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组蛋白去乙酰化酶 10 促进自噬作为一个可干预的药物靶点,以改善晚期神经母细胞瘤的治疗反应。

Histone deacetylase 10-promoted autophagy as a druggable point of interference to improve the treatment response of advanced neuroblastomas.

机构信息

Clinical Cooperation Unit Pediatric Oncology; German Cancer Research Center (DKFZ); Heidelberg, Germany.

出版信息

Autophagy. 2013 Dec;9(12):2163-5. doi: 10.4161/auto.26450. Epub 2013 Oct 8.

Abstract

Neuroblastoma is the most common extracranial solid tumor in childhood. Despite intense multimodal therapy and many improvements through basic scientific and clinical research, the successful response of advanced-stage patients to chemotherapy remains poor. Autophagy is a cytoprotective mechanism that may help advanced cancer cells survive stressful conditions such as chemotherapy. Here we review our recent findings describing HDAC10 as a promoter of autophagy-mediated survival in neuroblastoma cells and identifying this HDAC isozyme as a druggable regulator of advanced-stage tumor cell survival. These results propose a new and promising way to considerably improve treatment response in the neuroblastoma patient subgroup with the poorest outcome.

摘要

神经母细胞瘤是儿童期最常见的颅外实体瘤。尽管采用了强化的多模式治疗方法,并通过基础科学和临床研究取得了许多进展,但晚期患者对化疗的成功反应仍然不佳。自噬是一种细胞保护机制,可帮助晚期癌细胞在化疗等应激条件下存活。在这里,我们回顾了最近的发现,这些发现描述了 HDAC10 作为神经母细胞瘤细胞中自噬介导存活的促进因子,并将这种 HDAC 同工酶鉴定为晚期肿瘤细胞存活的可药物调节因子。这些结果提出了一种新的、有前途的方法,可以大大提高预后最差的神经母细胞瘤患者亚组的治疗反应。

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