Acute promyelocytic leukaemia: novel insights into the mechanisms of cure

被引：370

作者：

de The, Hugues ^{[1
,2
,4
]}

Chen, Zhu ^{[3
,4
]}

机构：

[1] CNRS, INSERM, F-75475 Paris 10, France

[2] Univ Paris Diderot UMR 944 7212, Inst Univ Hematol, Hop St Louis, Equipe Labellisee Ligue Canc,Serv Biochim, F-75475 Paris 10, France

[3] Shanghai Jiao Tong Univ, State Key Lab Med Genom, Shanghai Inst Haematol, Rui Jin Hosp,Sch Med, Shanghai 200025, Peoples R China

[4] Jiao Tong Univ, Sch Med, Shanghai 200025, Peoples R China

来源：

NATURE REVIEWS CANCER | 2010年 / 10卷 / 11期

基金：

中国国家自然科学基金;

关键词：

TRANS-RETINOIC ACID; PML-RAR-ALPHA; TUMOR-SELECTIVE APOPTOSIS; ARSENIC TRIOXIDE AS2O3; ACUTE MYELOID-LEUKEMIA; RECEPTOR-ALPHA; IN-VITRO; CELL-DIFFERENTIATION; HISTONE DEACETYLASE; NUCLEAR-BODIES;

D O I：

10.1038/nrc2943

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The fusion oncogene, promyelocytic leukaemia (PML)-retinoic acid receptor-alpha (RARA), initiates acute promyelocytic leukaemia (APL) through both a block to differentiation and increased self-renewal of leukaemic progenitor cells. The current standard of care is retinoic acid (RA) and chemotherapy, but arsenic trioxide also cures many patients with APL, and an RA plus arsenic trioxide combination cures most patients. This Review discusses the recent evidence that reveals surprising new insights into how RA and arsenic trioxide cure this leukaemia, by targeting PML-RAR alpha for degradation. Drug-triggered oncoprotein degradation may be a strategy that is applicable to many cancers.

引用

页码：775 / 783

页数：9

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