WASHINGTON (Reuters) - Smoking may turn on some genes in the body in a permanent and harmful way, scientists said on Thursday in a study that may help explain why the risk of cancer remains high even after smokers quit.

They found many genetic changes that stop when a smoker quits, but found several genes that stay turned on for years, including several not previously linked with tobacco use.

"These irreversible changes may account for the persistent lung cancer risk despite smoking cessation," the researchers wrote in their report, published in BioMed Central journal BMC Genomics.

In any cell, only about one-fifth of the genes are switched on at any given time.

Raj Chari of the British Columbia Cancer Research Centre in Vancouver and colleagues took tissue samples from 20 smokers and former smokers and compared their gene activity to one another and to the genes of four people who had never smoked.

They found some DNA repair genes were turned off in smokers and stayed off in the former smokers. Damage to the DNA is one of the main causes of cancer.

One gene that was switched on in smokers and former smokers was CABYR, a gene involved in helping sperm to swim.

It may also help other types of cells move. For instance, cells in the airways may be helped to move their tail-like cilia to push mucus along. And it has been associated with brain tumors, the researchers said.

Another gene that was switched on in smokers but not in people who had never smoked was called ENTPD8. It appears to play a role in damaging DNA.

Other genetic changes seen in smokers appeared to reverse themselves a year or more later in the former smokers. Some were involved in helping cells in the airways repair and regenerate.

"Fifty percent of newly diagnosed lung cancer patients are former smokers. It is therefore important to understand the effects of tobacco smoking on the (airways) in both active and former smokers," the researchers wrote.

The study is published on the Internet at http://www.biomedcentral.com/bmcgenomics/.