Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University, 269 Campus Drive West, CCSR Room 1255, Stanford, CA 94305, USA.
Br J Cancer. 2011 Jun 7;104(12):1805-9. doi: 10.1038/bjc.2011.169. Epub 2011 May 17.
Local recurrence of glioblastomas is a major cause of patient mortality after definitive treatment. This review discusses the roles of the chemokine stromal cell-derived factor-1 and its receptor CXC chemokine receptor 4 (CXCR4) in affecting the sensitivity of glioblastomas to irradiation. Blocking these molecules prevents or delays tumour recurrence after irradiation by inhibiting the recruitment of CD11b+ monocytes/macrophages that participate in revascularising the tumour. We review the literature pertaining to the mechanism by which revascularisation occurs following tumour irradiation using experimental models. Areas of interest and debate in the literature include the process by which endothelial cells die after irradiation and the identity/origin of the cells that reconstitute the tumour blood vessels after injury. Understanding the processes that mediate tumour revascularisation will guide the improvement of clinical strategies for preventing recurrence of glioblastoma after irradiation.
胶质母细胞瘤的局部复发是明确治疗后患者死亡的主要原因。本综述讨论趋化因子基质细胞衍生因子-1 及其受体 CXC 趋化因子受体 4(CXCR4)在影响胶质母细胞瘤对放疗敏感性中的作用。阻断这些分子可通过抑制参与肿瘤血管新生的 CD11b+单核细胞/巨噬细胞的募集来防止或延迟放疗后的肿瘤复发。我们回顾了使用实验模型探讨肿瘤放疗后血管新生机制的文献。文献中关注和争议的领域包括照射后内皮细胞死亡的过程以及损伤后重建肿瘤血管的细胞的身份/来源。了解介导肿瘤血管新生的过程将指导改善预防放疗后胶质母细胞瘤复发的临床策略。