Department of Radiation Oncology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Transl Oncol. 2010 Feb;3(1):50-5. doi: 10.1593/tlo.09244.
Proteasome inhibitors are emerging as a new class of cancer therapeutics, and bortezomib has shown promise in the treatment of multiple myeloma and mantle cell lymphoma. However, bortezomib has failed to have an effect in preclinical models of glioma. NPI-0052 is a new generation of proteasome inhibitors with increased potency and strong inhibition of all three catalytic activities of the 26S proteasome. In this article, we test the antitumor efficacy of NPI-0052 against glioma, as a single agent and in combination with temozolomide and radiation using five different glioma lines. The intrinsic radiation sensitivities differed for all the lines and correlated with their PTEN expression status. In vitro, NPI-0052 showed a dose-dependent toxicity, and its combination with temozolomide resulted in radiosensitization of only the cell lines with a mutated p53. The effect of NPI-0052 as a single agent on glioma xenografts in vivo was only modest in controlling tumor growth, and it failed to radiosensitize the glioma xenografts to fractionated radiation. We conclude that NPI-0052 is not a suitable drug for the treatment of malignant gliomas despite its efficacy in other cancer types.
蛋白酶体抑制剂作为一类新的癌症治疗药物正在兴起,硼替佐米已在多发性骨髓瘤和套细胞淋巴瘤的治疗中显示出前景。然而,硼替佐米在神经胶质瘤的临床前模型中并未发挥作用。NPI-0052 是新一代蛋白酶体抑制剂,具有更高的效力和对 26S 蛋白酶体的所有三种催化活性的强烈抑制作用。在本文中,我们测试了 NPI-0052 作为单一药物以及与替莫唑胺和放射治疗联合治疗五种不同神经胶质瘤系的抗肿瘤功效。所有系的固有放射敏感性均不同,并与它们的 PTEN 表达状态相关。在体外,NPI-0052 表现出剂量依赖性毒性,其与替莫唑胺联合使用仅导致 p53 突变的细胞系放射增敏。NPI-0052 作为单一药物对体内神经胶质瘤异种移植物的作用仅适度控制肿瘤生长,并且未能使神经胶质瘤异种移植物对分割放射增敏。我们得出结论,尽管 NPI-0052 在其他癌症类型中有效,但它不适合治疗恶性神经胶质瘤。