Targeting proteasomes as therapy in multiple myeloma
Targeting proteasomes as therapy in multiple myeloma
复制标题
DOI：
10.1007/978-1-4020-6554-5_12
复制
发表时间：
2008-01-01
期刊：
影响因子：
--
通讯作者：
Anderson, Kenneth C.
中科院分区：
文献类型：
--
作者：
Chauhan, Dharminder;Hideshima, Tern;Anderson, Kenneth C.
泛素蛋白酶体通路 (UPP) 调节正常的细胞内蛋白质降解过程，这对细胞周期进展、炎症、转录、DNA 复制和细胞凋亡至关重要。使用蛋白酶体抑制剂硼替佐米 (Velcade) 阻断 UPP 是治疗复发/难治性多发性骨髓瘤 (MM) 的有效疗法。寡核苷酸微阵列和蛋白质组学研究正在描绘介导硼替佐尼诱导的细胞毒性的分子机制，定义敏感性与耐药性的目标，允许开发下一代疗法，并提供联合疗法的基本原理。
The Ubiquitin-proteasome pathway (UPP) regulates normal intracellular protein degradation processes essential for cell cycle progression, inflammation, transcription, DNA replication, and apoptosis. Blockade of UPP using proteasome inhibitor Bortezomib (Velcade) is an effective therapy for relapsed/refractory multiple myeloma (MM). Both oligonucleotide microarrays and proteomic studies are delineating the molecular mechanisms mediating Bortezornib-induced cytotoxicity, defining targets of sensitivity vs resistance, allowing for the development of next generation therapies, and providing the rationale for combination therapies.