Skin cancer develops when skin cells accumulate genetic damage and other changes that disrupt normal control of growth and survival. Ultraviolet radiation from sunlight and artificial sources such as sunbeds is the principal environmental cause of many skin cancers. UV radiation can damage DNA directly and indirectly through oxidative processes, producing mutations in genes responsible for controlling cell division, DNA repair and tumour suppression. Repeated exposure provides repeated opportunities for damage to accumulate. The process is usually gradual and may involve many years between significant exposure and the eventual development of a clinically detectable cancer. This is why skin cancer risk reflects cumulative exposure as well as episodes of intense exposure and sunburn.
Ultraviolet radiation includes UVA and UVB, which have overlapping but distinct biological effects. UVB is strongly associated with direct DNA damage and sunburn, while UVA penetrates more deeply into the skin and contributes to oxidative DNA damage, photoageing and carcinogenesis. Both types of UV radiation can contribute to skin cancer. Sunbeds emit artificial UV radiation and are not a safe alternative to natural tanning. The International Agency for Research on Cancer classifies sunbed UV exposure as carcinogenic, and evidence links sunbed use to melanoma as well as non-melanoma skin cancers. Consequently, deliberately exposing the skin to UV in order to produce a tan increases rather than reduces skin-cancer risk.
Sunburn is particularly important because it indicates significant acute UV injury to the skin. A history of sunburn is associated with increased skin-cancer risk, and repeated sunburn increases concern. The risk is not restricted to sunburn occurring during childhood; Cancer Research UK notes that sunburn at any age can contribute to risk. Intermittent intense exposure, such as strong sunlight during holidays abroad, is particularly associated with melanoma risk. This differs somewhat from the pattern of chronic cumulative exposure that contributes strongly to many non-melanoma skin cancers, although the categories overlap. The distinction illustrates why both repeated everyday exposure and occasional intense exposure should be considered when assessing UV-related risk.
Skin type influences susceptibility because melanin provides some natural protection against UV radiation. People with fair or pale skin, particularly those who burn easily, generally have greater risk than people with darker skin. Fair or red hair, light-coloured eyes and extensive freckling are associated with increased melanoma and non-melanoma skin-cancer risk. People with brown or black skin can nevertheless develop skin cancer, including melanoma, and may experience delayed recognition because lesions can appear in locations such as the palms, soles and beneath nails. Albinism produces very little or no melanin and is associated with particularly high UV-related skin-cancer risk. Skin colour therefore modifies risk but never makes skin cancer impossible.
Age is another important risk factor because genetic damage and cumulative UV exposure can build over decades. Non-melanoma skin cancer is especially common in older adults, although younger people can develop it. Melanoma also becomes more common with age overall, while remaining relatively important among younger adults compared with many other cancers. Occupational exposure can increase cumulative UV exposure in people who work outdoors, including construction workers, agricultural workers and gardeners. Recreational exposure can be equally relevant, particularly repeated intentional tanning or intermittent high-intensity exposure. Risk therefore depends not only on age but on the pattern and duration of exposure over the person's lifetime.
Genetic and familial factors also influence risk. Some people inherit variants that affect DNA repair, pigment biology, immune surveillance or other mechanisms relevant to cancer susceptibility. A close family history of melanoma increases individual risk, and a small proportion of melanoma cases are associated with inherited gene changes such as variants involving CDKN2A. People with many ordinary moles or numerous atypical moles can also have elevated melanoma risk. These inherited or constitutional factors do not mean that cancer is inevitable. Rather, they alter baseline susceptibility and interact with environmental exposures such as UV radiation. A person with increased inherited risk can therefore still reduce avoidable environmental exposure and should be particularly attentive to changes in the skin.
Other factors can contribute to skin-cancer risk. Previous skin cancer increases the chance of developing another skin cancer. A weakened immune system, including immunosuppression following organ transplantation, can substantially increase the risk of certain skin cancers, particularly SCC. Previous radiotherapy can increase risk in treated areas, while exposure to certain carcinogenic chemicals can contribute to some forms of skin cancer. Chronic scars, wounds or areas of longstanding inflammation can occasionally give rise to SCC. These causes and risk factors are distinct from ordinary sun exposure, demonstrating that UV radiation is the major environmental factor but not the only possible contributor to malignant transformation of skin cells.
A risk factor is not the same thing as a direct guarantee of causation in an individual. Many people with substantial UV exposure never develop skin cancer, while some people develop skin cancer despite relatively limited recognised exposure. Cancer arises from interactions among DNA damage, cellular repair, immune surveillance, genetics, age and chance biological events. Nevertheless, the evidence linking UV radiation to skin cancer is strong, and reducing unnecessary UV exposure is an important prevention measure. Cancer Research UK estimates that a very large proportion of UK melanoma cases could be prevented through safer sun behaviour and avoiding sunbeds. This provides a practical distinction between unavoidable background susceptibility and modifiable environmental exposure.
