Marcu L, van Doorn T, Olver I
School of Chemistry and Physics, University of Adelaide, Adelaide, Australia.
Phys Med Biol. 2004 Aug 21;49(16):3767-79. doi: 10.1088/0031-9155/49/16/021.
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.
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。