Relationship between molecular changes in DNA and future cancer risks

Stem cells that have been exposed to inflammation pass on this open structure to their daughter cells. As a result, the body develops entire groups of cells that are biologically programmed to grow rapidly. In their normal state, these cells function normally, but their altered epigenome acts as a fertile ground. If a random cancerous mutation occurs in one of these cells over the years, the resulting tumor tends to be more aggressive and faster-growing than those in tissues without a history of inflammation.

This mechanism explains why lifestyle choices or dietary habits during adolescence can influence the risk of cancer in adulthood. Environmental factors may be temporary, but their impact on gene accessibility is fixed at the cellular level. This changes our understanding of the causes of disease: while a DNA mutation alone may not always lead to cancer, the accumulated “experience” of past exposures plays a crucial role.

In the future, identifying these molecular traces will enable us to detect disease predispositions long before the onset of clinical symptoms. Scientists are currently exploring ways to detect these markers through simple tests to provide timely interventions for tissue health. This opens the way to creating a therapy that can “erase” the cells’ memory of inflammation, thereby preventing the onset of tumor processes.