Abstract
We recently showed that mice and human tissues exposed to ionizing radiation (IR) have an increased expression of p16INK4a, a tumor suppressor gene and proven senescence marker. Expression of p16INK4a prevents adequate tissue renewal and is hypothesized to be an underlying mechanism by which most childhood cancer survivors develop IR treatment-related health conditions. Intriguingly, increased p16INK4a expression is delayed several weeks post exposure to IR. Hence, it is unclear if delayed expression occurs as an orchestred tumor suppressive pathway or simply as a bystandard effect to IR-induced loss of tissue homeostasis.
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