Institut National de Santé et de Recherche Médicale, Centre National de Recherche Scientifique, Institut Universitaire d'Hématologie, Université Paris-Diderot UMR 944/7212, Equipe labellisée par Ligue contre Cancer, Service de Biochimie, Hôpital St. Louis, 2 avenue C. Vellefaux, 75475 Paris, CEDEX 10, France.
Nat Rev Cancer. 2010 Nov;10(11):775-83. doi: 10.1038/nrc2943. Epub 2010 Oct 22.
The fusion oncogene, promyelocytic leukaemia (PML)-retinoic acid receptor-α (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-RARα for degradation. Drug-triggered oncoprotein degradation may be a strategy that is applicable to many cancers.
融合癌基因早幼粒细胞白血病(PML)-维甲酸受体-α(RARA)通过阻止分化和增加白血病祖细胞的自我更新来引发急性早幼粒细胞白血病(APL)。目前的标准治疗方法是维甲酸(RA)和化疗,但三氧化二砷也能治愈许多 APL 患者,RA 和三氧化二砷联合治疗能治愈大多数 APL 患者。这篇综述讨论了最近的证据,这些证据揭示了 RA 和三氧化二砷通过靶向 PML-RARα 降解来治愈这种白血病的令人惊讶的新见解。药物触发的癌蛋白降解可能是一种适用于许多癌症的策略。