Most basal cell and squamous cell skin cancers are caused by unprotected ultraviolet (UV) radiation exposure to the area of skin that develops the cancer. Most of this radiation comes from sunlight, but some may come from manmade sources such as tanning booths.

Some of this exposure may have occurred within the few years of the development of the cancer, particularly for squamous cell carcinoma. But many of the cases may be caused by exposures that happened many years earlier. Children and young adults often receive a lot of intense sun exposure that may not result in an actual cancer until many years or decades later. Repeated and unprotected sun exposure over many years increases the person's risk of skin cancer.

DNA is the genetic material in each of our cells. It passes along genetic information to the next generation that makes children resemble their parents. Along with information about how we look, DNA also contains information that tells the cells of our body how to grow and how to perform all the activities needed for life.

UV radiation (from sunlight or tanning lamps) damages DNA. Sometimes this damage affects certain genes (segments of DNA with a specific function) that control how and when cells grow and divide. Usually the body can repair the DNA damage. But if there is too much, in some situations, this results in the start of a cancer.

Researchers don't yet know all of the DNA changes that result in skin cancer, but they have found that many skin cancers contain changes in tumor suppressor genes. These genes normally function to help keep cells from growing out of control.

The gene most often found to be altered in squamous cell cancers is called p53. This gene normally causes damaged cells to die. When this gene is altered, these abnormal cells may live longer and perhaps go on to become cancerous.

A gene commonly found to be mutated in basal cell cancers is the "patched" (PTCH) gene. This tumor suppressor gene normally helps keep cell growth in check, so changes in this gene can allow cells to grow out of control.

These are not the only gene changes that may play a role in the development of skin cancer. There are likely to be many others as well.

People with xeroderma pigmentosum (XP) have a high risk for skin cancer. XP is a rare, inherited condition resulting from a defect in an enzyme that repairs damage to DNA. Because people with XP are less able to repair DNA damage caused by sunlight, they develop huge numbers of cancers on sun-exposed areas of their skin.

The link between squamous cell skin cancer and human papilloma virus (HPV) infection also involves DNA and genes. These viruses contain genes that instruct infected cells to make certain proteins that affect the growth-regulating proteins of normal skin cells. This can cause skin cells to grow too much and to not die when they're supposed to.

Scientists are studying other links between DNA changes and skin cancer. In the future, better understanding of how damaged DNA leads to skin cancer might be used to design treatments to overcome or repair that damage.