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Molecular cancerization identified in airway epithelium of smokers
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Smoking may be linked to the formation of molecular features of cancer in the large airway epithelium of healthy smokers, according to data presented at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer: Biology, Therapy and Personalized Medicine meeting in San Diego.
Based on the premise that gene expression changes reflect genomic and epigenomic alterations preceding the development of pathologic lesions, researchers investigated whether characteristics of molecular cancerization can be detected early in healthy smokers, based on the expression of specific genes linked to lung cancer development. During the study, researchers also examined the possible association of chronic obstructive pulmonary disease with greater accumulation of cancerization features.
“We are striving to find the earliest molecular changes that are induced by environmental stressors — in this case, smoking,” Renat Shaykhiev, MD, PhD, assistant professor of genetic medicine at Weill Cornell Medical College, said in a press release. “Our goal is to understand the early pathogenesis of lung cancer and to develop strategies to prevent lung cancer in susceptible individuals.”
Using obtained bronchoscopic brushings, researchers analyzed the large airway epithelium of 21 healthy nonsmokers and 31 healthy smokers, the small airway epithelium of 63 healthy nonsmokers with 73 healthy smokers, and additional samples from 37 smokers with chronic obstructive pulmonary disease.
According to the study analysis, researchers found considerably more cancerous gene expression changes in the large airway epithelia of smokers than in those of nonsmokers. When researchers analyzed the small airway epithelium, no significant differences were found between healthy smokers and nonsmokers, but significant overall upregulation of cancerization genes were observed in smokers with chronic obstructive pulmonary disease.
From these results, the researchers determined that smoking is associated with acquisition of the molecular features of cancerization in the large airway epithelium and likely precedes accumulation in the small airway epithelium — identification of early cancerizationfeatures are crucial to understanding the early pathogenesis of lung cancer, as well as the development of cancer prevention strategies in cancer-prone individuals.
“Ideally, we would use these genes to do very routine analysis to determine which smokers or even nonsmokers are at risk for development of lung cancer,” Shaykhiev said.
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