and patient survival. Incidence of posterior uveal melanoma is highest among people with light skin and blue eyes. Other risk factors, such as blue light exposure and arc welding have been put forward, but are still debated in the field. Mobile phone use is not a risk factor for uveal melanoma.

It has been demonstrated that acral lentiginous melanoma has a poorer prognosis compared to that of cutaneous malignant melanoma (CMM).

The treatment protocol for uveal melanoma has been directed by many clinical studies, the most important being The Collaborative Ocular Melanoma Study (COMS). The treatment varies depending upon many factors, chief among them, the size of the tumor and results from testing of biopsied material from the tumor. Primary treatment can involve removal of the affected eye (enucleation); however, this is now reserved for cases of extreme tumor burden or other secondary problems. Advances in radiation therapies have significantly decreased the number of patients treated by enucleation in developed countries. The most common radiation treatment is plaque brachytherapy, in which a small disc-shaped shield (plaque) encasing radioactive seeds (most often Iodine-125, though Ruthenium-106 and Palladium-103 are also used) is attached to the outside surface of the eye, overlying the tumor. The plaque is left in place for a few days and then removed. The risk of metastasis after plaque radiotherapy is the same as that of enucleation, suggesting that micrometastatic spread occurs prior to treatment of the primary tumor. Other modalities of treatment include transpupillary thermotherapy, external beam proton therapy, resection of the tumor, Gamma Knife stereotactic radiosurgery or a combination of different modalities. Different surgical resection techniques can include trans-scleral partial choroidectomy, and transretinal endoresection.

A newly discovered virus called Merkel cell polyomavirus (MCV) likely contributes to the development of the majority of MCC. Approximately 80% of MCC have this virus integrated in a monoclonal pattern, indicating that the infection was present in a precursor cell before it became cancerous. At least 20% of MCC tumors are not infected with MCV, suggesting that MCC may have other causes as well.

Polyomaviruses have been known to be oncogenic (cancer-causing) viruses in animals since the 1950s, but MCV is the first polyomavirus strongly suspected to cause tumors in humans. Like other tumor viruses, most people who are infected with MCV probably do not develop MCC. It is currently unknown what other steps or co-factors are required for MCC-type cancers to develop. MCC can also occur together with other sun exposure-related skin cancers that are not infected with MCV (i.e. basal cell carcinoma, squamous cell carcinoma, melanoma). Intriguingly, most MCV viruses obtained so far from tumors have specific mutations that render the virus uninfectious. It is unknown whether these particular mutations result from sun exposure. MCC also occurs more frequently than would otherwise be expected among immunosuppressed patients, such as transplant patients, AIDS patients, and the elderly persons, suggesting that the initiation and progression of the disease is modulated by the immune system.

While infection with MCV is common in humans, MCC patients whose tumors contain MCV have higher antibody levels against the virus than similarly infected healthy adults. A recent study of a large patient registry from Finland suggests that individuals with MCV-positive MCC's have better prognoses than do MCC patients without MCV infection. While MCV-positive MCC may be a less aggressive form of the disease, the results of the aforementioned study may instead be due to significant differences in other confounding factors, including tumor stage at the time of diagnosis, the age of the patient, or the location of the tumor rather than any intrinsic difference in disease aggressiveness or response to therapy.

Since 80% of grey horses will develop a melanoma tumor at some point in their lives, it is important to know what kind of treatments are available. There are several treatment options when a horse is found to have a melanoma tumor including surgical or injections:

Grey horses have a higher susceptibility to melanoma than any other coat color, with up to 80% of grey horses developing some kind of melanoma in their lifetime and some sources state that 66% of those melanomas will become malignant. The grey coat color comes from a gene that is responsible for the gradual depigmentation of the horse’s coat; horses with this gene are born darker and over time, they lose their coat pigmentation. The grey gene is the strongest coat modifier, and will act on any base color. The grey coat color is the result of an autosomal dominant trait that is caused by a 4.6-kb duplication in the 6th intron of the gene syntaxin-17 (STX17). The region of this mutation contains four genes: NR4A3 (nuclear receptor subfamily 4, group A, member 3), STX17, TXNDC4 (thioredoxin domain–containing-4¢) and INVS (inversin). To determine what makes grey horses more susceptible to melanomas, researchers have used different techniques such as the Northern Blot technique and Real-Time PCR. From these studies, it was concluded that the STX17 gene and the NR4A3 gene are both being over expressed in grey horses, which is responsible for the increased incidences of melanoma in horses with the grey gene.

Therapies for metastatic melanoma include the biologic immunotherapy agents ipilimumab, pembrolizumab, and nivolumab; BRAF inhibitors, such as vemurafenib and dabrafenib; and a MEK inhibitor trametinib.

Acral lentiginous melanoma is due as a result of malignant melanocytes. This occurs at the membrane of the skin (outer layers). It should be noted that the pathogenesis of acral lentiginous melanoma remains unknown at this time.

Lentigo maligna melanoma is a melanoma that has evolved from a lentigo maligna. They are usually found on chronically sun damaged skin such as the face and the forearms of the elderly. The nomenclature is very confusing to both patients and physicians alike.

Lentigo maligna is the non-invasive skin growth that some pathologists consider to be a melanoma-in-situ. A few pathologists do not consider lentigo maligna to be a melanoma at all, but a precursor to melanomas. Once a lentigo maligna becomes a lentigo maligna melanoma, it is treated as if it were an invasive melanoma.

Ultraviolet light from the sun causes premature aging of the skin and skin damage that can lead to melanoma. Some scientists hypothesize that overexposure to UV, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed to determine the complex interaction between genetic makeup and overall exposure to ultraviolet light. Some strong indications that this is so (but falling short of proof), are:

- The relative lack of moles on the buttocks of people with dysplastic nevi.

- Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.

Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is "in addition to" those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring "benign" moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever one's shadow is shorter than one's height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses.

Lentigo maligna (also known as "lentiginous melanoma on sun-damaged skin") is a melanoma "in situ" that consists of malignant cells but does not show invasive growth. Lentigo maligna is not the same as lentigo maligna melanoma, and should be discussed separately. It typically progresses very slowly and can remain in a non-invasive form for years. The transition to true melanoma is marked by the appearance of a bumpy surface (itself a marker of vertical growth and invasion), at which point it is called lentigo maligna melanoma. It is normally found in the elderly (peak incidence in the 9th decade), on skin areas with high levels of sun exposure like the face and forearms. Some authors do not consider lentigo maligna to be a melanoma. It is commonly thought of as a melanoma precursor. Incidence of evolution to lentigo maligna melanoma is very low, about 2.2% to 5% in elderly patients.

It is also known as "Hutchinson's melanotic freckle". This is named for Jonathan Hutchinson.

An invasive tumor arising from a classical lentigo maligna. Usually a darkly pigmented raised papule or nodule, arising from a patch of irregularly pigmented flat brown to dark brown lesion of sun exposed skin of the face or arms in an elderly patient.

Desmoplastic melanoma (also known as a "Neurotropic melanoma," or "Spindled melanoma") is a rare cutaneous condition characterized by a deeply infiltrating type of melanoma with an abundance of fibrous matrix. It usually occurs in the head and neck region of older people with sun-damaged skin. Diagnosis can be difficult as it has a similar appearance to sclerosing melanocytic nevi as well as some nonmelanocytic skin lesions such as scars, fibromas, or cysts.

Desmoplastic melanomas tend to recur locally, with distant metastasis being less common.

Nodular melanoma (NM) is the most aggressive form of melanoma. It tends to grow more rapidly in thickness (penetrate the skin) than in diameter. Instead of arising from a pre-existing mole, it may appear in a spot where a lesion did not previously exist . Since NM tends to grow in depth more quickly than it does in width, and can occur in a place that did not have a previous lesion, the prognosis is often worse because it takes longer for a person to be aware of the changes. NM is most often darkly pigmented; however, some NM lesions can be light brown, multicolored or even colorless (non-pigmented). A light-colored or non-pigmented NM lesion may escape detection because the appearance is not alarming, however an ulcerated and/or bleeding lesion is common. Polypoid melanoma is a virulent variant of nodular melanoma.

The microscopic hallmarks are:

- Dome-shaped at low power

- Epidermis thin or normal

- Dermal nodule of melanocytes with a 'pushing' growth pattern

- No "radial growth phase"

The best treatment of lentigo maligna is not clear as it has not been well studied.

Standard excision is still being done by most surgeons. Unfortunately, the recurrence rate is high (up to 50%). This is due to the ill defined visible surgical margin, and the facial location of the lesions (often forcing the surgeon to use a narrow surgical margin). The use of dermatoscopy can significantly improve the surgeon's ability to identify the surgical margin. The narrow surgical margin used (smaller than the standard of care of 5 mm), combined with the limitation of the standard bread loafing technique of fixed tissue histology - result in a high "false negative" error rate, and frequent recurrences. Margin controlled (peripheral margins) is necessary to eliminate the false negative errors. If breadloafing is utilized, distances from sections should approach 0.1 mm to assure that the method approaches complete margin control.

Where the lesion is on the face and either large or 5mm margins are possible, a skin flap or skin graft may be indicated/required. Grafts have their own risks of failure and poor cosmetic outcomes. Flaps can require extensive incision resulting in long scars and may be better done by plastic surgeons (and possibly better again by those with extensive LM or "suspicious of early malignant melanoma" experience.

Mohs surgery has been done with cure rate reported to be 77%. The "double scalpel" peripheral margin controlled excision method approximates the Mohs method in margin control, but requires a pathologist intimately familiar with the complexity of managing the vertical margin on the thin peripheral sections and staining methods.

Some melanocytic nevi, and melanoma-in-situ (lentigo maligna) have resolved with an experimental treatment, imiquimod (Aldara) topical cream, an immune enhancing agent. In view of the very poor cure rate with standard excision, some surgeons combine the two methods: surgical excision of the lesion, then three months treatment of the area with imiquimod cream.

Studies seem to conflict about the level of certainty associated with using imiquimod.

Another treatment to be considered where standard margins cannot be achieved or cosmetics are a major consideration is ultra-soft x-ray/grenz-ray radiation.

In the very elderly or those with otherwise limited life expectancy, the impact of major day surgery for excision with 5mm margins and large skin flap could be worse than doing nothing or the possibility of failed treatments with imiquimod or Grenz ray.

Experts, such as the American Academy of Dermatology, say that vast majority of moles are benign. Nonetheless, the U.S. National Cancer Institute estimated that 62,480 new cases of melanoma and 8,420 related deaths would appear in the United States in the year 2008.

Data on the chances of transformation from melanocytic nevi to melanoma is controversial, but it appears that about 10% of malignant melanomas have a precursor lesion, of which about 10% are melanocytic nevi. Therefore, it appears that malignant melanoma quite seldomly (1% of cases) has a melanocytic nevi as a precursor.

A study by You et al. was only able to evaluate the 47 documented cases that have been made to date. According to this study, intraocular schwannomas are more prevalent in females as compared to males with a ratio of 3:1. Additionally, individuals are more likely to present with intraocular schwannomas at a younger age than with uveal melanomas, the most common intraocular tumor. According to the participants evaluated in this study, the average age of occurrence was 37 years old, however, it is important to note that the age range documented represented individuals 9–76 years old.

When the tumor is large and there is presence of necrosis and local recurrence, the prognosis is poor. Presence of metastasis occurs in more than 50% cases and the common places of its occurrence are the bone, lymph node and lungs. Five-year survival rates, which are reported to be between 50-65%, can be misleading because the disease is prone to late metastasis or recurrence. Ten and twenty-year survival rates are 33% and 10%, respectively.