<unk> s are usually caused by DNA damage resulting from exposure to UV light from the sun. Genetics also play a role.<unk>  can also occur in skin areas with little sun exposure (i.e. mouth, soles of feet, palms of hands, genital areas). People with dysplastic nevus syndrome, also known as familial atypical multiple mole<unk> , are at increased risk for the development of<unk> . Having more than 50 moles indicates an increased risk<unk>  might arise. A weakened immune system makes cancer development easier due to the body's weakened ability to fight cancer cells. UV radiation The UV radiation from tanning beds increases the risk of<unk> . 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<unk> . Those who work in airplanes also appear to have an increased risk, believed to be due to greater exposure to UV. UVB light (wavelengths between 315 and 280 nm) from the sun is absorbed by skin cell DNA and results in a type of direct DNA damage called cyclobutane pyrimidine dimers. 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 and 315 nm) from the sun or from tanning beds can also be directly absorbed by skin DNA (at about 1/100 to 1/1000 of the efficiency of UVB). Exposure to radiation (UVA and UVB) is one of the major contributors to the development of<unk> . Occasional extreme sun exposure (resulting in "sunburn") is causally related to<unk> .<unk>  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 socioeconomic 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<unk> . 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.<unk>  rates tend to be highest in countries settled by migrants from Northern Europe who have a large amount of direct, intense sunlight to which the skin of the settlers is not adapted, 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<unk>  due to cumulative damage. The sun and tanning beds are the main sources of UV radiation that increase the risk for<unk>  and living close to the equator increases exposure to UV radiation. Genetics A number of rare mutations, which often run in families, greatly increase<unk>  susceptibility. Several genes increase risks. Some rare genes have a relatively high risk of causing<unk> ; some more common genes, such as a gene called MC1R that causes red hair, have a relatively lower elevated risk. Genetic testing can be used to search for the mutations. One class of mutations affects the gene CDKN2A. An alternative reading frame mutation in this gene leads to the destabilization of p53, a transcription factor involved in apoptosis and in 50% of human cancers. Another mutation in the same gene results in a nonfunctional inhibitor of CDK4, a cyclin-dependent kinase that promotes cell division. Mutations that cause the skin condition xeroderma pigmentosum (XP) also increase<unk>  susceptibility. Scattered throughout the genome, these mutations reduce a cell's ability to repair DNA. Both CDKN2A and XP mutations are highly penetrant (the chances of a carrier to express the phenotype is high). Familial<unk>  is genetically heterogeneous, and loci for familial<unk>  appear on the chromosome arms 1p, 9p and 12q. Multiple genetic events have been related to<unk> 's pathogenesis (disease development). The multiple tumor suppressor 1 (CDKN2A/MTS1) gene encodes p16INK4a – a low-molecular weight protein inhibitor of cyclin-dependent protein kinases (CDKs) – which has been localised to the p21 region of human chromosome 9. FAMMM is typically characterized by having 50 or more combined moles in addition to a family history of<unk> . It is transmitted autosomal dominantly and mostly associated with the CDKN2A mutations. People who have CDKN2A mutation associated FAMMM have a 38 fold increased risk of pancreatic cancer. Other mutations confer lower risk, but are more common in the population. People with mutations in the MC1R gene are two to four times more likely to develop<unk>  than those with two wild-type (typical unaffected type) copies. MC1R mutations are very common, and all red-haired people have a mutated copy. Mutation of the MDM2 SNP309 gene is associated with increased risks for younger women. Fair- and red-haired people, persons with multiple atypical nevi or dysplastic nevi and persons born with giant congenital melanocytic nevi are at increased risk. A family history of<unk>  greatly increases a person's risk, because mutations in several genes have been found in<unk> -prone families. People with a history of one<unk>  are at increased risk of developing a second primary tumor. Fair skin is the result of having less melanin in the skin, which means less protection from UV radiation exists. A family history could indicate a genetic predisposition to<unk> .
Melanoma
Blue nevus
Pseudomelanoma
Seborrheic keratosis
Xanthoma
Lentigo
Nodular melanoma
Dermatofibroma