Certain types of cancer are common in the United States and are often influenced by lifestyle choices. For example, skin cancers like melanoma can result from extended exposure to ultraviolet (UV) light, while lung cancers are frequently linked to tobacco use.
While it’s known that these choices can increase cancer risk, it has been challenging for scientists to determine how much each individual’s cancer is due to preventable actions versus natural aging or random genetic changes.
A recent study from Yale University offers new insights into this question. Researchers aimed to identify which factors contribute the most to the DNA changes that drive cancer growth across various tumor types.
They focused on 24 major types of cancer and analyzed how specific mutations might indicate the extent to which exposure to certain preventable factors contributed to tumor development.
By combining their data on genetic mutations with a method to estimate the impact of each mutation, the researchers could identify what percentage of cancer growth could be attributed to known factors like UV light or tobacco use.
They found that certain cancers are more strongly influenced by lifestyle or environmental exposures than others.
For example, preventable factors play a large role in the development of bladder and skin cancers, suggesting that careful management of exposures could help reduce the risk of these cancers.
On the other hand, cancers such as prostate cancer and brain tumors (gliomas) appear to be driven more by internal, age-related processes rather than external factors.
This means that while lifestyle adjustments may reduce some cancer risks, other cancers are more associated with natural aging and internal cell changes.
These findings could be valuable for specific communities or occupations where cancer rates are unusually high.
By better understanding the proportion of preventable and non-preventable causes, health officials may be able to pinpoint environmental or lifestyle factors that contribute to increased cancer risk in these populations.
While this research marks a step forward, it does not capture every type of genetic change that can lead to tumors. For example, complex alterations, such as duplicated genes or entire chromosomes, require further investigation.
Still, the findings open new possibilities for quickly identifying preventable sources of cancer, potentially helping public health officials address high-risk factors and prevent more cases.
Led by Jeffrey Townsend, this study was published in Molecular Biology and Evolution and highlights how tracking DNA changes related to lifestyle factors could play a role in cancer prevention efforts.
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