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细胞间凋亡诱导对低剂量辐射致癌作用的影响。

Impact of intercellular induction of apoptosis on low-dose radiation carcinogenesis.

作者信息

Kundrát P, Friedland W

机构信息

Institute of Radiation Protection, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg, Germany

Institute of Radiation Protection, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg, Germany.

出版信息

Radiat Prot Dosimetry. 2015 Sep;166(1-4):170-3. doi: 10.1093/rpd/ncv169. Epub 2015 Apr 21.

Abstract

In vitro data indicate that selective removal of oncogenic transformed cells by apoptosis induced via signalling by neighbouring cells may represent an important anti-carcinogenic process. Mechanistic modelling supports this concept and predicts that the phenomenon can stop the growth of a transformed cell population, forming a dormant pre-neoplastic lesion, or even remove the transformed clone completely. Radiation has been shown to enhance the underpinning signalling and increase the extent and rate of apoptosis induction in precancerous cells. Implications for low-dose radiation carcinogenesis are discussed based on in vitro data and mechanistic modelling. The possibility is outlined for radiation to act in a pro-carcinogenic manner, i.e. to reduce rather than enhance the removal of transformed cells by apoptosis. The effects of radiation exposure during early or late carcinogenesis are discussed.

摘要

体外数据表明,通过相邻细胞发出的信号诱导凋亡来选择性清除致癌转化细胞可能是一个重要的抗癌过程。机制建模支持这一概念,并预测该现象可以阻止转化细胞群体的生长,形成休眠的癌前病变,甚至完全清除转化克隆。已表明辐射可增强基础信号传导,并增加癌前细胞中凋亡诱导的程度和速率。基于体外数据和机制建模讨论了低剂量辐射致癌的影响。概述了辐射以促癌方式起作用的可能性,即减少而非增强通过凋亡清除转化细胞的能力。还讨论了早期或晚期致癌过程中辐射暴露的影响。

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