LONDON (Reuters) - An international research team has identified two genetic variations that appear to increase a person’s risk of developing lung cancer by up to 60 percent, they reported on Sunday.
In April the same researchers identified another gene that raised lung cancer risk and they said their latest finding was relevant for both smokers and non-smokers.
“We are looking at differences in the DNA that makes you more or less likely to develop lung cancer,” said Paul Brennan, a cancer epidemiologist at the World Health Organisation’s International Agency for Research on Cancer.
“The idea is if you can identify genes then that might indicate why people develop lung cancer.”
Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death among women worldwide, according to the American Cancer Society, with about 975,000 men and 376,000 women forecast to die annually.
Smoking is the leading risk factor but increasingly scientists are looking to genetics to help explain why some long-time smokers never develop the disease and why some non-smokers do.
The study published in the journal Nature Genetics included researchers from 18 countries who analyzed genetic mutations in more than 15,000 people -- 6,000 with lung cancer and 9,000 without the disease.
The researchers discovered a region on the fifth chromosome containing two genes -- TERT and CRR9 -- where they believe variations can boost the likelihood of lung cancer by as much as 60 percent.
“We are looking at versions of genes that everybody has,” Brennan said in a telephone interview.
Not much is known about CRR9 but pinpointing the TERT gene is promising because it activates an enzyme called telomerase which is key to aging and cancer, Brennan said.
Cancer is caused by defects in DNA, the basic genetic material. All chromosomes, which carry the DNA, also have little caps on each end called telomeres.
Each time a cell divides, these telomeres become a little more frayed. When they are too worn out, the cell dies.
But when cells become cancerous, they produce telomerase, which can renew the telomeres and lets the cells reproduce out of control, eventually to form a tumor.
So implicating the TERT gene in a specific cancer can help lead to a better understanding of how cancer develops and boost the design of new drugs to stop tumors, Brennan added.
“The principle is there,” he said. “If one can identify what goes wrong, it may be possible to identify targeted drugs.” (Reporting by Michael Kahn; Editing by Maggie Fox and Matthew Jones)
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