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Oncology›Condition·Updated Jul 11, 2026·v1

Glioblastoma

Glioblastoma is an IDH-wildtype, WHO grade 4 glioma with a median survival of 12-15 months. The Stupp protocol (maximal safe resection, radiotherapy with concurrent and adjuvant temozolomide) remains the standard of care, with tumor-treating fields providing a modest additional survival benefit. MGMT promoter methylation is the key predictive biomarker for temozolomide response. Bevacizumab is not recommended for newly diagnosed disease. Elderly patients benefit from hypofractionated radiotherapy with temozolomide. Despite decades of research, no systemic therapy has surpassed temozolomide in the upfront setting, and recurrence is inevitable.

High Evidence509 references·1,892 words·8 min read·v1
glioblastomaGBMbrain tumorneuro-oncologytemozolomideMGMTStupp protocoltumor-treating fields

Quick Reference

RxDrug of choiceTemozolomide 75 mg/m² PO daily during radiotherapy, then 150-200 mg/m² PO days 1-5 of 28-day cycles for 6 cycles
AltAlternativesLomustine 90-110 mg/m² PO every 6 weeks for recurrent disease; bevacizumab 10 mg/kg IV q2w for symptom control (no OS benefit)
⊘AvoidBevacizumab in newly diagnosed GBM; non-dihydropyridine CCBs; anticonvulsant prophylaxis
DxTest of choiceMRI brain with contrast + histopathology with IDH1/2 sequencing and MGMT promoter methylation analysis
ScKey scoreRTOG RPA class (age, KPS, MMSE, extent of resection, neurologic function); NRG-GBM-RPA model (adds MGMT protein, c-Met, age); Park scale for recurrent surgery
→When to referNeurosurgery for resection, radiation oncology, neuro-oncology, palliative care, clinical trials
The Stupp protocol (RT + concurrent/adjuvant temozolomide) remains the cornerstone of therapy; only TTFields added a survival benefit in newly diagnosed disease. No systemic therapy has surpassed temozolomide in 20 years. MGMT methylation is the key predictive biomarker.
Glioblastoma is the most common and most aggressive primary malignant brain tumor in adults, defined by IDH-wildtype status and WHO grade 4. Despite multimodality therapy, prognosis remains poor with median survival of 12-15 months. The Stupp protocol (radiotherapy with concurrent and adjuvant temozolomide) is the cornerstone of treatment. This concise reference summarizes key clinical facts, drug doses, critical thresholds, and management strategies for bedside use.

Overview and Recommendations

Background

  • •Glioblastoma is an IDH-wildtype, WHO grade 4 diffuse glioma of neuroglial progenitor origin, representing the most common malignant primary brain tumor in adults with an incidence of ~3.2 per 100,000 person-years in the United States. It accounts for 61.5% of all adult gliomas and carries a uniformly fatal prognosis despite multimodality therapy.
  • •The disease is defined molecularly by the absence of IDH1/2 mutations, which separates it from IDH-mutant astrocytomas (grade 4). The 2021 WHO classification also requires the presence of microvascular proliferation, pseudopalisading necrosis, or molecular grade 4 features such as TERT promoter mutation, EGFR amplification, or combined chromosome 7 gain/10 loss.
  • •Incidence rises with age: ~80% of cases occur in patients ≥45 years, and nearly half are ≥65 years. Males are affected 60% more often than females. The only established risk factors are rare genetic syndromes (Li-Fraumeni, Lynch, neurofibromatosis type 1) and prior therapeutic cranial irradiation; no modifiable environmental or lifestyle factors have been identified.
  • •Four transcriptional subtypes, proneural, neural, classical, and mesenchymal, were defined by TCGA, with the mesenchymal subtype associated with radioresistance and a shift toward this phenotype at recurrence. Single-cell studies reveal intratumoral heterogeneity, with cells from multiple subtypes coexisting within the same tumor.
  • •The core driver pathways universally dysregulated in GBM are RTK/RAS/PI3K (>90% of tumors), p53 (~87%), and RB (~79%). Key alterations include EGFR amplification (~40%), TERT promoter mutations (~80%), PTEN loss, and CDKN2A/B deletion. MGMT promoter methylation is the most important predictive biomarker, silencing the DNA repair enzyme that confers sensitivity to temozolomide.

Evaluation

  • •Suspect glioblastoma in any adult presenting with progressive headache, new-onset focal neurological deficit (hemiparesis, aphasia, visual field cut), unexplained seizure, or cognitive decline evolving over weeks to a few months. The classic triad of headache, seizure, and focal deficit is present in ~50% of patients.
  • •Ask about the tempo of symptom onset, presence of nausea/vomiting (suggesting elevated ICP), seizure semiology, medication use (especially anticoagulants), family history of brain tumors or cancer syndromes, and prior radiation exposure.
  • •Examine for contralateral pyramidal weakness, hyperreflexia, Babinski sign, sensory loss, neglect, homonymous hemianopia, central facial weakness, and aphasia. Assess mental status with attention to executive function and memory. Funduscopy may reveal papilledema but is often absent in the era of early imaging.
  • •Order urgent MRI brain with and without gadolinium as the imaging gold standard. The typical appearance is a ring-enhancing mass with central necrosis, surrounding T2/FLAIR hyperintensity (edema/infiltration), and restricted diffusion. Volume ≥50 cm³ and multifocality are poor prognostic signs.
  • •Obtain tissue for histopathologic and molecular diagnosis via maximal safe resection or stereotactic biopsy. The gold-standard diagnostic test is histopathologic evaluation with IDH1/2 mutational status determination. Immunohistochemistry should include GFAP, OLIG2, ATRX, IDH1 R132H, p53, and Ki-67.
  • •Mandatory molecular testing includes IDH1/2 sequencing (to confirm wild-type status), MGMT promoter methylation analysis (by pyrosequencing, threshold ≥11% for methylated), and TERT promoter mutation testing. Optional but useful markers include EGFR amplification, CDKN2A/B deletion, and BRAF V600E mutation.
  • •Apply the 2021 WHO diagnostic criteria: IDH-wildtype status plus at least one of microvascular proliferation, pseudopalisading necrosis, or molecular grade 4 features (TERT promoter mutation, EGFR amplification, +7/-10 chromosome signature). The presence of IDH mutation reclassifies the tumor as IDH-mutant astrocytoma grade 4.
  • •Assess baseline laboratory values including CBC, comprehensive metabolic panel, and coagulation profile before surgery. Consider pregnancy testing in women of childbearing age.
  • •Perform postoperative contrast-enhanced MRI within 48 hours to determine extent of resection. Gross total resection (no residual enhancement) is the goal and roughly doubles survival compared with biopsy alone.
  • •Use the RTOG RPA classification for pretreatment prognostic staging, incorporating age, Karnofsky Performance Status (KPS), Mini-Mental State Exam score, extent of resection, and neurologic function. For recurrent disease, the Park scale (0-3 points based on eloquent cortex involvement, KPS ≤80, volume ≥50 cm³) predicts survival after repeat surgery.

Management

  • •Initiate therapy with maximal safe resection of contrast-enhancing tumor. Gross total resection reduces 1-year mortality by 38% (RR 0.62, NNT=9) compared with subtotal resection. Intraoperative MRI or 5-ALA fluorescence guidance improves complete resection rates.
  • •Within 4-6 weeks of surgery, start involved-field radiotherapy (60 Gy in 30 fractions over 6 weeks) with concurrent temozolomide 75 mg/m² orally daily, 7 days per week. This is the Stupp protocol, which improved median OS from 12.1 to 14.6 months (HR 0.63) and 5-year OS from 1.9% to 9.8%.
  • •After a 28-day break following chemoradiation, administer adjuvant temozolomide 150-200 mg/m² orally on days 1-5 of each 28-day cycle for 6 cycles. The ASCO-SNO guideline recommends 6 cycles; longer treatment may be considered in selected patients.
  • •Add tumor-treating fields (TTFields) to adjuvant temozolomide for eligible patients with newly diagnosed GBM. The EF-14 trial showed improved median OS (20.9 vs 16.0 months; HR 0.67) and PFS (6.7 vs 4.0 months) without worsening quality of life except for itchy skin.
  • •For elderly patients (≥65 years) with good performance status (KPS ≥70), use hypofractionated radiotherapy (40 Gy in 15 fractions) with concurrent and adjuvant temozolomide. The Perry trial showed median OS 9.3 vs 7.6 months (HR 0.67). For MGMT-methylated patients, median OS was 13.5 vs 7.7 months.
  • •For frail elderly patients (KPS 50-70%), short-course radiotherapy alone (25 Gy in 5 fractions) is non-inferior to 40 Gy in 15 fractions (median OS 7.9 months). Alternatively, temozolomide alone (100 mg/m² days 1-7 of 1-week-on/1-week-off) is non-inferior to radiotherapy in patients >65 years with MGMT-methylated tumors.
  • •At recurrence, evaluate for repeat surgery, re-irradiation, or systemic therapy. The Park scale (0-3 points) guides surgical decision: score 0 → median OS 10.8 months; score 3 → 1.0 month. Re-irradiation (35 Gy in 10 fractions) with concurrent bevacizumab improves PFS but not OS vs bevacizumab alone.
  • •For first recurrence, consider lomustine 90-110 mg/m² orally every 6 weeks (median OS 8.6 months in EORTC 26101). Bevacizumab 10 mg/kg IV every 2 weeks improves PFS and reduces steroid dependence but does not extend OS when added to lomustine. It is not recommended for newly diagnosed disease.
  • •Do NOT use bevacizumab in the upfront setting, two phase III trials (AVAglio, RTOG 0825) showed no OS benefit and worse quality of life. Avoid non-dihydropyridine CCBs (diltiazem, verapamil) as they may exacerbate cerebral edema. Anticonvulsant prophylaxis is not indicated; only treat patients with a history of seizures.
  • •Refer all patients to a neuro-oncology specialist, radiation oncologist, and palliative care team early. Consider clinical trials for novel therapies (e.g., checkpoint inhibitors, CAR-T cells, targeted agents) at any point in the disease course. Monitor with MRI every 2-4 months, with awareness that pseudoprogression within 12 weeks of chemoradiation is common and requires a confirmatory scan before declaring progression.

Board Review — High Yield

  • •Stupp protocol, RT 60 Gy/30 fractions + concurrent temozolomide 75 mg/m² daily, then adjuvant TMZ 150-200 mg/m² days 1-5/28 for 6 cycles; improves median OS from 12.1 to 14.6 months.
  • •MGMT promoter methylation, strongest predictive biomarker for temozolomide benefit; pyrosequencing threshold ≥11% defines methylated; associated with median OS ~28 months when combined with GTR and chemoradiation.
  • •IDH-wildtype, required for GBM diagnosis per WHO 2021; IDH mutation reclassifies as IDH-mutant astrocytoma grade 4 with better prognosis (median OS 3.6 vs 1.2 years).
  • •TERT promoter mutation, present in 70-80% of IDH-wildtype GBM; a defining molecular alteration; portends worse survival (aHR 2.93).
  • •Pseudoprogression, transient increase in enhancement within 12 weeks of chemoradiation, more common in MGMT-methylated tumors; do not declare progression without confirmatory scan.
  • •TTFields, low-intensity alternating electric fields added to adjuvant TMZ; EF-14 trial showed median OS 20.9 vs 16.0 months (HR 0.67); FDA-approved for newly diagnosed GBM.
  • •Bevacizumab, no OS benefit in newly diagnosed GBM (two phase III trials); used in recurrent disease for PFS and steroid reduction but not recommended by ASCO-SNO upfront.
  • •Elderly GBM, hypofractionated RT (40 Gy/15 fractions) + TMZ is standard for fit patients ≥65; TMZ alone is non-inferior to RT for MGMT-methylated patients.
  • •Mesenchymal subtype, associated with radioresistance via NF-κB activation; tumors shift toward this phenotype at recurrence.
  • •CSF ctDNA, liquid biopsy alternative when tissue unavailable; 84% concordance with tumor genotyping; higher variant allele frequency correlates with worse survival.

Deep Dive — Evidence Details

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