Tobacco Smoke Causes Inflammation, Promotes Cancer Growth

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 University of California, 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 January 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, PhD, 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. Read more

Diet May Protect Against Lung Cancer In Smokers

Leafy green vegetables, folate, and some multivitamins could serve as protective factors against lung cancer in current and former smokers, according to a study that is a first step in understanding a complex association. The study was led by Steve Belinsky, Ph.D. and other researchers at the institute in ABQ, NM. It was supported by the National Cancer Institute (NCI), part of the National Institutes of Health. The study appeared online Jan. 12, 2010, in Cancer Research .

Researchers examined cells that were coughed up by current and former smokers for gene methylation, a chemical modification used by the cell to control gene expression. Upon careful study of the cells and by comparing those cells with profiles of smokers’ dietary intake of leafy green vegetables, folate, and some multivitamins, they found an association between those particular substances was associated with a reduced prevalence for cellular gene methylation.

As seen in previous studies, gene methylation is likely to be a major mechanism in lung cancer development and progression, as well as a potential marker for the early detection of lung cancer. Dr. Belinsky said, “This study suggests that diet and dietary supplements could help in preventing lung cancer.” Read more

Cancer/Inflamation Link Discovered By University Of Montreal

Canadian researchers have discovered a novel molecular mechanism that prevents cancer. In the December 11 edition of the prestigious journal Molecular Cell, scientists from the Université de Montréal and the Université de Sherbrooke explain how they found that the SOCS1 molecule prevents the cancer-causing activity of cytokines, hormones that are culprits in cancer-prone chronic inflammation diseases such as Crohns, in smokers and people exposed to asbestos.

“Excessive cytokine activity promotes cancer,” says Dr. Gerardo Ferbeyre, senior author and a Université de Montréal biochemistry professor. “Discovery of these mechanisms will enable scientists to design a cancer-prevention strategy for people with chronic inflammatory diseases and lead to better understanding of the human body’s natural defenses against cancer.”

The research team didn’t anticipate that SOCS1 would turn out to be linked to p53, the master regulator of natural anticancer defenses. “We were surprised to realize that SOCS1 was directly linked to p53,” says first author and Université de Montréal student, Viviane Calabrese.
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