Researchers studying the effects of cigarette smoke on the lungs have determined that smoking causes changes to the gene expression of lung cells, priming them for the uncontrolled growth associated with lung cancer.
The science of epigenetics has advanced rapidly over the past two decades, telling us more about how environmental factors can have their impact at a genetic level. Where our genes contain the DNA blueprint for how to make a human body such as ours, epigenetics determines whether and to what degree the various aspects of that blueprint will become activated.
Thus, while DNA is a fixed plan, how gene expression will be carried out is variable, with research showing that gene expression can be influenced by both inherited characteristics as well as environmental factors during one’s lifetime.
Research has concluded, for example, that chemical exposure, especially during developmental years, can alter gene expression. Thalidomide, a sedative given to pregnant women in the 1950s, is a well-known case, where resulting birth defects involved epigenetic alterations. A more current example is the toxin Bisphenol A (BPA) which has been linked to cancers and other health impacts as a result of changes in gene expression.
Now, researchers at the Johns Hopkins University School of Medicine in Baltimore, Maryland, have concluded that cigarette smoke produces epigenetic changes that lead to lung cancer, involving increased activity of cell signals that have been linked with cell mutation.
The researchers grew health bronchial cells in the lab and exposed them to liquid cigarette smoke for a period of ten to 15 months, producing the equivalent effect of smoking one to two packs of cigarettes a day for 20 to 30 years. They found that at the ten-month mark, the cells’ DNA had developed epigenetic markers that were repressing the cells’ ability to protect themselves from abnormal growth.
“When you’re smoking, you are building up a substrate of epigenetic changes that we hypothesize are increasing your mathematics for developing lung cancer, because if you’re not a smoker, your risk of lung cancer is very low,” say Stephen B. Baylin and Hari Easwaran, both of Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins and co-authors of the new study, in a statement.
But the researchers also found that these epigenetic changes to lung cells are potentially reversible, if further environmental changes (such as quitting smoking) happen soon enough. The team introduced a genetic mutation into the lung cells of two groups of mice, those exposed to cigarette smoke extract for six months and those exposed for 15 months. The team found that the mutation produced cancerous cells only in the mice of the 15 month group.
“This work suggests the possibility that unlike mutations, which are harder to reverse, if you stop smoking at a certain time and duration, then you have a chance to decrease your likelihood of getting cancer that might be due to the buildup of epigenetic changes,” says first author Michelle Vaz, postdoctoral researcher at Johns Hopkins University School of Medicine.
The new research is published in the journal Cancer Cell.