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Chronic exposure to cigarette smoke may reprogram different populations of lung stem cells, which maintain and repair lung tissue, in ways that make them vulnerable to specific cancer-causing gene alterations and ultimately help determine the type of lung cancer that develops.

Using laboratory-grown lung organoids, researchers at the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center followed changes in lung cells over six months of exposure to cigarette smoke condensate, a collection of chemicals and particles contained in cigarette smoke. They found that chronic exposure altered both the epigenetic programming that regulates gene activity and the genes being expressed in different populations of lung stem cells, creating distinct precancerous cell states.

When researchers subsequently introduced two genetic alterations commonly associated with smoking-related lung cancer, involving KRAS and TP53, the altered stem cell populations responded differently. KRAS mutations drove lung adenocarcinomas primarily from cells derived from bronchioalveolar stem cells, while loss of the tumor suppressor gene TP53 produced squamous cell carcinomas derived from basal stem cells.

The findings, reported Oct. 5 in the Proceedings of the National Academy of Sciences, help explain how environmental exposure, epigenetic changes and genetic mutations may work together during the earliest stages of non-small cell lung cancer (NSCLC), the most common type of lung cancer.

Epigenetic alterations are chemical changes that affect how genes are turned on or off without changing the DNA sequence, while genetic alterations, such as mutations, permanently alter the DNA sequence.

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