n(steroids) = 2; n(no steroids) = 28. n (RT) = 5; n(RT + TMZ) = 22; n(TMZ) = 3. Two-sided Kruskal–Wallis test with Dunn’s multiple comparison ( b). c, Gating strategy for flow cytometric effector sub-phenotyping of peripheral IDH1-vac-induced T cells shown in Fig. 2c. FM2, fluorescence minus two; FMO, fluorescence minus one; MOG, negative control. Extended Data Fig. 5 | Definition of the MSS and PLA. a, Exemplary MSS of patients ID12 and ID05. Mathematical differences between specific spot counts for IDH1(R132H) (red) and wild-type IDH1 (blue) are calculated (light blue) for all immunogenicity testing visits. MSS is defined as the sum of the three largest differences. For MSS of the IDS please refer to Supplementary Table 7. b, Exemplary PLA of patients ID12 and ID05. For relative PLA values of the IDS please refer to Fig. 2 . Scale bars, 80 μm. PLA was performed once per patient. c, Relative PLA signals of primary and recurrent tissues from patient ID25. Article Extended Data Fig. 6 | Probabilities of progression and death in the SDS. Overall (left) and progression-free (right) survival estimates with number of patients at risk are shown for all patients of the SDS ( a), according to SOC treatment ( b), extent of resection ( c), and WHO grade ( d). CR, complete resection; ST, subtotal resection. n (all patients) = 32; n (RT, aTMZ) = 4; n (RT) = 2; n(TMZ + RT, aTMZ) = 22; n (TMZ + RT) = 1; n(TMZ) = 3; n(CR) = 17; n(ST) = 12; n(biopsy) = 3; n(grade 3) = 21; n (grade 4) = 11. Time, months from first diagnosis. Extended Data Fig. 7 | Determinants of pseudoprogression. a, Time points of PsPD diagnosed by MRI and onset of early immune response are shown in weeks and study visits. Black diamond, onset of immune response; red asterisk, PsPD. Visits with immune monitoring (V03, V05, V07, V10, and V12) are depicted. MRI was performed at clinical screening, V07, V10, V12 and V13. The onset of an early immune response was defined as antibody titre ≥ 1:333 (B cell), and/or T cell response detectable after negative control subtraction. n = 12 patients with PsPD. b , Violin plots showing MSS according to disease progression. Solid line, median; dotted lines, quartiles. n (SD) = 15; n(PsPD) = 11; n(PD) = 4. Two-sided Kruskal–Wallis test with Dunn’s multiple comparison. c, Incidence of disease progression in patients with molecularly defined astrocytomas according to CNV-L, methylation class, and CDKN2A/B status. d, Correlation between predicted and actual occurrence of molecular markers in groups of disease outcomes. Two-sided Fisher’s exact test (PsPD versus SD + PD). n(all patients) = 23 ( c, d). Article Extended Data Fig. 8 | Probabilities of progression and death in the molecular dataset. Overall (left) and progression-free (right) survival estimates with number of patients at risk are shown according to methylation class ( a), CDKN2A/B status and grade ( b), and CDKN2A/B status and CNV-L ( c). H, methylation class high; L, methylation class low; het, heterozygous CDKN2A/B deletion; 0, no CDKN2A/B deletion; homo, homozygous CDKN2A/B deletion. n (all patients) = 24; n(methylation class H) = 10; n (methylation class L) = 14; n(CDKN2A/B het and 0 + grade 3) = 13; n (CDKN2A/B het and 0 + grade 4) = 7; n(CDKN2A/B het and 0 + CNV-L high) = 4; n (CDKN2A/B het and 0 + CNV-L low) = 16; n(CDKN2A/B homo) = 4. Extended Data Fig. 9 | Outcomes, standard treatment and peripheral immune cell composition in the IDS. a, Frequencies of T cells, monocytes, regulatory T cells (Tregs), and monocytic myeloid-derived suppressor cells (mo-MDSC) within PBMCs were determined at V07 by flow cytometry and are shown according to disease course at EOS (top) and SOC treatment (bottom). CD3 +, T cells. n (SD) = 15; n(PsPD) = 11; n(PD) = 4; n(RT) = 5; n(RT + TMZ) = 22; n(TMZ) = 3. Red line, median; dotted lines, quartiles. Two-sided Kruskal–Wallis test with Dunn’s multiple comparison. b, Gating strategy for flow cytometric analysis. Article Extended Data Fig. 10 | Longitudinal TCRB deep sequencing of PBMC. Tree maps of longitudinal TCRB deep sequencing of PBMCs. Black outlines highlight time points of PsPD. TCRB deep sequencing was performed if PBMCs were available for exploratory analyses. n = 25 patients of the SDS. Extended Data Fig. 11 | Ex vivo cytotoxic T cell responses, CD8+ T cell clone-specific cytokine production and TCR-transgenic cell reactivity of PsPD LILs from patient ID08. a, Top, visualization of TNF- and IFNγ- expressing T cells by UMAP (Fig. 4). Bottom, relative percentages of cells expressing IFNγ and TNF among CD8+ cells, each expressing one of the top ten TCRs. b, c, Flow cytometric gating strategy ( b) and quantification ( c) of ex vivo cytotoxic T cell responses of PsPD CD8+ LILs from patient ID08 upon re-stimulation with IDH1(R132H). d , CD8+ T cell clonotype-retrieved TCR-transgenic cell reactivity in luciferase NFAT reporter assays. TCR1, overall top abundant ID08 PsPD CD8 + T cell clonotype; TCR3, ID08 PsPD CD8+ T cell clonotype with top TNF/IFNγ percentage ( a). InfHA (influenza HA peptide; PKYVKQNTLKLAT) and its respective TCR-transgenic cells were used as positive control. Technical triplicates with mean, experiment performed once. Article Extended Data Fig. 12 | S ingle-cell RNA-TCR-seq and TCRB deep sequencing of PsPD from patient ID08. a, Bottom left, abundance of T cells relative to non-T cells in PsPD from patient ID08 versus control IDH1(R132H)+ astrocytoma and glioblastoma tissues. Dashed line, median; dotted lines, quartiles. Top and right, gating strategy of ID08-PsPD T cell sorting. b , Heat map of RNA expression of single-cell cluster-defining genes (see Fig. 4). c, Co-visualization of top 5 CD8+ and CD4+ TCR clonotypes and corresponding RNA single-T cell clusters by UMAP (see Fig. 4). d, Combined visualization of TCRB deep sequencing and scRNA-TCR-seq of PBMCs from patient ID08 at V07 versus LILs from PsPD of patient ID08. The frequency of TCR14 is highlighted. e, Longitudinal T cell response of patient ID08 assessed by IFNγ ELISpot.