Additional file 1: Table S1. of Genetic and epigenetic stability of oligodendrogliomas at recurrence

Clinical characteristics of the patient cohort. Table S2. Sequence data summary. Table S3. List of the somatic mutations in this study. (XLSX 163 kb

Additional file 2: Figure S1. of Genetic and epigenetic stability of oligodendrogliomas at recurrence

Histopathological features of primary and recurrent tumors in a 34 year-old female (patient 6). The primary tumor was diagnosed as anaplastic oligodendroglioma (WHO grade III) (A). Postoperatively, the patient was treated with 8 courses of PAV chemotherapy. Eight years after the initial surgery, an MRI FLAIR-high lesion was noticeably enlarged and this region showed high uptake in Methionine PET. Tumor recurrence was therefore suspected and surgical resection was performed. In the recurrent tumor, atypia of the nucleus was improved and numbers of mitotic cells were decreased compared to the primary tumor, and the tumor was diagnosed as oligodendroglioma (WHO grade II) (B). Formalin-fixed paraffin-embedded tissues were sectioned and stained with Hematoxylin and Eosin (bar = 100 μm). Figure S2. Histopathological features of different tumor portions from the same patient as listed in Additional file 1: Table S1. Formalin-fixed paraffin-embedded tissues were sectioned and stained with Hematoxylin and Eosin (bar = 100 μm). A. Patient 13, Methionine PET low uptake, grade II; B. Patient 13, Methionine PET high uptake, grade III; C. Patient 14, Gadolinium enhanced -, grade II; D. Patient 14, Gadolinium enhanced +, grade III; E. Patient 15, Methionine PET low uptake, grade II; F. Patient 15, Methionine PET high uptake, grade II; G. Patient 16, Methionine PET low uptake, grade III; H. Patient 16, Methionine PET high uptake, grade III. (PPTX 1597 kb

Additional file 2: Table S1. of A combination of TERT promoter mutation and MGMT methylation status predicts clinically relevant subgroups of newly diagnosed glioblastomas

Molecular and clinical characteristics of Cohort 1 (n = 758). Table S2. Molecular and clinical characteristics of GBM cohort (n = 453). Table S3. Univariate and multivariate Cox regression analyses for Group A (IDH mutated-TERT mutated) tumors in Cohort 1 (n = 155). Table S4. Univariate and multivariate Cox regression analyses for Group B (IDH mutated-TERT wild-type) tumors in Cohort 1 (n = 131). Table S5. Univariate and multivariate Cox regression analyses for Group C (IDH wild-type-TERT wild-type) tumors in Cohort 1 (n = 237). Table S6. Univariate and multivariate Cox regression analyses for Group D (IDH wild-type-TERT mutated) tumors in Cohort 1 (n = 235). Table S7. Univariate and multivariate Cox regression analyses for GBM in Cohort 1 (n = 260). Table S8. Univariate and multivariate Cox regression analyses for GBM in Cohort 2 (n = 193). Table S9. Background of combined GBM cohort stratified by TERT and MGMT status (n = 453). Table S10. Survival time and WHO grade in each molecular subgroup of Cohort 1 (n = 758). (XLSX 254 kb

Additional file 3: Figure S1. of A combination of TERT promoter mutation and MGMT methylation status predicts clinically relevant subgroups of newly diagnosed glioblastomas

Distributions of molecular alterations according to histology in Cohort 1. Figure S2. Kaplan-Meier analysis for Group A cases stratified by 1p/19q status. Figure S3. Kaplan-Meier analyses for GBM cases in Cohorts 1 and 2. (PPTX 172 kb

Additional file 1: of A combination of TERT promoter mutation and MGMT methylation status predicts clinically relevant subgroups of newly diagnosed glioblastomas

Supplementary Information. (DOCX 141 kb