Studies suggests that cancer risk is not just down to lifestyle
Three independent genetic studies have found some of the strongest evidence yet that your genes influence your risk of developing lung cancer.
Lung cancer, the most common killer cancer in the world, is largely caused by smoking. Tobacco is thought to be responsible for about 5 million premature deaths every year and smoking is still clearly the largest risk factor. But the new results suggest that, amongst smokers, some people may be as much as 80% more at risk than others thanks to their genes.
People who have never smoked might also have a slightly increased risk of developing lung cancer and similar problems, although the three studies disagree on whether this is actually the case. It is not clear whether the genetic effect occurs independently of smoking, or whether the genes raise the risk of cancer by exacerbating nicotine addiction.
The cancer region
By scanning the entire genomes of lung-cancer patients and healthy controls, the three research teams all identified a region on chromosome 15 that seems to influence the likelihood of developing cancer. People possessing a certain set of mutations at this genetic location are more likely than others to have the disease.
About 50% of the general population carries a single copy of this cancer gene variant, members of the three research groups suggest. Data from all three studies — some of which did not include non-smokers — show that possessing this single copy raises the risk of lung cancer by about 30%.
What's more, another 10% of the population is likely to carry two copies of this set of mutations, raising cancer risk by as much as 80% relative to people with equivalent lifestyles without the cancer-linked gene variant.
Smoking is still the mostly significant contributor to lung cancer, says Kari Stefansson of deCODE Genetics in Reykjavik, Iceland, who led one of the studies1, which featured almost 11,000 Icelandic smokers. "Just smoking itself is the overwhelming risk factor," he says.
Source: www.nature.com (2 April 2008)
Read more: HERE
Three independent genetic studies have found some of the strongest evidence yet that your genes influence your risk of developing lung cancer.
Lung cancer, the most common killer cancer in the world, is largely caused by smoking. Tobacco is thought to be responsible for about 5 million premature deaths every year and smoking is still clearly the largest risk factor. But the new results suggest that, amongst smokers, some people may be as much as 80% more at risk than others thanks to their genes.
People who have never smoked might also have a slightly increased risk of developing lung cancer and similar problems, although the three studies disagree on whether this is actually the case. It is not clear whether the genetic effect occurs independently of smoking, or whether the genes raise the risk of cancer by exacerbating nicotine addiction.
The cancer region
By scanning the entire genomes of lung-cancer patients and healthy controls, the three research teams all identified a region on chromosome 15 that seems to influence the likelihood of developing cancer. People possessing a certain set of mutations at this genetic location are more likely than others to have the disease.
About 50% of the general population carries a single copy of this cancer gene variant, members of the three research groups suggest. Data from all three studies — some of which did not include non-smokers — show that possessing this single copy raises the risk of lung cancer by about 30%.
What's more, another 10% of the population is likely to carry two copies of this set of mutations, raising cancer risk by as much as 80% relative to people with equivalent lifestyles without the cancer-linked gene variant.
Smoking is still the mostly significant contributor to lung cancer, says Kari Stefansson of deCODE Genetics in Reykjavik, Iceland, who led one of the studies1, which featured almost 11,000 Icelandic smokers. "Just smoking itself is the overwhelming risk factor," he says.
Source: www.nature.com (2 April 2008)
Read more: HERE
