Gene May Increase Risk of Lung Cancer : Medicine: The finding by Louisiana researchers supports the theory that the disease can result from an interaction between genetics and lifestyle.
A new examination of lung cancer within families suggests that an unidentified gene may increase a person’s risk of the disease--a finding that supports the theory that lung cancer, like other diseases, can result from an interaction of genetics and lifestyle.
The study, published todaywed in the Journal of the National Cancer Institute, suggests that people with the gene are more likely than others to develop lung cancer relatively early in life, particularly if they smoke or are exposed to certain other carcinogens. Traditionally, it was thought that lung cancer resulted solely from environmental causes.
The researchers emphasized Tuesday that the theory remains to be proven by pinpointing the gene and determining how it works. The current study was based solely on observation of lung cancer patterns in families, not on an analysis of genetic material.
“It would mean that . . . it’s a disease that has many different causes,” said Dr. Henry Rothschild, a co-author of the paper. “(If) there is a group of people that have a gene that makes them more susceptible . . . preventive measures (such as anti-smoking programs) could be taken in those people.”
The researchers also stressed that smoking and other environmental factors are more important than genetics in lung cancer.
It has been known for several decades that lung cancer can “cluster” in families. It is also well known that smoking and exposure to workplace carcinogens can cause lung cancer, although some people are believed to be more susceptible than others.
In the new study, researchers at Louisiana State University Medical Center studied 337 families of people who had died of cancer. Many of Louisiana’s parishes have lung cancer death rates that rank among the highest in the nation.
The researchers explored who in each family had developed cancer, at what age and under what conditions. Taking those factors into account, they say they found disease patterns consistent with accepted patterns of inheritance first identified by Gregor Mendel, founder of modern genetics.
The group suggested that the gene accelerates the early onset of cancer. It appeared to play a significant role in cancers that developed in middle age. By contrast, most cancers occurring in old age were attributed to smoking alone.
It is not known how the gene might exert its effect. But epidemiologist Thomas A. Sellers, who headed the study, said the gene might affect the way people metabolize potentially carcinogenic material in cigarette smoke.
“The importance (of this) is that once you isolate one specific mechanism, you can see how that disease is caused,” Rothschild said.
Sellers acknowledged that it is possible his theory is wrong and that perhaps unidentified environmental factors are mimicking genetic patterns. But he said that seemed unlikely because “the genetic model fits the data so well.”
He said the group intends next to try to identify the gene through studies of DNA.
In an editorial accompanying the paper in the journal, George E. Bonney of Howard University Cancer Center said the paper provides some of “the first strong evidence for gene-environment-lifestyle interactions” in the development of lung cancer.
But Bonney added, “Finding (the gene) will provide the ultimate proof of its existence.”
Dr. Arno G. Motulsky, a professor of medicine and genetics at the University of Washington , said the study adds new information to the field of so-called ecogenetics--the study of the interaction of heredity and environment.
“If one could find out that you, and not I, are highly susceptible to the carcinogenic effects of cigarette smoking, you might think twice about smoking,” he said.
