Two more genes linked to common skin cancer

A basal cell carcinoma papule is seen in a handout photo from the National Cancer Institute.

LONDON (Reuters) - Scientists have found two new genetic variations that appear to increase the risk of the most common skin cancer among people of European descent.

The variations play no role in skin color but people with both of them are nearly three times more likely to develop basal cell carcinoma compared with people without the changes, researchers from Iceland's Decode Genetics said on Sunday.

Darker skin is traditionally regarded as an important protection against skin cancer.

"Here we have two variants that have no impact on pigmentation and only affect the risk of basal cell carcinoma," Kari Stefansson, Decode's chief executive, who led the study, said in a telephone interview. "We don't know why that is."

Basal cell carcinoma is the most common form of cancer worldwide, and in the vast majority of cases are thought to be caused by exposure to ultraviolet rays of the sun, according to the American Academy of Dermatology.

Most cases are easy to treat when detected early, but in rare instances the cancer is resistant to treatment, causing damage to skin and sometimes invading bone and cartilage.

The researchers at Decode, a biotech company hunting for new drugs using Iceland's unique gene pool dating back to the Vikings, analyzed genes of more than 30,000 people to identify the impact of the genetic variations located on chromosome 1.

These variations differed from past genetic changes linked to basal cell carcinoma in that unlike the others they were not associated with fair skin or pigmentation.

The study published in Nature Genetics also found that the risk of developing basal cell carcinoma was 12 times higher for people with these new variations along with the three other genetic changes already linked to the cancer.

"Exposure to the sun has no direct impact on the genes, which add to the total risk of basal cell carcinoma," Stefansson said.

(Reporting by Michael Kahn; Editing by Charles Dick)