Biological basis for chemo-radiotherapy interactions
Biological basis for chemo-radiotherapy interactions
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DOI：
10.1016/s0959-8049(01)00360-4
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发表时间：
2002-01-01
影响因子：
8.4
通讯作者：
Favaudon, V
中科院分区：
文献类型：
--
作者：
Hennequin, C;Favaudon, V
10多年来，放化疗组合一直被用于治疗局部晚期上皮性肿瘤。这些组合的理由取决于各种模式之间的空间合作或相互作用。相互作用可发生在分子水平上，与药物或辐射引起的损伤的DNA修复或修饰改变，(Ii)在细胞水平上，特别是通过细胞周期各部分对药物或辐射的不同敏感性而产生的细胞动力学合作，以及(Iii)在组织水平上，包括复氧、药物摄取增加或抑制再繁殖或血管生成。本文描述了辐射与顺铂、5-氟-2‘-脱氧尿苷、紫杉烷和吉西他滨相互作用的一些机制。它显示了包括细胞同步化和复氧在内的各种机制如何与紫杉醇诱导的放射增敏相一致。在未来，应该实现针对肿瘤的特定靶向，例如，使用表皮生长因子受体(EGFR)或血管生成抑制剂，以提高治疗指数。(C)2002年由爱思唯尔科学有限公司出版。
For over 10 years, chemo-radiotherapeutic combinations have been used to treat locally advanced epithelial tumours. The rationale for these combinations relies on spatial cooperation or interaction between modalities. Interactions may take place (i) at the molecular level, with altered DNA repair or modification of the lesions induced by drugs or radiation, (ii) at the cellular level, notably through cytokinetic cooperation arising from differential sensitivity of the various compartments of the cell cycle to the drug or radiation, and (iii) at the tissue level, including reoxygenation, increased drug uptake or inhibition of repopulation or angiogenesis. Some mechanisms underlying interaction of radiation with cis-diammino-platinum (II) (cis-Pt), 5-fluoro-2'-deoxy-uridine (5-FU), taxanes and gemcitabine are described. It is shown how various mechanisms including cell synchronisation and reoxygenation concur to paclitaxel-induced radiosensitisation. In the future, specific targeting of tumours, for example, with the epidermal growth factor receptor (EGFR) or angiogenesis inhibitors, should be achieved in order to increase the therapeutic index. (C) 2002 Published by Elsevier Science Ltd.