A Yale University study has offered a clearer picture of why cancers develop and how much some of them may be influenced by preventable causes.
By examining patterns of DNA damage across many cancer types, researchers estimated how strongly outside exposures contribute to the mutations that help tumors grow.
Cancer begins when changes build up in a cell’s DNA, the biological instructions that control how cells work. Some mutations allow damaged cells to grow and divide when they should not, eventually helping a tumor form.
But these mutations can arise for very different reasons. Some result from outside exposures such as cigarette smoke or ultraviolet radiation from sunlight, while others happen through natural processes inside the body as cells age and repeatedly copy their DNA.
The Yale researchers wanted to separate these influences more clearly. They studied mutation patterns across 24 types of cancer and used mathematical methods to estimate how much different causes contributed to cancer-driving mutations.
Certain exposures leave recognizable patterns of damage in DNA, almost like fingerprints. Tobacco smoke and ultraviolet light, for example, can produce characteristic mutation patterns that scientists can identify when examining tumor cells.
The analysis showed that some cancers have a large preventable component. Skin cancers were strongly connected with ultraviolet radiation, supporting decades of evidence that sunlight and tanning beds can damage DNA and increase cancer risk.
Lung cancer was another clear example. Tobacco smoke contributes heavily to the mutations that cause many lung cancers, which is why avoiding smoking remains one of the most powerful ways to reduce cancer risk.
Bladder cancer also showed an important contribution from outside exposures. Smoking is a known risk factor for bladder cancer because harmful chemicals from tobacco can enter the bloodstream, be filtered by the kidneys and collect in urine before leaving the body.
Other cancers appeared much less connected to known preventable exposures. Prostate cancer and gliomas, a group of tumors that develop in the brain or spinal cord, were among those in which internal biological processes appeared to play a larger role.
This does not mean that these cancers happen for no reason or that researchers understand every cause. Instead, it suggests that much of their mutation burden cannot currently be explained by familiar environmental or lifestyle exposures.
Age is an important part of the picture because DNA changes naturally accumulate over time. Every time a cell divides, it must copy billions of pieces of genetic information, and occasional copying errors can occur even when a person lives a very healthy life.
The findings could help public health experts focus prevention efforts where they are most likely to have an impact. They may also help researchers investigate cancers in workers or communities exposed to suspected cancer-causing chemicals and determine whether unusual mutation patterns are present.
The method could even point scientists toward cancer causes that have not yet been identified. If researchers find a large share of mutations that cannot be explained by known processes, that may provide clues that an overlooked environmental or biological factor is involved.
However, the study does not capture every kind of genetic change involved in cancer. Tumors can also gain or lose large sections of DNA or entire chromosomes, and these more complicated changes require additional research.
The research was led by Jeffrey Townsend and published in the journal Molecular Biology and Evolution.
The results underline an important message: people cannot prevent every cancer, but reducing well-established risks such as tobacco use and excessive ultraviolet exposure can prevent some of the DNA damage that helps certain cancers develop.
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