Department of Radiology and Biomedical Imaging Yale University School of Medicine 330 Cedar St, TE 2-230 New Haven, CT 06520.
Radiology. 2017 Jun;283(3):621-623. doi: 10.1148/radiol.2017170358.
In this issue of Radiology, Gade et al ( 1 ) describe a unique mechanism of hepatocellular carcinoma (HCC) cells for surviving ischemia induced by transarterial embolization (TAE)/transarterial chemoembolization (TACE) in a state of cell cycle arrest-a function that may serve as a defensive shield against conventional chemotherapeutic agents. This finding adds to our knowledge and establishes a previously poorly understood mechanism of chemoresistance in HCC. As the Achilles heel in terms of this process, a concurrent upregulation of autophagic flux as an adaptive response to TAE-like ischemia was found by the authors. This is a targetable mechanism that can potentially be exploited for combined therapeutic approaches of embolotherapy and autophagy inhibition in HCC.
在本期《放射学》杂志中，Gade 等人(1)描述了肝细胞癌（HCC）细胞在细胞周期停滞状态下对经动脉栓塞（TAE）/经动脉化疗栓塞（TACE）引起的缺血产生适应性的独特生存机制——该功能可能作为对抗传统化疗药物的防御盾牌。这一发现增加了我们对 HCC 化疗耐药性的认识，并建立了一个以前了解甚少的机制。作为这一过程的致命弱点，作者发现自噬通量的同时上调是对 TAE 样缺血的适应性反应。这是一个可靶向的机制，有可能被用于 HCC 的栓塞治疗和自噬抑制联合治疗方法。
