Nobusawa Sumihito, Yokoo Hideaki
Department of Human Pathology, Gunma University Graduate School of Medicine, Gunma, Japan.
Brain Nerve. 2011 Dec;63(12):1378-86.
The NADP+-dependent isocitrate dehydrogenases 1 and 2 (IDH1/2) catalyze the oxidative decarboxylation of isocitrate into α-ketoglutarate (α-KG). IDH1 and IDH2 mutations have been frequently found in some types of gliomas (low-grade diffuse gliomas WHO grade II, anaplastic gliomas WHO grade III, and secondary glioblastomas WHO grade IV), and have received significant attention because of their specificity to single codons. Since the unveiling of IDH1/2 mutations, many studies have investigated their clinical impact on gliomas. While the favorable influence of these mutations in high-grade gliomas has been well established, their prognostic impact on low-grade diffuse gliomas is much less clear. While the mechanism of IDH1/2 mutations in gliomagenesis remains to be clarified, its elucidation might lead to novel therapeutic strategies against gliomas.
烟酰胺腺嘌呤二核苷酸磷酸(NADP⁺)依赖性异柠檬酸脱氢酶1和2(IDH1/2)催化异柠檬酸氧化脱羧生成α-酮戊二酸(α-KG)。IDH1和IDH2突变在某些类型的胶质瘤中经常被发现(世界卫生组织二级低级别弥漫性胶质瘤、世界卫生组织三级间变性胶质瘤和世界卫生组织四级继发性胶质母细胞瘤),并且由于它们对单个密码子的特异性而受到了极大关注。自IDH1/2突变被发现以来,许多研究都调查了它们对胶质瘤的临床影响。虽然这些突变在高级别胶质瘤中的有利影响已经得到充分证实,但它们对低级别弥漫性胶质瘤的预后影响却远不那么清晰。虽然IDH1/2突变在胶质瘤发生中的机制仍有待阐明,但其阐明可能会带来针对胶质瘤的新治疗策略。