Smoking is the most powerful known cause of lung cancer. The question is: Why do some smokers for a long time to descend to the deadly disease, while others escape? New genetic research reveals a culprit who was also upping praying for the person likely to become addicted to cigarettes.
Two new studies linking a variation in a gene residing on chromosome 15 (a person of 23 pairs of chromosomes) with an increased risk of developing lung cancer, a third study suggests that the same mutation affects a person tends to become addicted to cigarettes and, by extension, to develop the terrible disease. Lung cancer is diagnosed in about 200000 Americans and kills more than 150000 annually.
The new research published in both Nature and Nature Genetics, suggests that people with this gene have a loophole 30 percent greater chance of developing the disease, which is often fatal. But studies differ on the potential risk of dependency. The results allow a better understanding of how this genetic variation and smoking interact to cause lung cancer. They provide "new targets to begin to think about how to treat drug addiction and, also, of course, for the prevention or treatment of lung cancer," says Nora Volkow, director of the National Institute on Drug Abuse (NIDA) in Bethesda, Md., who was not involved in the study.
The research teams scanned a list of 300000 minutes changes in the genome where a (unit of genetic material) has been either deleted, duplicated or replaced. (These changes are called single nucleotide polymorphisms, or SNPs.) In one study, scientists at the Iceland-based biotechnology company deCODE genetics tried to correlate these genetic variations of a person to smoke, other research efforts have tried to bind them for lung cancer.
DeCODE Icelandic 50000 The group questioned about their smoking habits, using the information gleaned from this investigation as well as 40000 genome scans of smokers admitted to the pack, researchers have zeroed on a CHRNA variant of the gene, which codes for a receptor on nerve cells can be stimulated by nicotine. The amended version of the gene was more common among the heaviest smokers than it was in the rest of the population. "Non-smokers have a higher frequency of this variant that smokers who smoke between one and 10 cigs a day," says the neurologist Kári Stefánsson, deCODE's CEO, "because if you smoke and you have this variant You tend to smoke more than 10 cigs per day. "
When the team Stefánsson applied statistics on the incidence of lung cancer, she found that people with two copies of the altered gene had a huge 70 percent more likely to develop lung cancer, those with a copy had an increased risk of 30 percent.
These results are almost identical to those of other studies and one (in the wild) conducted by the International Agency for Research on Cancer (IARC) in Lyon, France (which is based on the examination of about 11000 volunteers, 7500 d 'Among them were smokers) and the other (in Nature Genetics), by a team at the University of Texas MD Anderson Cancer Center in Houston, who reviewed 9000 people, about 4000 of them were smokers.
Paul Brennan, who led the study of the CIRC, said he initially believed that the risk of lung cancer was raised by genetic predisposition to become addicted. "The genes that made you more likely to smoke, are you more likely to smoke, you are less likely to give up, and therefore more likely to develop lung cancer," he says. But his research has shown that, in fact, the gene seemed an independent person increase the risk of developing the disease-at arm's length.
NIDA's Volkow suggests that the gene variant may lead some people to smoke more because of its effect on the reward centers of the brain (associated with addictive behavior), and may increase the risk of cancer, too, because it also plays a role in lung tissue function. Epidemiologist Christopher Amos, Texas, who led the study, notes that even nicotine receptor involved in this study has been shown in previous research to stimulate tumor growth in other areas of the body, including the thymus (an body located near the lungs, which produces immune cells). "The nicotine or its derivatives can stimulate the cells to proliferate, to participate in the development of new blood vessels and also not to undergo cell death," he says, all of which are characteristics of tumor formation and the growth. "So that raises the possibility that there is a direct effect through the nicotine in the activation of the cells become cancerous."
Two new studies linking a variation in a gene residing on chromosome 15 (a person of 23 pairs of chromosomes) with an increased risk of developing lung cancer, a third study suggests that the same mutation affects a person tends to become addicted to cigarettes and, by extension, to develop the terrible disease. Lung cancer is diagnosed in about 200000 Americans and kills more than 150000 annually.
The new research published in both Nature and Nature Genetics, suggests that people with this gene have a loophole 30 percent greater chance of developing the disease, which is often fatal. But studies differ on the potential risk of dependency. The results allow a better understanding of how this genetic variation and smoking interact to cause lung cancer. They provide "new targets to begin to think about how to treat drug addiction and, also, of course, for the prevention or treatment of lung cancer," says Nora Volkow, director of the National Institute on Drug Abuse (NIDA) in Bethesda, Md., who was not involved in the study.
The research teams scanned a list of 300000 minutes changes in the genome where a (unit of genetic material) has been either deleted, duplicated or replaced. (These changes are called single nucleotide polymorphisms, or SNPs.) In one study, scientists at the Iceland-based biotechnology company deCODE genetics tried to correlate these genetic variations of a person to smoke, other research efforts have tried to bind them for lung cancer.
DeCODE Icelandic 50000 The group questioned about their smoking habits, using the information gleaned from this investigation as well as 40000 genome scans of smokers admitted to the pack, researchers have zeroed on a CHRNA variant of the gene, which codes for a receptor on nerve cells can be stimulated by nicotine. The amended version of the gene was more common among the heaviest smokers than it was in the rest of the population. "Non-smokers have a higher frequency of this variant that smokers who smoke between one and 10 cigs a day," says the neurologist Kári Stefánsson, deCODE's CEO, "because if you smoke and you have this variant You tend to smoke more than 10 cigs per day. "
When the team Stefánsson applied statistics on the incidence of lung cancer, she found that people with two copies of the altered gene had a huge 70 percent more likely to develop lung cancer, those with a copy had an increased risk of 30 percent.
These results are almost identical to those of other studies and one (in the wild) conducted by the International Agency for Research on Cancer (IARC) in Lyon, France (which is based on the examination of about 11000 volunteers, 7500 d 'Among them were smokers) and the other (in Nature Genetics), by a team at the University of Texas MD Anderson Cancer Center in Houston, who reviewed 9000 people, about 4000 of them were smokers.
Paul Brennan, who led the study of the CIRC, said he initially believed that the risk of lung cancer was raised by genetic predisposition to become addicted. "The genes that made you more likely to smoke, are you more likely to smoke, you are less likely to give up, and therefore more likely to develop lung cancer," he says. But his research has shown that, in fact, the gene seemed an independent person increase the risk of developing the disease-at arm's length.
NIDA's Volkow suggests that the gene variant may lead some people to smoke more because of its effect on the reward centers of the brain (associated with addictive behavior), and may increase the risk of cancer, too, because it also plays a role in lung tissue function. Epidemiologist Christopher Amos, Texas, who led the study, notes that even nicotine receptor involved in this study has been shown in previous research to stimulate tumor growth in other areas of the body, including the thymus (an body located near the lungs, which produces immune cells). "The nicotine or its derivatives can stimulate the cells to proliferate, to participate in the development of new blood vessels and also not to undergo cell death," he says, all of which are characteristics of tumor formation and the growth. "So that raises the possibility that there is a direct effect through the nicotine in the activation of the cells become cancerous."
