Cigarette smoke exposure has been shown to activate genes that promote cancer and deactivate genes that stop tumour growth.
They found that alteration in DNA methylation, a vital process, which regulates gene expression during normal development, might explain why former smokers develop lung cancer.
With the help of endoscope, the research team led by Emily A. Vucic, a graduate student at the British Columbia Cancer Research Centre, Vancouver, B.C. collected bronchial epithelial cells, which are cells that line the lungs, from 16 former smokers.
The participants quit smoking more than 10 years ago. Eight participants had surgical removal of non-small cell lung cancer; eight were disease free.
The study showed differences in methylation levels in lung epithelial cells between former smokers with and without lung cancer.
"Alteration to DNA methylation might potentially explain why some former smokers sustain additional genetic damage resulting in lung cancer," Vucic said.
"As methylation is a reversible DNA modification, this knowledge could prompt the development and application of chemopreventive agents and unique therapeutic strategies that target DNA methylation in these patients."
The researchers are pursuing additional studies to confirm their initial results.