Cancer develops when cells collect DNA changes that allow them to grow and divide in harmful ways.
But scientists have long debated how many of these changes come from preventable exposures and how many happen because of aging and normal processes inside the body.
A study from Yale University offers a new way to examine this question. The research, led by Jeffrey Townsend and his team, was published in the journal Molecular Biology and Evolution.
The researchers studied genetic changes in tumors from 24 types of cancer. Their goal was to estimate how much different causes contributed to the mutations that helped each cancer develop.
Some cancer risks are already well known. Tobacco smoke contains chemicals that can damage DNA and is a major cause of lung cancer, while too much ultraviolet, or UV, radiation from sunlight can damage skin cells and increase the risk of skin cancer.
These exposures can leave recognizable patterns of damage in DNA. Scientists sometimes describe these patterns as genetic signatures because they can provide clues about what happened to a cell before it became cancerous.
The Yale team used these patterns to examine the causes behind mutations found in different tumors. They then estimated how strongly particular types of DNA damage contributed to the growth of each cancer.
The results showed major differences between cancer types. For some cancers, outside exposures appeared to play a large role, suggesting that prevention could potentially reduce many cases.
Skin cancer was one clear example because UV radiation can cause characteristic DNA damage. Bladder tumors also showed a relatively strong contribution from preventable or environmental exposures.
Other cancers appeared to be driven much more by processes that occur naturally inside the body. Prostate cancer and gliomas, a group of tumors that develop in the brain or spinal cord, were among the cancers in which aging and internal biological processes appeared more important.
Aging itself increases cancer risk because cells continue to divide and copy their DNA throughout life. Small copying errors can occur during this process, and DNA can also become damaged naturally over time.
Most of these changes do not cause cancer. However, if important genes controlling cell growth or DNA repair are damaged, a cell may eventually begin growing in an uncontrolled way.
The research could also help scientists investigate cancer clusters in particular workplaces or communities. If people in one location develop unusually high rates of a certain cancer, patterns in their tumors could potentially provide clues about an unknown environmental exposure.
That could have important public health benefits. Finding a harmful chemical or other cancer-causing exposure early could allow governments, workplaces, and communities to reduce contact with it before more people become sick.
However, the method does not yet capture every type of genetic change involved in cancer. The researchers noted that more complicated changes, such as duplicated sections of DNA or abnormal numbers of chromosomes, were not fully included in the analysis.
This means the findings cannot explain every cause behind every tumor. Cancer usually develops through a complicated combination of inherited risk, aging, random biological events, environmental exposures, and lifestyle factors.
Still, the study provides another tool for understanding why different cancers develop. Knowing which cancers are strongly influenced by preventable exposures could help researchers and health officials focus prevention efforts where they are most likely to make a difference.
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