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A groundbreaking study by Van Andel Institute (VAI) scientists reveals that a person’s lifetime risk for cancer may be determined before they are even born. The research, published in Nature Cancer, identifies two distinct epigenetic states arising during development, each linked to differing cancer risks later in life. One state is associated with a lower risk, while the other carries a higher risk.
Interestingly, the study suggests that if cancer develops in the lower-risk state, it is more likely to be a liquid tumor, such as leukemia or lymphoma. In contrast, if cancer arises from the higher-risk state, it is more likely to manifest as a solid tumor, such as lung or prostate cancer.
“Most cancers occur later in life and are often attributed to mutations or genetic changes. However, our findings suggest that the foundation for cancer risk may be set much earlier, during the developmental phase,” said J. Andrew Pospisilik, Ph.D., chair of VAI’s Department of Epigenetics and co-corresponding author of the study. “These two epigenetic states represent a completely new avenue of exploration in understanding cancer risk.”
Cancer risk generally increases with age due to the accumulation of DNA damage and other factors. Yet not every abnormal cell turns cancerous. In recent years, scientists have recognized the role of epigenetic changes—processes that affect how genes are expressed without altering the underlying DNA sequence—as critical contributors to cancer development.
Epigenetic errors can disrupt cellular quality control, allowing abnormal cells to survive and proliferate. In this study, Pospisilik and his team discovered that mice with reduced levels of the gene Trim28 exhibit one of two distinct epigenetic patterns related to cancer genes, even though the mice are genetically identical. These epigenetic patterns, which arise during development, play a key role in determining the cancer risk associated with each mouse.
“Our findings challenge the notion that cancer is simply a result of ‘bad luck,'” said Ilaria Panzeri, Ph.D., a research scientist in Pospisilik’s lab and the study’s first author. “While bad luck does play a role, it doesn’t explain why some people develop cancer and others don’t. More importantly, luck cannot be targeted for treatment, but epigenetic changes can. This study opens up new possibilities for understanding cancer from a developmental perspective and could lead to novel diagnostic and therapeutic approaches.”
The research also suggests that the two epigenetic states may be common across various types of cancer, raising the possibility of a broader application in cancer prevention and treatment.
Looking ahead, the VAI team plans to further investigate how these epigenetic states impact different types of cancer, with the hope of providing new insights into how to detect, treat, and potentially prevent cancer from an early stage.
For more details, refer to the study: TRIM28-dependent developmental heterogeneity determines cancer susceptibility through distinct epigenetic states, published in Nature Cancer (2025).
Disclaimer: The findings discussed in this article are based on research conducted by the Van Andel Institute and published in Nature Cancer. These results may not be universally applicable or applicable to every individual case of cancer. Further research is needed to understand the full implications of epigenetic changes in cancer risk. Always consult a healthcare provider for advice on medical conditions.
