Cancer develops when changes occur with one or more genes in our cells. A change in a gene is called a defect or mutation.
The gene mutations found in this study, are passed from parent to child and are common in the population. However, not all individuals significantly increase the risk of cancer.
Instead, these mutations together work to increase the risk of cancer. They do not directly cause cancer, but are more likely to interact with many other risk factors or random mutations that accumulate over a person ‘s lifetime.
Cancers caused by defective genes were previously thought to be inherited, as opposed to mutations that occur by chance as we age or other risk factors such as smoking or sunlight.
Further analysis of these genes may help to design more effective early detection and analysis strategies for the general population, scientists say.
The findings, published in Cancer Research, a journal of the American Society for Cancer Research, this may also help to develop more effective personalized cancer treatments, as some patients respond differently to treatments depending on their genetics.
Previous research found that these types of hereditary mutations alone were not responsible for significantly increasing cancer risk and were often excluded from further study.
However, it is possible that large numbers of these mutations may increase cancer risk, as the majority of cancer cases are caused by mutations in several genes.
Researchers at the University of Edinburgh have developed a new method, called Bayesian Gene HERitability Analysis (BAGHERA) to estimate whether these mutations together could increase cancer risk.
The team analyzed 38 cancers reported in Biobank UK – a large-scale biochemical database containing detailed genetic and health information for half a million people in the UK.
The BAGHERA approach, which aggregates mutations according to the genes they affect, makes it easier to study a number of mutations that have very flexible effects, but together raise the risk of cancer. .
The findings showed that these accumulation mutations contribute to the development of the appearance of cancers, including late forms such as prostate cancer and bladder cancer.
Previously many late cancers were not thought to be caused by hereditary mutations, except in rare cases. They were thought to be caused by mutations built up over several years.
Hereditary defective genes were thought to be very rare and often involve a single gene that greatly increases cancer risk – such as the BRCA gene linked to breast cancer.
They are usually only found in a small number of families and make up a small percentage of known cancers.
However, the study suggests that, in some cases, a person’s genetic background, the presence of large numbers of these other types of inheritance, may increase the risk of cancer.
In total, the team identified 1146 genes, known as cancer heritability genes (CHGs), that contribute to the likelihood of developing cancer during a lifetime.
Many of these genes are known to play important roles in protecting the body against cancer – preventing tumors from forming or controlling the transformation from normal to cancer cells.
The team’s next step is to do further analysis to find out if these genes are linked and how they affect biological pathways that increase cancer risk.
They will also examine whether the genes interact with other known risk factors to increase cancer risk, such as obesity.
Dr Giovanni Stracquadanio, Senior Lecturer in Synthetic Biology, Institute of Cellular Biology, School of Biological Sciences, University of Edinburgh, said:
“It is reasonable to think that inherited mutations in some genes can benefit malignant cells to escape the tumor defenses in our cells. Integrating genetic information with tumor mutational status can help tailor-made patient treatment. “
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The study was conducted in partnership with the Universities of Oxford and Essex. The data biology laboratory, within the School of Biological Sciences, is supported by the Wellcome Trust.
For more information contact Marie-Anne Robertson, Science Communications Manager, School of Biological Sciences, University of Edinburgh [email protected]
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