New Delhi: Inherited genes shape cancer risk by interacting with environmental damage like UV rays or cigarette smoke, states a new study. This genetic background controls how cells handle errors, how tumours grow, and why identical exposures affect people differently.
Researchers at the University of Cambridge conducted the study. It was published on 27 July in the journal Nature. The research was led by Professor Duncan Odom, Sarah Aitken and Professor Martin Taylor, in collaboration with scientists from the University of Edinburgh and institutions across Europe and the US.
“Responses to DNA-damaging cancer treatments could differ depending on a patient’s background genetics, strengthening the case for a more personalised approach to treatment,” states the study, adding that tumours arise when our DNA accumulates errors, or mutations, causing the cells to grow faster and ignore signals that would otherwise instruct damaged cells to die before they can cause harm.
“Environmental exposures – for example, cigarette smoke or sunlight – influence how much DNA damage occurs, and inherited genetic alterations can alter how many mutations accumulate,” the study adds.
While lifestyle and environmental exposures influence cancer risk, researchers have long suspected that inherited genetic differences also play a role. Proving this has been difficult in humans because people differ in their lifestyles, environments and exposure histories.
To study the impact of genetic inheritance on cancer development in mice, researchers conducted controlled experiments on mice with different genetic backgrounds. The researchers analysed nearly 600 tumours from mice. Although the tumours followed the same overall development pattern, the genetic background of the mice influenced the mutations that developed within those tumours.
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‘Cancer doesn’t arise entirely by chance’
Researchers found that while tumours across different mouse strains often involved the same cancer-driving pathway, inherited genetics influenced the mutations and changes that developed within those tumours.
“Cancer does not arise entirely by chance. Although tumours often reach the same biological endpoint, the path to that endpoint is determined by an individual’s genetic background,” Professor Duncan Odom said. “We’ve been able to show for the first time the extent to which genetic background influences both the mutation processes and the pathways leading to tumour development.”
However, the researchers caution that these results were obtained using mice and more studies are needed to determine if similar results can be obtained from human subjects.
The researchers said their findings could lead to changes in the way cancer is evaluated in the future.
“If genetic background influences both cancer risk and the evolutionary trajectory of tumours, future cancer prevention and screening strategies will need to take into account inherited genetics and population diversity,” Sarah Aitken, a researcher who worked on the project, said.
Meanwhile, another researcher, Sam Godfrey, said the study hints that our inherited genes might have a big influence on the way that cancers develop after DNA damage.
“We still need to see more research before we can understand what this means in humans, but this finding could change our understanding of how cancer starts, and lead to more powerful and precise ways of tackling cancer,” he added.
(Edited by Saptak Datta)

