TP53 Mutant Acute Myeloid Leukemia: The Immune and Metabolic Perspective

被引:0
作者
Zingarelli, Federico [1 ]
Zannoni, Letizia [1 ]
Curti, Antonio [2 ]
机构
[1] Univ Bologna, Dipartimento Med Specialist Diagnost & Sperimental, I-40138 Bologna, Italy
[2] IRCCS Azienda Osped Univ Bologna, Ist Ematol Seragnoli, I-40138 Bologna, Italy
来源
HEMATO | 2022年 / 3卷 / 04期
关键词
acute myeloid leukemia; TP53; mutation; metabolism; immunotherapy; COMPLEX KARYOTYPE; STEM-CELLS; PHASE-II; P53; MUTATIONS; INHIBITION; VENETOCLAX; GENE; AZACITIDINE; EXPRESSION;
D O I
10.3390/hemato3040050
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
TP53 mutated/deleted acute myeloid leukemia (AML) stands out as one of the poorest prognosis forms of acute leukemia with a median overall survival not reaching one year in most cases, even in selected cases when allogenic stem-cell transplantation is performed. This aggressive behavior relies on intrinsic chemoresistance of blast cells and on high rates of relapse. New insights into the biology of the disease have shown strong linkage between TP53 mutant AML, altered metabolic features and immunoregulation uncovering new scenarios and leading to possibilities beyond current treatment approaches. Furthermore, new targeted therapies acting on misfolded/dysfunctional p53 protein are under current investigation with the aim to improve outcomes. In this review, we sought to offer an insight into TP53 mutant AML current biology and treatment approaches, with a special focus on leukemia-associated immune and metabolic changes.
引用
收藏
页码:742 / 757
页数:16
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