Are we moving the needle for patients with tp53-mutated acute myeloid leukemia?

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SUMMARY

    TP53 is a critical tumor suppressor gene located on chromosome 17p13.1 that encodes the p53 protein, which, in response to cellular stress, including deoxyribonucleic_acid (DNA) damage, increases in level and ultimately induces the transcription of the genes responsible for DNA damage repair and cell cycle arrest/apoptosis, among others. Among patients with a new diagnosis of acute myeloid leukemia (AML), at least 10% will have disease-harboring mutations in TP53 (TP53m-AML) but up to 30% in certain 2 of 19 subpopulations such as those with secondary AML, therapy-related AML (t-AML . . .

     

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