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Background  Mutations in isocitrate dehydrogenase 1 ( IDH1 ) and isocitrate dehydrogenase 2 ( IDH2 ) are frequent in low-grade gliomas and secondary glioblastomas (sGBM). Because they yield the same oncometabolite, D-2-hydroxyglutarate, they are often treated as equivalent and pooled. The objective of this study was to provide insight into the differences between  IDH1  and  IDH2  mutant gliomas.    Methods  To investigate the different clinical and molecular characterization between  IDH1  mutant and  IDH2  mutant gliomas, we studied 811 patients with  IDH1  mutations,  IDH2  mutations and  IDH1/2  wild-type. In addition, whole-transcriptome sequencing and DNA methylation data were used to assess the distribution of genetic changes in  IDH1  and  IDH2  mutant gliomas in a Chinese population-based cohort.    Results  Among 811 gliomas in our cohort, 448 cases (55.2 %) harbored an  IDH1  mutation, 18 cases (2.2 %) harbored an  IDH2  mutation and 345 cases (42.6 %) harbored an  IDH1/2  wild-type. We found that  IDH1  and  IDH2  are mutually exclusive in gliomas, and  IDH2  mutations are mutually exclusive with  PTEN ,  P53  and  ATRX  mutations. Patients with  IDH2  mutations had a higher frequency of  1p/19q  co-deletion ( p  < 0.05) than  IDH1  mutant patients. In addition, a Gene Set Enrichment Analysis (GSEA) showed that  IDH2  mutant gliomas were associated with the oxidative phosphorylation gene set, and the four most representative biological processes for genes commonly altered by hypermethylation in  IDH2  mutant gliomas were the regulation of cell proliferation, cell motion, cell migration and response to hypoxia. Patients with  IDH2  mutant gliomas exhibited longer Overall survival (OS) ( p  < 0.05) and longer Progression-free survival (PFS) ( p  < 0.05) than patients with  IDH1/2  wild-type gliomas. However, their OS and PFS did not differ from that of  IDH1  mutant patients.    Conclusions  Our study revealed an intrinsic distinction between  IDH1  and  IDH2  mutant gliomas, and these mutations should be considered separately because their differences could have implications for the diagnosis and treatment of  IDH1/2  mutant gliomas.

The comparison of clinical and biological characteristics between IDH1 and IDH2 mutations in gliomas