Suppr超能文献

鳞状细胞癌放疗后加速再增殖的模型构建

Modelling of post-irradiation accelerated repopulation in squamous cell carcinomas.

作者信息

Marcu L, van Doorn T, Olver I

机构信息

School of Chemistry and Physics, University of Adelaide, Adelaide, Australia.

出版信息

Phys Med Biol. 2004 Aug 21;49(16):3767-79. doi: 10.1088/0031-9155/49/16/021.

Abstract

The mechanisms postulated to be responsible for the accelerated repopulation of squamous cell carcinomas during radiotherapy are the loss of asymmetry of stem cell division, acceleration of stem cell division, abortive division and/or recruitment of the non-cycling cell with proliferative capacity. Although accelerated repopulation was observed with recruitment and accelerated cell cycles, it was not sufficient to cause an observable change to the survival curve. However, modelling the loss of asymmetry in stem cell division has reshaped the curve with a 'growth' shoulder. Cell recruitment was not found to be a major contributor to accelerated tumour repopulation. A more significant contribution was provided through the multiplication of surviving tumour stem cells during radiotherapy, by reducing their cell cycle time, and due to loss of asymmetry of stem cell division.

摘要

据推测,放疗期间鳞状细胞癌再增殖加速的机制包括干细胞分裂不对称性的丧失、干细胞分裂加速、流产性分裂和/或具有增殖能力的非循环细胞的募集。尽管观察到募集和细胞周期加速会导致再增殖加速,但这不足以使生存曲线发生可观察到的变化。然而,对干细胞分裂不对称性丧失进行建模后,生存曲线出现了带有“生长”平台期的重塑。未发现细胞募集是肿瘤再增殖加速的主要因素。放疗期间存活肿瘤干细胞的增殖、细胞周期时间的缩短以及干细胞分裂不对称性的丧失起到了更为重要的作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验