Repeated exposure to tobacco smoke makes lung cancer much worse, and one reason is that it steps up inflammation in the lung. Scientists at the UC San Diego School of Medicine have found that mice with early lung cancer lesions that were repeatedly exposed to tobacco smoke developed larger tumors — and developed tumors more quickly — than unexposed animals. The key contributing factor was lung tissue inflammation.

The results of their study, to be published Jan. 19 in the journal Cancer Cell, provide definitive evidence for the role of lung inflammation brought on by chronic exposure to tobacco smoke in promoting lung cancer growth. The findings also establish new lung cancer models, provide insights into both the development and growth of lung cancer, and suggest the possibility of using anti-inflammatory agents to prevent or slow lung cancer progression, said Michael Karin, Ph.D., Distinguished Professor of Pharmacology and Pathology at the UC San Diego School of Medicine, who led the work.

“We’ve shown for the first time that tobacco smoke is a tumor promoter — not only a tumor initiator — and that it works through inflammation,” said Karin, director of the Laboratory of Gene Regulation and Signal Transduction and a member of the Moores UCSD Cancer Center. “Other particulate materials, such as fine silicon dust, asbestos and coal dust, may promote lung cancer development through similar mechanisms. Such substances were never found to induce mutations, which are the essence of tumor formation. More research is needed to explore the role and biochemical mechanisms of exposure to pro-inflammatory substances in the environment in early stages of cancer development.”

Lung cancer killed nearly 160,000 Americans in 2009, according to the American Cancer Society, making it the leading cause of cancer death in both men and women.

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