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Peer-Reviewed Publication
Blood2022;140(1):58-72.July 7, 2022Journal Article

TP53 copy number and protein expression inform mutation status across risk categories in acute myeloid leukemia.

Mehrnoosh Tashakori1,2, Tapan Kadia3, Sanam Loghavi1, Naval Daver3, Rashmi Kanagal-Shamanna1, Sherry Pierce3, Dawen Sui4, Peng Wei4, Farnoosh Khodakarami5, Zhenya Tang1, Mark Routbort1, Carol A Bivins3, Elias J Jabbour3, L Jeffrey Medeiros1, Kapil Bhalla3, Hagop M Kantarjian3, Farhad Ravandi3, Joseph D Khoury1
1Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX.
2Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.
3Department of Leukemia, and.
4Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX; and.
5Cyclica Inc, Toronto, ON, Canada.

Abstract

Mutant TP53 is an adverse risk factor in acute myeloid leukemia (AML), but large-scale integrated genomic-proteomic analyses of TP53 alterations in patients with AML remain limited. We analyzed TP53 mutational status, copy number (CN), and protein expression data in AML (N = 528) and provide a compilation of mutation sites and types across disease subgroups among treated and untreated patients. Ou…

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