Mayo Clinic researchers found that the genetic mutation, alpha-1 antitrypsin deficiency (Ą1ATD), could explain up to about 12 percent of lung cancer patients in this study and likely represents the same widespread risk in the general population. The World Health Organization estimates that at least 120 million people worldwide are Ą1ATD carriers.
A normal Ą1AT gene produces a protein that stops enzymes from breaking down elastin, which keeps lung tissue elastic for normal function. However, the mutated gene produced less of the lung-protecting chemical from the protein, increasing the odds of developing lung cancer.
In the particular study, a team of 12 researchers looked at three different groups: 1,443 patients with lung cancer treated at Mayo Clinic from 1997 to 2003; a control group of 797 residents in the community; and a second control group of 902 siblings of the lung cancer patients. They found that:The Ą1ATD carrier rate among 1,443 genotyped patients with lung cancer was 13.4 percent, compared to 7.8 percent among unrelated control participants.
All Ą1ATD gene carriers were at a similarly greater risk of developing lung cancer, regardless of smoking status. Also, the estimated attributable risk for Ą1ATD carriers in this study among those who never smoked and among heavy smokers was 11 percent to 12 percent, suggesting that the genetic disorder might explain a significant proportion of lung cancer in the general population.
Although the study helps explain why people who have never smoked can develop lung cancer, it doesn't mean that people who don't have the gene won't develop lung cancer. "Smoking remains the overwhelming risk factor for lung cancer development."
Reference
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Leigh Frazer 4143927

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