Ultraviolet (UV) radiation is the leading cause of skin cancer, responsible for more than 80% of melanoma cases worldwide. But UV exposure isn’t the only cause. Chemical exposures, a weakened immune system, certain viruses, and genetic factors all play a role, and some skin cancers develop on parts of the body that rarely see sunlight.
UV Radiation and DNA Damage
Sunlight contains two types of UV radiation that damage skin cells in different ways. UVB rays, the kind that cause sunburn, are the more directly dangerous of the two. When UVB light hits your skin cells, it forces neighboring molecules in your DNA to bond together abnormally, creating structural defects called pyrimidine dimers. About 75% of UVB-related DNA damage takes this form. The remaining 25% involves a slightly different type of molecular bonding error. Both types block the cell’s ability to copy its DNA correctly, and they can also physically break DNA strands.
Your cells have built-in repair systems that fix most of this damage. But with repeated UV exposure over years, some errors slip through. When those errors land in genes that control cell growth, a normal skin cell can begin dividing without the usual checks. That’s how a cancer begins.
A 2025 analysis from the International Agency for Research on Cancer found that 83% of all new melanoma cases worldwide in 2022 were caused by UV radiation exposure. The proportion was higher in men (86%) than in women (79%), likely reflecting differences in outdoor occupational exposure and sun protection habits. For non-melanoma skin cancers like squamous cell and basal cell carcinoma, UV radiation is similarly dominant as a cause.
How Skin Type Affects Your Risk
Not everyone’s skin responds to UV radiation the same way, and that difference has a direct impact on cancer risk. The Fitzpatrick scale, developed in 1975, classifies skin into six types based on how it reacts to sun exposure. Type I skin is very fair, always burns, and never tans. Type II is fair and burns easily. Types III and IV fall in the middle, with Type IV skin (beige-olive) burning minimally and tanning well. Type V (moderate brown) rarely burns, and Type VI (dark brown or black) essentially never burns.
People with Type I and II skin face the highest risk of UV-related skin cancer because their skin produces less of the pigment that absorbs UV radiation before it reaches vulnerable DNA. Epidemiological data shows the highest sunburn rates occur among non-Hispanic White and Native American populations. But darker skin types are not immune to skin cancer, and they face a particular risk from a form of melanoma that isn’t driven by sun exposure at all.
Skin Cancer That Isn’t Caused by the Sun
Acral lentiginous melanoma (ALM) develops on the palms, soles of the feet, and under fingernails or toenails, areas that get very little UV exposure. This type of melanoma has a different genetic profile from sun-related melanomas, with a lower overall number of DNA mutations and less immune system activity within the tumor. It is more commonly diagnosed in people with darker skin.
Because UV radiation doesn’t explain ALM, researchers have looked at other contributing factors. Genetic predisposition and physical trauma to the skin are the leading candidates. ALM has been commonly reported following injury to the affected area, though the exact mechanism connecting trauma to cancer development in these sites isn’t fully understood.
Gene Mutations That Drive Cancer Growth
Whether triggered by UV light or something else, skin cancer ultimately comes down to specific genetic errors accumulating in a single cell. Two of the most important involve genes that act as a gas pedal and a brake on cell growth.
About 80% of common moles carry a mutation in a gene that locks a key growth-signaling pathway into the “on” position. Normally, when a skin cell acquires this kind of always-on growth signal, the cell recognizes something is wrong and enters a permanent state of dormancy. That’s why most moles stay harmless for life. The problem arises when a second mutation knocks out the cell’s primary tumor-suppressing gene, which functions as an emergency brake. Research has shown that disabling this brake in cells that already carry the growth mutation causes them to bypass dormancy entirely, begin multiplying rapidly, and take on the early characteristics of melanoma. In short, one mutation alone usually isn’t enough. It takes a combination of a stuck accelerator and a broken brake to push a mole toward cancer.
Chemical and Industrial Exposures
UV radiation gets most of the attention, but certain chemical exposures cause skin cancer through entirely separate pathways. Coal tar and coal-tar pitch, both of which contain carcinogens like benzene, are among the best-documented examples. Occupational exposure to these substances increases skin cancer risk, and workers at foundries, coke production facilities, coal gasification plants, and aluminum smelters face the highest levels of exposure. Roofers, pavement workers, and people who apply coal-tar coatings or paints are also at elevated risk.
The general public encounters coal tar on a smaller scale. It’s an active ingredient in some over-the-counter shampoos and skin treatments for eczema, psoriasis, and dandruff. The doses in these products are far lower than occupational exposures, but the connection between coal tar and skin cancer is well established at higher levels. Arsenic, found in contaminated groundwater in some regions, is another recognized skin carcinogen that works independently of UV damage.
Weakened Immune Systems
Your immune system doesn’t just fight infections. It also identifies and destroys abnormal cells before they can grow into tumors. When that surveillance system is suppressed, skin cancer risk rises sharply.
The clearest evidence comes from organ transplant recipients, who take medications to prevent their body from rejecting the new organ. These drugs deliberately dampen immune function, and the tradeoff is a significantly higher rate of skin cancer. In studies of transplant recipients who developed skin cancer, squamous cell carcinoma accounted for 71% of cases, basal cell carcinoma for 26%, and melanoma for 3%. That heavy tilt toward squamous cell carcinoma is notable because in the general population, basal cell carcinoma is the more common type. A suppressed immune system appears to be especially permissive for squamous cell growth.
Viruses Linked to Skin Cancer
Certain viruses contribute to skin cancer by inserting their genetic material into skin cells and hijacking the cell’s growth controls. The most dramatic example is the Merkel cell polyomavirus, discovered in 2008, which drives about 80% of Merkel cell carcinomas, a rare but aggressive skin cancer. In these tumors, the viral DNA is physically stitched into the cell’s own DNA. The virus produces proteins that disable the cell’s normal growth restraints, forcing it to keep dividing. If researchers shut down those viral proteins in lab experiments, the cancer cells stop growing, confirming that the virus isn’t just a bystander but an active driver.
Human papillomavirus (HPV) also plays a role, though a subtler one. Several strains of the beta-HPV family, particularly HPV8 and HPV38, have been linked to squamous cell carcinoma of the skin. Unlike Merkel cell polyomavirus, these HPV strains likely act as co-factors alongside UV damage rather than single-handedly causing cancer. Because multiple HPV strains frequently infect the same person, isolating the effect of any single strain has been challenging for researchers.
Multiple Causes, One Disease
Skin cancer is rarely the result of a single event. In most cases, it develops from a combination of factors: cumulative UV damage over decades, inherited traits that affect how well your skin repairs itself, immune function that may be compromised by medication or age, and in some cases viral infections or chemical exposures layered on top. Even virus-driven Merkel cell carcinoma typically involves UV radiation as a catalyst. The causes are different enough that no single prevention strategy eliminates all risk, but reducing UV exposure remains the single most impactful step because it accounts for the vast majority of cases.