Acute Promyelocytic Leukemia: A Paradigm for Oncoprotein-Targeted Cure

被引：244

作者：

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

Pandolfi, Pier Paolo ^{[3
]}

Chen, Zhu ^{[4
]}

机构：

[1] PSL Res Univ, Chaire Oncol Cellulaire & Mol, Coll France, Paris, France

[2] Univ Paris Diderot, CNRS UMR 7212, Sorbonne Paris Cite, Hop St Louis,INSERM UMR 944, Paris, France

[3] Harvard Med Sch, Canc Res Inst, Beth Israel Deaconess Canc Ctr, Dept Pathol & Med,Beth Israel Deaconess Med Ctr, Boston, MA USA

[4] Shanghai Jiao Tong Univ, Shanghai Inst Hematol, Ruijin Hosp, Sch Med, Shanghai 200025, Peoples R China

来源：

CANCER CELL | 2017年 / 32卷 / 05期

关键词：

TRANS-RETINOIC ACID; PML-RAR-ALPHA; ARSENIC TRIOXIDE AS2O3; TUMOR-SUPPRESSOR PML; FOLLOW-UP; IN-VITRO; T(15-17) TRANSLOCATION; CELLULAR SENESCENCE; GROWTH-SUPPRESSOR; INTERFERON-ALPHA;

D O I：

10.1016/j.ccell.2017.10.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Recent clinical trials have demonstrated that the immense majority of acute promyelocytic leukemia (APL) patients can be definitively cured by the combination of two targeted therapies: retinoic acid (RA) and arsenic. Mouse models have provided unexpected insights into the mechanisms involved. Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is essential, while RA-triggered transcriptional activation is dispensable for APL eradication. Mutations of the arsenic-binding site of PML/RARA, but also PML, have been detected in therapy-resistant patients, demonstrating the key role of PML in APL cure. PML nuclear bodies are druggable and could be harnessed in other conditions.

引用

页码：552 / 560

页数：9

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