TP53突变型急性髓细胞白血病的免疫和代谢研究

IF 0.9 Q4 HEMATOLOGY Hemato Pub Date : 2022-11-15 DOI:10.3390/hemato3040050
F. Zingarelli, L. Zannoni, A. Curti
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引用次数: 0

摘要

TP53突变/缺失型急性髓细胞白血病(AML)是急性白血病预后最差的形式之一,在大多数情况下,即使在进行同种异体干细胞移植的选定病例中,中位总生存期也达不到一年。这种攻击性行为依赖于母细胞固有的化学耐药性和高复发率。对该疾病生物学的新见解表明,TP53突变AML、代谢特征的改变和免疫调节之间存在着强烈的联系,揭示了新的情况,并带来了超越当前治疗方法的可能性。此外,目前正在研究针对错误折叠/功能失调的p53蛋白的新靶向疗法,以改善疗效。在这篇综述中,我们试图深入了解TP53突变AML的当前生物学和治疗方法,特别关注白血病相关的免疫和代谢变化。
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TP53 Mutant Acute Myeloid Leukemia: The Immune and Metabolic Perspective
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.
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CiteScore
1.30
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审稿时长
11 weeks
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