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Genes may increase lung cancer risk among smokers, according to lung cancer study

Genes may increase lung cancer risk among smokers, according to lung cancer study

In the latest project to use the findings of human genome research to assess individual health risks, a suite of new studies has found a genetic variant that can increase smokers’ risk of getting lung cancer by as much as 80 percent.

One of the research teams, deCODE Genetics of Iceland, already has incorporated the discovery into a package of tests it sells to the public, offering consumers genetic profiles that estimate a person’s risk for 26 conditions including prostate cancer, diabetes and even male-pattern baldness.

Authors of the three cancer reports published Wednesday in the journal Nature employed a powerful new method to scan thousands of people’s genomes looking for links to disease. The results suggest that scientists are beginning to reap the benefits of the Human Genome Project, which promised a new era of personalized medicine based on an individual’s genetic risks.

But experts caution that many of the emerging tests are brand new and have severe limitations.

For example, none of the new findings in the new lung cancer study would change doctors’ basic advice regarding cigarettes: If you don’t smoke, don’t start, and if you do smoke, try to quit.

Kari Stefansson, chief executive officer of the Icelandic company, conceded that its lung cancer test would not aid a typical person’s health decisions but argued that “knowledge is never evil in and of itself.”

“As a diagnostic test, I think, it is of no value,” said Stefansson, who also co-wrote his team’s report. “I am actually even a little bit afraid that some may look at it as a green light to smoke, and that’s something I would not want to contribute to.”

Several experts pointed out that although an 80 percent higher risk may sound significant, all smokers are at high risk of lung cancer. The risk for smokers without the genetic variant is about 14 percent, compared with 23 percent for those with the variant.

The usefulness of such genetic information for ordinary consumers is a subject of intense debate among researchers and genetic counselors. Genome-wide tests are at such an early stage that the risk assessment a consumer gets today may well be obsolete next year, if not next month.

“There’s a serious concern that people will be flooded with information that changes over time, and they’ll have little idea how to use it to improve their health,” said Dr. David Hunter, a professor of epidemiology at the Harvard School of Public Health, who co-wrote a commentary on the research in Nature.

Yet Stefansson said the field is moving so fast that he thinks wide-ranging genetic profiles of individual patients will be common practice within five years.

The road to such tests began in 2001 with the completion of the Human Genome Project, which mapped out all the genes that most people possess. That blueprint varies slightly from person to person, often in the form of tiny variations called SNPs, or “snips.” Scientists have made steady progress this decade in cataloging millions of points where people’s genomes frequently vary.

The lung cancer studies released Wednesday used a type of analysis called genome-wide association, scanning about 300,000 genetic markers for variation and seeing how they match up with people’s diseases and habits.

Scores of similar genome-wide analysis studies have been published since early 2007, as improved lab techniques made such work almost routine. In March, groups from America, Britain and the deCODE team published papers showing about a dozen genome regions that affect the risk of prostate cancer.

“The effect of any one of these genetic markers is small, but we’re looking at complex diseases where many genes have a role,” said Dr. Stephen J. Chanock, chief of translational genomics at the National Cancer Institute, who led one of the recent prostate cancer studies.

Each of the three new lung cancer studies used data from thousands of people, and the deCODE study had the largest sample with about 40,000 participants. All three research groups zeroed in on variation in a portion of chromosome 15 that was previously known to affect cells that respond to nicotine.

The researchers disagreed on whether the genetic variants make people more likely to stay hooked on cigarettes or if they directly affected the development of cancer. The deCODE group found a direct link with smoking behavior, but the other two teams did not.

“Future studies will tell us whether the effect has more to do with smoking or lung cancer, but my intuition is it’s a combination,” said Chanock, who co-wrote the Nature commentary on the lung cancer studies.

Stefansson said his study found that smokers who had one copy of the genetic variant smoked an average of one more cigarette per day than people who lacked the variant. Smokers with two copies of the variant smoked two more cigarettes per day than those without the genetic quirk.

Some of the genes involved play a role in how the brain handles nicotine, which lends credence to the idea that the genetic variants influenced smokers’ behavior. The genes also can affect how other parts of the body respond to nicotine, said Dr. Chris Amos, whose University of Texas group published one of the new studies.

“It raises the possibility that there’s a direct effect through nicotine in activating cells that go on to become cancerous,” Amos said.

Several experts pointed out that a test for the variant would not greatly improve doctors’ ability to predict which smokers will get lung cancer. “Because the predictive value is so low, [the test] seems unlikely to be something that people will clamor to have,” wrote Nancy Cox, a professor of human genetics at the University of Chicago, in an e-mail response to questions.

If the genetic variation does affect whether a person gets hooked on cigarettes, that could lead to targeted interventions for people at high risk of nicotine dependence. Stefansson said the link to smoking behavior shows how complicated the role of genes can be.

“We’ve always looked at lung cancer as a purely environmental disease caused by smoking, but now we have a genetic variant that makes you go into this environment repeatedly,” Stefansson said. “The distinction between nature and nurture gets completely blurred.”

You all seem to be in the dark concerning types of smokers. There are tobacco smokers and users that do not inhale smoke into their lungs. Then there are those cigarette smokers, most of which do inhale smoke into their lungs inviting lung cancer. Almost all pipe and cigar smokers don’t inhale smoke into their lungs, since there are no taste buds in the lungs, and smoking a pipe or cigars is not about getting a nicotine fix, it’s about taste. Smoking a pipe or cigars is as harmless as drinking a cup of tea. Then of course there are the tobacco chewers and sniffers; since direct and prolonged contact with a tobacco product is required, this activity can cause cancer. If anyone is going to get even with the system, deservedly so, it should be pipe and cigar smokers, since they practice safe smoking and do not get cancer.

It seems to me that the most important thought to take from this article, is that since this genetic programming exists in this disease,it likely exists for every disease there is. Take the genetic factor, combine it with environment and habits, and you have “Life Programming”. This cancer evidence shows how totally important it is to clean up our air. We are all forced to smoke because of pollution.

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