Published in Vaccine Weekly, January 4th, 2006
According to a study from the United States, "Although TP53 mutations are rare in AML, inactivation of wild-type p53 protein frequently occurs through overexpression of its negative regulator MDM2. Recently, small-molecule antagonists of MDM2, Nutlins, have been developed that inhibit the p53-MDM2 interaction and activate p53 signaling."
"Here, we study the effects of p53 activation by Nutlin-3 in AML cells. Treatment with MDM2 inhibitor triggered several molecular events consistent with induction of apoptosis: loss of mitochondrial membrane...
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