After a certain age, cancer becomes a less frequent threat, contrary to what one might think. A recent study sheds light on the mechanisms behind this surprising phenomenon.
As cells age, they change the way they work. The Memorial Sloan Kettering Cancer Center (MSK) team discovered that in aged mice, lung cells accumulate fer but act as if they lack it. This dysfunction reduces their capacity for regeneration, a key factor in slowing the appearance of tumors.
The researchers highlighted the role of a protein called NUPR1. With age, its production increases, disrupting iron metabolism in cells. This reaction limits the multiplication cellular anarchy, a process central to the development of cancers. By studying mice genetically engineered to develop lung cancer, they observed a significant reduction in tumors in older rodents. On the other hand, treatments administering iron or inhibiting NUPR1 restored cell regeneration… and tumor risk.
These results raise questions about current therapeutic approaches. Treatments targeting ferroptosis, a form of iron-induced cell death, appear less effective in older patients. Aging cells, resistant to this mechanism, require adapted strategies to maximize benefits and reduce risks.
This study also raises questions about prevention. Researchers point out that carcinogenic exposures in youth, such as smoking or excessive tanning, have potentially more serious effects than previously thought. Focusing on preventive actions at these critical stages could limit the incidence of cancer in the long term.
Beyond cancer, these discoveries open avenues for treating disorders linked to poor cell regeneration, such as certain chronic lung diseases. But researchers warn: stimulating regeneration could unintentionally promote tumors in at-risk patients.
Age therefore transforms cells and their response to therapies, reminding us of the importance of personalized medicine. Understanding these biological changes is a crucial step in developing treatments adapted to each stage of life.
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