London: Shedding new light on why some people develop cancer while others do not, a new study has found that a person's risk of developing cancer is affected by genetic variations in regions of DNA that do not code for proteins, previously dismissed as "junk DNA".
This study, published in the British Journal of Cancer, shows that inherited cancer risk is not only affected by mutations in key cancer genes, but that variations in the DNA that controls the expression of these genes can also drive the disease.
The researchers believe that understanding how non-coding DNA affects the development of this disease could one day improve genetic screening for cancer risk. And in the future, this could lead to new prevention strategies, or help doctors diagnose the disease earlier, when it is more likely to be treated successfully.
"What we found surprised us as it had never been reported before -- our results show that small genetic variations work collectively to subtly shift the activity of genes that drive cancer," said lead researcher of the study John Quackenbush, Professor at Harvard T.H. Chan School of Public Health in the US.
"We hope that this approach could one day save lives by helping to identify people at risk of cancer, as well as other complex diseases," Quackenbush said. The researchers investigated 846 genetic changes within non-coding stretches of DNA, identified by previous studies as affecting cancer risk.
These Single Nucleotide Polymorphisms (SNPs) are particular positions in the human genome where a single letter of the genetic code varies between people. Unlike mutations in coding DNA, such as BRCA, that are rare but significantly raise a person's risk of developing cancer, non-coding SNPs are relatively common in the population but only slightly increase cancer risk.
