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Preclinical Study Suggests E-Cigarettes May Contribute to Lung Cancer in High-Risk Individuals

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Key Points

  • A study of human bronchial epithelial cells carrying mutations in the TP53 and KRAS genes has found that e-cigarette vapors enhanced the cells’ cancerous behaviors.
  • Although e-cigarettes are advertised as a safer alternative to tobacco cigarettes, very few studies have investigated their impact on lung function and whether they can promote lung cancer.
  • Further studies are underway to determine the impact of electronic cigarette exposure on lung carcinogenicity and provide scientific guidance to the FDA regarding the physiologic effects of e-cigarettes.

A study of human bronchial epithelial cells carrying mutations in the TP53 and KRAS genes has found that e-cigarette vapors enhanced the cells’ cancerous behaviors. The study suggests that e-cigarette exposure may contribute to lung cancer in individuals at high risk for the disease. The preliminary results were presented at the AACR-IASLC Joint Conference on the Molecular Origins of Lung Cancer, held in San Diego.

According to the American Cancer Society, lung cancer is by far the leading cause of cancer death among both men and women in the United States and at least 80% of those deaths are thought to be the result from smoking. Although electronic cigarettes (e-cigarettes), which use a battery-powered electronic nicotine delivery system to supply nicotine without combusting tobacco or producing smoke, are advertised as a safer alternative to tobacco cigarettes, very few studies have investigated the impact they have on lung function and whether they can promote lung cancer.

Study Methodology

Because TP53 and KRAS mutations are often found in the airway of current and former smokers at risk for lung cancer, Stacy J. Park, PhD, a postdoctoral fellow at the University of California, Los Angeles, and colleagues, assessed the impact of e-cigarette exposure on the carcinogenic potential of immortalized human bronchial epithelial cells on a background of silenced TP53 and KRAS. The cells were grown in a liquid medium that had been previously exposed for 4 hours to e-cigarette vapor or tobacco smoke. Nicotine levels were estimated to be similar to the levels to which lung airway cells are exposed during e-cigarette smoking.

Findings

The researchers found that the human bronchial epithelial cells showed cancer-like behaviors regardless of whether the medium had been generated using e-cigarette vapor or tobacco smoke. Cells grown in both groups demonstrated an enhanced ability to become invasive and to exhibit colony formation, a process fundamental to the survival and metastasis of cancer cells.

The researchers also observed that the changes in gene expression following growth in the medium generated by e-cigarette vapor were very similar to those changes found when the cells were grown for the same period of time in the medium generated using tobacco smoke.

In immortalized human bronchial epithelial cells with normal TP53 and KRAS genes (similar to normal airways), the high-nicotine medium generated using e-cigarette vapor was found to be toxic, reducing cell growth and triggering cells death. However, it did not cause the cells to develop cancerous behaviors, according to Dr. Park. “Since many users of e-cigarettes are smokers who generally have an elevated risk of developing lung cancer due to the presence of mutations, our data suggest that within this population at high risk for lung cancer, e-cigarettes may be harmful,” Dr. Park said in a statement.

“We will next compare the [e-cigarette]-induced gene expression signature to carcinogenicity-related gene signatures established in previous and ongoing clinical investigations and test [e-cigarette]-altered candidate genes for their ability to drive the malignant transformation of airway epithelial cells. These studies will determine the impact of [e-cigarette] exposure on lung carcinogenicity and provide needed scientific guidance to the FDA regarding the physiologic effects of [e-cigarettes],” wrote the researchers.

The study was supported by funds from the National Institutes of Health; the National Cancer Institute; the National Heart, Lung, and Blood Institute; and the University of California Tobacco-Related Disease Research Program. Dr. Park reported no potential conflicts of interest.

The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.


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