Smoking isn’t healthy, but a new study has shown strong evidence that tobacco use can chemically modify and affect the activity of genes known to increase the risk of developing cancer.
The scientists published their findings in the journal Human Molecular Genetics¹ and hope that this finding will give them a new tool to assess cancer risk among smokers.
Chemical compounds that affect the functioning of genes can bind to genetic material, turning genes on and off. These epigenetic modifications can influence a variety of traits and scientists have identified specific epigenetic patterns on the genes of smokers. However, none of these genes has a direct link to cancer, so it’s unclear whether these chemical alterations increase the risk of developing cancer.
In this new study, the epigenetic signatures in blood cells from 374 different individuals were analyzed. The subjects were part of the European Prospective Investigation into Cancer and Nutrition (EPIC), which is aimed at linking diet, lifestyle, and environmental factors to the incidence of cancer and other chronic diseases. Half of the group went on to develop colon or breast cancer 5 to 7 years after joining the study. The other half remained healthy.
Researchers, led by James Flanagan, a human geneticist at Imperial College London, discovered a distinct epigenetic footprint in the study subjects who smoked. Smokers had fewer methyl groups on 20 different regions of their DNA. Analysis showed that the epigenetic modifications were tied to sites located in four genes, which were weakly linked to cancer before. All of the changes increase the activity of these genes and it’s unclear why the increase of activity in the genes would cause cancer, but individual who don’t have cancer tend not to have these modifications.
This is the first study to establish a link between epigenetic modifications on a cancer gene and the risk of developing the disease. This may lead to new ways to assess cancer risk from smoking.
- Shenker, N. S., et al., Hum. Mol. Genet. (2012) doi: 10.1093/hmg/dds488