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Using a knock-in mouse that expresses a wild-typep53–oestrogen receptor fusion protein (p53ERTAM) which is dependent upon4-hydroxytamoxifen (4-OHT) for activity, Christophorou and colleagues [195]showed that the restoration of p53 function 6 days before administering a singlewhole-body dose of ionizing radiation led to widespread p53-dependent cell deathin radiosensitive tissues in a manner similar to that observed in wild-type mice.However, although there was a substantial p53 response, it provided no protectionagainst the subsequent onset of lymphoma development. Industrial activities, such as mining and manu-facturing, often concentrate metals from natural mineralsand this increases the potential for human exposure.

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