"All of those differences are evidence there may be something different going on with their tumors," Thu said.
The new study confirmed earlier findings that nonsmokers were more likely to have the EGFR mutation, Thu said.
Never-smokers with lung cancer were also less likely to have the KRAS mutation, which has also been shown in prior research.
In smokers, it's believed that the carcinogens in tobacco and cigarettes cause DNA mutations that lead to the uncontrolled growth of cancer cells, Thu said.
In nonsmokers, the added genetic mutations suggest other mechanisms are driving the tumor growth, Thu said. "We hypothesize there is more genomic instability in the never-smokers than the smokers, and that leads us to believe there may be some other molecular mechanism that is driving the tumor development," she said.
Dr. David Carbone, a professor of medicine and cancer biology at Vanderbilt University, said the new study supports the idea that cancer in people who've never smoked vs. current and former smokers is different.
In never-smokers, the challenge is not only coming up with treatments that target the genetic mutations of their tumor, but in identifying people soon enough to help them, said Carbone, a member of the Lung Cancer Foundation of America's scientific advisory board.
Nonsmokers tend to take longer to be diagnosed with lung cancer because few suspect they have it, he said.
"We often see never-smokers present with advanced, incurable disease," he said.
Drugs that target particular genetic pathways have been very successful. Erlotinib (Tarceva), for example, has been shown to extend the lives of lung cancer patients with the EGFR mutation, present in about 10 percent of lung cancers, Carbone said.
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