Glioma & glioblastoma
Prepared with OnCo (onco.cc/prep/glioblastoma/). Orientation, not medical advice; your team knows your case.
My details
What I know, what is unclear, changes to discuss
Saved in this browserMy questions
28 on the sheet- 1.What is my exact diagnosis, stage, and grade, and which tests established them?
- 2.Which biomarkers have been tested on my tumour (for example IDH1/2, 1p/19q codeletion, MGMT methylation, H3K27M, EGFR amplification), and what were the results?
- 3.Which subtype is my cancer, and does that change the recommended treatment?
- 4.Is germline (inherited) genetic testing recommended for me or my family?
- 5.For my situation (glioblastoma), which of the standard options do you recommend and why?
- 6.Am I a candidate for Optune / Optune Pax (TTFields), and what side effects should I expect?
- 7.For my situation (idh-mutant grade 2), which of the standard options do you recommend and why?
- 8.Am I a candidate for Vorasidenib, and what side effects should I expect?
- 9.For my situation (diagnosis), which of the standard options do you recommend and why?
- 10.For my situation (glioblastoma, newly diagnosed), which of the standard options do you recommend and why?
- 11.Am I a candidate for Temozolomide, Optune / Optune Pax (TTFields), and what side effects should I expect?
- 12.How do the results of EORTC 26981 / NCIC CE.3 (Stupp trial) and CCTG CE.6 / EORTC 26062-22061 (Perry trial) apply to someone like me?
- 13.For my situation (glioblastoma, recurrent), which of the standard options do you recommend and why?
- 14.Am I a candidate for Lomustine (CCNU), Bevacizumab (glioblastoma use), and what side effects should I expect?
- 15.For my situation (idh-mutant grade 2 glioma), which of the standard options do you recommend and why?
- 16.Am I a candidate for Vorasidenib, and what side effects should I expect?
- 17.How do the results of INDIGO apply to someone like me?
- 18.For my situation (oligodendroglioma grade 3 / astrocytoma grade 3), which of the standard options do you recommend and why?
- 19.Am I a candidate for Temozolomide, and what side effects should I expect?
- 20.For my situation (h3 k27m diffuse midline glioma), which of the standard options do you recommend and why?
- 21.Am I a candidate for Dordaviprone, and what side effects should I expect?
- 22.For my situation (paediatric low-grade glioma), which of the standard options do you recommend and why?
- 23.Am I a candidate for Tovorafenib, and what side effects should I expect?
- 24.Are there clinical trials I could join, for example of Armoured, logic-gated & next-gen CARs, Boron neutron capture therapy, Hyperthermia, LAM561?
- 25.Would a second opinion at a high-volume centre change anything, and can you help arrange it?
- 26.What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?
- 27.I read that “Blood-brain barrier”. How does that affect my plan?
- 28.I read that “Immunologically cold, heterogeneous, infiltrative”. How does that affect my plan?
The words I may hear
- EGFRvIII: EGFRvIII is a mutant, tumour-only version of the EGFR receptor found in about a third of glioblastomas.
- Necrosis: Messy, uncontrolled cell death, where the cell bursts and spills its contents.
- Extent of resection (RANO resect classes): How much of a brain tumour the surgeon removes, measured on an MRI scan soon after the operation.
- Accelerated approval: FDA approval based on early evidence (like tumour shrinkage) on condition that a confirmatory trial follows.
- Hot vs cold tumours: 'Hot' tumours are full of immune cells and respond to immunotherapy; 'cold' tumours have kept the immune system out.
- Metabolic theory of cancer: from Warburg to oncometabolites: Otto Warburg noticed a century ago that cancer cells ferment glucose even when oxygen is plentiful and concluded that damaged respiration causes cancer.
- Bioelectric theory of cancer (Levin): Cells hold a voltage across their membranes, and tissues share these voltages as patterns that guide growth and regeneration.
- MGMT promoter methylation: A chemical switch that turns off a DNA-repair gene.
- H3 K27M (diffuse midline glioma): A single change in a histone protein that defines diffuse midline glioma, the childhood brain tumour with the fewest treatment options, and now the target of the first approved drug for it.
- Cancer stem cell theory and phenotypic plasticity: The idea that a tumour is organised like a tissue, with a small pool of stem-like cells that renew it and a bulk that cannot, so killing the bulk shrinks the tumour but the stem-like cells regrow it.
Tests and results to bring
Diagnosis: MRI with contrast; maximal safe resection with 5-ALA and intraoperative mapping, with early postoperative MRI to measure the extent of resection; integrated histo-molecular diagnosis with methylation classification where available.
Glioblastoma, newly diagnosed: Radiotherapy 60 Gy in 30 fractions with concurrent and 6 cycles adjuvant temozolomide; from age 65, short-course radiotherapy (40 Gy in 15 fractions) with temozolomide (CCTG CE.6); for older patients unfit for combined treatment, temozolomide alone or hypofractionated radiotherapy alone, chosen by MGMT status (Nordic, NOA-08); TTFields with maintenance temozolomide; trials for MGMT-unmethylated patients.
Biomarker results to ask for: IDH1/2, 1p/19q codeletion, MGMT methylation, H3K27M, EGFR amplification, Methylation class, IDH1/2 mutation (vorasidenib eligibility), MGMT promoter methylation (temozolomide benefit), H3 K27M (dordaviprone eligibility), BRAF fusion / V600E (tovorafenib, dabrafenib-trametinib), TERT promoter, EGFR amplification, +7/−10 (molecular glioblastoma), CDKN2A/B homozygous deletion (grade 4 astrocytoma), DNA methylation class (Heidelberg classifier), NTRK/ALK/ROS1 fusions (infant gliomas), TMB / mismatch repair (rare hypermutant, IO-responsive).
Scans and tests linked to this cancer: MRI, PET (positron emission tomography), PET/CT, DNA methylation profiling, Fluorescence-guided surgery, Intraoperative fluorescence and Cerenkov imaging systems (SPY, Firefly, LumiSystem, LightPath).
Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.
The treatments I may be offered
- Glioblastoma: Resection → RT + temozolomide → TTFields; lomustine/bevacizumab at relapse. (Fluorescence-guided surgery, IMRT / IGRT (modern external beam), Optune / Optune Pax (TTFields))
- IDH-mutant grade 2: Resection → vorasidenib or observation; RT/PCV for high-risk. (Vorasidenib)
- Glioblastoma, recurrent: Re-resection or LITT if feasible; lomustine; bevacizumab for oedema/steroid sparing; re-irradiation; clinical trial (CAR-T, FUS-BBB, vaccines) strongly preferred. (Lomustine (CCNU), Bevacizumab (glioblastoma use), Laser interstitial thermal therapy (LITT), CAR-T for glioma (IL13Rα2, GD2, EGFRvIII, multi-target), Focused-ultrasound blood-brain barrier opening, SBRT / SABR (stereotactic radiotherapy))
- IDH-mutant grade 2 glioma: Maximal resection; vorasidenib for residual/recurrent disease (INDIGO); radiotherapy plus PCV or temozolomide for high-risk or progressive disease. (Vorasidenib, INDIGO)
- Oligodendroglioma grade 3 / astrocytoma grade 3: Radiotherapy plus PCV (RTOG 9402, EORTC 26951) or temozolomide (CATNON). (Temozolomide, IMRT / IGRT (modern external beam))
- H3 K27M diffuse midline glioma: Radiotherapy; dordaviprone at progression (2025); GD2 CAR-T and ONC201 first-line trials. (Dordaviprone, CAR-T for glioma (IL13Rα2, GD2, EGFRvIII, multi-target))
- Paediatric low-grade glioma: Resection where safe; chemotherapy (carboplatin/vincristine) or tovorafenib / dabrafenib-trametinib for BRAF-altered relapsed disease; avoid radiation in young children. (Tovorafenib)
From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.