摘要
血管增生和侵袭性生长是恶性胶质瘤重要的生物学特征，也是其临床治疗失败的主要因素。随着对胶质瘤血管生成的分子生物学机制研究的深入，以贝伐单抗为主的抗血管生成药物在临床试验中取得了积极的治疗效果，但在治疗过程中也增强了胶质瘤细胞的侵袭迁移能力。目前，研究认为基质金属蛋白酶（MMP）、缺氧诱导因子1（HIF-1）和需肌醇酶1（IRE-1）与胶质瘤细胞的侵袭改变存在一定相关性，但具体的分子生物学机制尚需进一步探讨。
Angiogenesis and invasion are two remarkable features of spongioblastoma, which lead to the failure of clinical treatment. With the development of the gliomab molecular biology mechanism in the realm of angiogenesis, some anti-angiogenesis drugs have got a positive therapeutic efficacy in the clinical trials, such as bevacizumab. However, it is reported that these drugs maybe also enhance the invasion and migration ability of glioma cells in the process of anti-angiogenesis therapy. Matrix metalloproteinases, hypoxia induced factor-1 and the inositol-requiring enzyme-1 maybe have some correlations with the change of the invasion and migration, but the molecular biological mechanism needs further research.
出处
《国际肿瘤学杂志》
CAS
2012年第4期259-261,共3页
Journal of International Oncology
基金
湖北省自然科学基金资助项目（2010CDB05507）
