Polish Mother's Health Center Research Institute, Lodz, Poland.
Arch Immunol Ther Exp (Warsz). 2011 Aug;59(4):301-7. doi: 10.1007/s00005-011-0132-3. Epub 2011 May 28.
Hypoxia that originates from disturbed growth of solid tumors initiates a cascade of intracellular events engaging hypoxia-inducible factors, HIF-1 and HIF-2. Overexpression of HIF has been confirmed in solid tumors and was unfortunately accompanied with chemo- and radioresistance observed in many patients. Multiple cellular pathways resulting in HIF activation could be successfully inhibited by use of different kinds of drugs (e.g. topotecan, heat shock protein 90 and mTOR inhibitors, YC-1, pleurotin or 2-methoxyestradiol), which are being subjected into intensive investigation in clinical trials.
缺氧起源于实体瘤生长的紊乱,引发一系列涉及缺氧诱导因子(HIF-1 和 HIF-2)的细胞内事件。在实体瘤中已经证实 HIF 的过表达,不幸的是,这种过表达与许多患者中观察到的化疗和放疗耐药性相伴出现。多种细胞通路导致 HIF 的激活,可以通过使用不同种类的药物(如拓扑替康、热休克蛋白 90 和 mTOR 抑制剂、YC-1、pleurotin 或 2-甲氧基雌二醇)成功抑制,这些药物正在临床试验中进行深入研究。