Skin cancer develops when DNA inside skin cells becomes damaged and the cells begin growing out of control. The most common cause by far is ultraviolet (UV) radiation from sunlight or tanning beds, but genetics, immune system function, certain viruses, chemical exposures, and even chronic wounds can also trigger it. Understanding these causes helps explain why skin cancer is so common and who faces the greatest risk.
How UV Radiation Damages Skin Cell DNA
Sunlight contains two types of ultraviolet radiation that harm skin in different ways. UVB rays are absorbed directly by DNA, creating structural defects called pyrimidine dimers, which are essentially kinks in the DNA strand that distort the genetic code. UVA rays work more indirectly. They activate molecules already present in your skin that generate what’s known as oxidative stress, a burst of reactive particles that attack DNA and other cell components from the inside.
Your cells have a built-in repair system designed to find and fix these DNA defects before they cause problems. This system recognizes the damaged sections and cuts them out so the correct code can be restored. But the system isn’t perfect. When UV exposure is frequent or intense, repairs can’t keep up. Unrepaired damage accumulates and eventually becomes permanent mutations during cell division. These mutations can disable tumor suppressor genes, the very genes responsible for keeping cell growth in check. Once enough of these protective genes stop working, cells lose their brakes and begin multiplying unchecked.
Why Sunburns Early in Life Matter So Much
Not all sun exposure carries equal weight. A large study that followed nearly 109,000 women for about 20 years found that those who had five or more blistering sunburns between ages 15 and 20 had an 80 percent increased risk of melanoma and a 68 percent increased risk of the two other major skin cancers (basal cell carcinoma and squamous cell carcinoma) compared to those who didn’t. Severe burns during adolescence appear especially dangerous because young skin cells are dividing rapidly, and mutations introduced at that stage get copied into a much larger population of cells over a lifetime.
Tanning Beds and Artificial UV
Indoor tanning is not a safer alternative to sunlight. Tanning beds emit mostly UVA radiation, which penetrates deeper into the skin than UVB. According to the American Academy of Dermatology, indoor tanning increases the risk of squamous cell carcinoma by 58 percent and basal cell carcinoma by 24 percent. The common belief that a “base tan” from a tanning bed offers protection is a myth. Any tan is a visible sign that DNA damage has already occurred and the skin is trying to defend itself by producing more pigment.
Skin Type and Natural Protection
Your natural skin color plays a significant role in how vulnerable you are. Dermatologists use a six-point scale called the Fitzpatrick classification, ranging from very fair skin that always burns (type I) to deeply pigmented skin that rarely burns (type VI). People with skin types I and II face the highest risk of skin cancer because they have less melanin, the pigment that absorbs and scatters UV radiation before it reaches DNA. Those with types V and VI have substantially more built-in protection.
This doesn’t mean darker-skinned individuals are immune. Skin cancer can develop in anyone, and when it does occur in people with more pigment, it’s often diagnosed later because it appears in less obvious locations like the palms, soles of the feet, or under nails.
Genetics and Family History
About 5 to 10 percent of all melanomas run in families and follow a hereditary pattern. The most significant genetic factor is a mutation in a gene called CDKN2A, which acts as a tumor suppressor. Mutations in this single gene account for an estimated 35 to 40 percent of all familial melanomas. Several other genes also raise melanoma risk when mutated, including one called BAP1 that’s linked to both skin and eye melanomas as part of a broader cancer predisposition syndrome.
Basal cell carcinoma has its own genetic vulnerabilities. Gorlin syndrome, a rare inherited condition caused by mutations in a gene called PTCH1, leads to the development of numerous basal cell carcinomas starting at a young age. People with this syndrome may develop dozens or even hundreds of these tumors over their lifetime. While these hereditary conditions are uncommon, having even one close relative with melanoma meaningfully increases your own risk.
A Weakened Immune System
Your immune system doesn’t just fight infections. It also patrols for abnormal cells and destroys them before they can form tumors. When that surveillance system is suppressed, skin cancer risk rises dramatically. The clearest example 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 consequences for skin cancer are striking.
In a Canadian study of more than 10,000 transplant recipients, nearly 17 percent developed a skin cancer after transplant, with a median time to diagnosis of just under four years. Their overall skin cancer rate was almost seven times higher than the general population. Squamous cell carcinoma, which is normally less common than basal cell carcinoma, actually becomes the dominant type in transplant patients, a reversal of the usual pattern.
Viruses That Promote Skin Cancer
Certain strains of human papillomavirus (HPV) contribute to skin cancer development, particularly squamous cell carcinoma. HPV produces proteins that interfere with two of the cell’s most important tumor suppressors, p53 and the retinoblastoma protein, effectively disabling the cell’s ability to stop abnormal growth and repair damaged DNA.
The connection between HPV and skin cancer is strongest in people with weakened immune systems. In immunocompetent people, a group of HPV strains called beta types may play an early role in cancer development by amplifying the damaging effects of UV radiation on skin cells, even if the virus itself is no longer active by the time the cancer is established. Researchers describe this as a “hit-and-run” mechanism: the virus sets the stage for cancer, then becomes unnecessary for its continued growth. Under the fingernails and toenails, a different HPV type (HPV-16, more commonly associated with cervical cancer) is found in roughly half of squamous cell carcinomas at that site.
Chemical and Environmental Exposures
Arsenic is the best-documented chemical cause of skin cancer. This naturally occurring element contaminates drinking water in many parts of the world, particularly in regions with certain geological formations or near mining and metal smelting operations. Prolonged exposure to arsenic-contaminated water is associated with increased rates of both skin and bladder cancer. Until the mid-1900s, arsenic compounds were also widely used as pesticides, and they appeared in some medical treatments through the 1970s. People can still be exposed through contaminated groundwater, tobacco smoke, and food grown with contaminated irrigation water.
Ionizing radiation from medical treatments is another recognized cause. People who received radiation therapy, particularly with older techniques that delivered broader exposure to surrounding skin, have elevated rates of skin cancer in the treated area, sometimes appearing years or decades later.
Chronic Wounds and Scars
Skin cancer can also develop in areas that have nothing to do with sun exposure. When a wound fails to heal for months or years, whether from a burn, a chronic ulcer, or an old scar, the constant cycle of inflammation and attempted repair can eventually trigger cancerous changes. This type of cancer, known as a Marjolin’s ulcer, most commonly takes the form of squamous cell carcinoma. It accounts for roughly 2 to 5 percent of all squamous cell carcinoma cases and is more common in men, typically appearing after age 50.
The exact mechanism isn’t fully understood, but chronic inflammation, reduced oxygen supply to the tissue, and localized immune suppression in the wound area all appear to contribute. These cancers can be aggressive, partly because they often go unrecognized for a long time. Any non-healing wound that changes in appearance, starts to grow, or develops raised edges deserves prompt evaluation.