A study suggests that nicotine promotes the spread of brain metastases by suppressing the innate immune function of cells present in the nervous system.
In itself, nicotine is not a carcinogenic compound. However, this molecule is partly responsible for tobacco addiction. This is why it is used in products aimed at relieving withdrawal symptoms. We are thinking in particular of anti-smoking patches, chewing gum, or even certain inhalers and tablets. If these nicotine substitutes have already proven themselves, they may not be systematically indicated.
According to a recent study published in the Journal of Experimental Medicine , nicotine may indeed be more harmful than previously thought, promoting the spread of lung cancer to the brain.
About 40% of people with lung cancer develop metastases (cancer cells separate from the main tumor to attach to other organs). However, approximately 90% of lung cancer deaths are directly attributed to the latter, and metastatic brain cancer is among the most common .
While smoking is known to be associated with lung cancer, the impact of smoking on the development of brain metastases has until now remained elusive. In an effort to learn more, researchers at the Wake Forest School of Medicine reviewed the medical records of 281 lung cancer patients .
They then very quickly brought to light that metastatic brain cancer was considerably more common among smokers. Based on the principle that nicotine is a molecule capable of crossing the blood-brain barrier, it has therefore been suggested that it could be involved in the proliferation of lung cancer.
To test this theory, the researchers used mice that were genetically modified to develop lung cancer. It actually turned out that all those who were subsequently treated with nicotine were more likely to develop brain tumors as well.
Analyses then found that nicotine molecules bind to receptors on the surface of microgliocytes , immune cells present in the central nervous system (brain, spinal cord and retina).
These cells, normally programmed to destroy cancerous tumors (M1 form), then tended to do the opposite (M2 form):they supported tumor growth by inhibiting their innate immune functions . The authors concluded that nicotine promotes the spread of cancer cells from the lungs to the brain by diverting microgliocyte cells.
Researchers nevertheless mention good news. Indeed, it appears that a certain compound called parthenolide can prevent microgliocyte cells from transforming into their M2 form, thereby reducing the risk of spreading metastases. This compound is naturally produced by feverfew (Tanacetum parthenium ).
Although for the time being this work has only been carried out on mouse models, the researchers aim to follow this lead with the idea of eventually proposing a means of treat or prevent brain metastases.
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