A pioneering study conducted by scientists at the Van Andel Institute has unveiled that cancer risk could potentially start even before birth.
This important research, featured in Nature Cancer, identifies two unique epigenetic states that form during early development, each profoundly affecting an individual’s susceptibility to cancer.
Impact of Epigenetic States on Cancer Risk
Interestingly, these epigenetic states are linked to varying lifetime cancer risks.
One state is associated with a lower risk of developing cancer, while the other increases risk significantly.
In individuals who develop cancer from the lower-risk state, the tumor is more likely to be a liquid form, such as leukemia or lymphoma.
Conversely, those from the higher-risk state tend to be more susceptible to solid tumors, including types like lung or prostate cancer.
Dr. J. Andrew Pospisilik, chair of the Department of Epigenetics at VAI and a leading author of the study, pointed out a crucial oversight in the traditional approach to understanding cancer.
While it has long been viewed primarily as a disease driven by genetic mutations, this new research highlights the potential impact of developmental factors on cancer risk.
Identifying these two epigenetic states signals a transformative moment in cancer research, paving the way for deeper investigations into its fundamental mechanisms.
Understanding Epigenetic Changes
As individuals age, the likelihood of developing cancer generally rises due to an accumulation of DNA damage among other factors.
However, the study emphasizes that not every abnormal cell progresses to cancer.
This anomaly has prompted scientists to explore additional influences, such as epigenetic changes, that may contribute to the evolution of cancer.
Epigenetics involves the biological processes that manage how genes are expressed, determining when and how genetic information is activated.
When these processes are disrupted, it can lead to a breakdown in cellular quality control, allowing unhealthy cells to survive and multiply.
In their experiments, Pospisilik and his team discovered that mice missing the Trim28 gene exhibited two distinct epigenetic patterns tied to cancer-related genes, despite their genetic similarity.
These patterns, established early in development, ultimately influence the cancer risk configuration that the organism will experience later in life.
Future Directions in Cancer Research
Dr. Ilaria Panzeri, a research scientist in Pospisilik’s lab and the study’s first co-author, offered an insightful perspective.
While everyone carries some degree of cancer risk, she argued that attributing cancer to sheer chance doesn’t sufficiently account for why some people develop the disease while others remain unaffected.
Unlike random chance—which we can’t manipulate—epigenetic factors may offer pathways for targeted treatments.
The findings suggest that the origins of cancer risk arise during critical stages of development, potentially leading to innovative approaches in diagnosing and treating cancer.
This research underscores the importance of early-life environmental and genetic interactions in shaping long-term health outcomes.
By identifying epigenetic markers linked to cancer susceptibility, scientists may eventually develop targeted interventions, much like the recent advancements seen with the new genetic test for IBD.
Such breakthroughs pave the way for more precise diagnostics and personalized treatment strategies, ultimately improving patient outcomes.
The researchers also observed signs of these epigenetic states across various tissues in the body, indicating a shared developmental epigenetic risk that could apply to multiple cancer types.
Future studies are set to delve deeper into how these epigenetic states uniquely impact specific kinds of cancer, continuing this exciting line of research.
Source: Science daily