If this is where you are
Newly diagnosedReports arriving, no plan yetAlready tested elsewhereYou have results you cannot readOn treatment nowYou want to know it is workingOr
Finished treatmentWatching for anything left behindWorried about familyInherited risk, and relativesWanting a second opinionA decision you are unsure aboutDecide
Blueprint CareThe flagship decision report and a dedicated clinical teamSignalOne free question answered on WhatsApp within four hoursNavigationRecords you already have, turned into a clarity timelineDecipherInterpretation of sequencing already done elsewhereTest
Signature, all tiersSolid tumour and blood cancer panels comparedSignature STb33 genes from a blood drawSignature STb O118 genes from a blood drawSignature STb O+523 genes, with TMB and MSISignature STt OProfiling from an existing tissue blockMonitor
SentinelSerial monitoring while treatment is runningSentinel SolidctDNA monitoring for solid tumoursClearMolecular residual disease surveillanceClear SolidTumour-informed surveillanceProtect
HeritageInherited risk, assessed properlyHeritage CoreA broad inherited-risk assessmentHeritage AdhocFocused testing for named relativesCancer DictionaryWhat is discussed in your specific cancerReference
Cancer DictionaryOne structured entry per cancer typeBiomarker LibraryOne page per marker, in plain languagePatient ResourcesGlossary, guides and how to use themWatch, read and ask
Video LibraryShort explainers, captioned and translatedStoriesPatient and clinician experiences, consentedFAQThe questions we are asked mostCancer Dictionary · Central nervous system
The classification of adult diffuse glioma was rebuilt around molecular features. IDH status and 1p/19q codeletion define the three main adult types, and a tumour that looks like one entity under a microscope may be classified as another once molecular results arrive. MGMT promoter methylation is a separate, treatment-relevant test.
Also called Glioblastoma, Astrocytoma, Oligodendroglioma, GBM.
Start here
Adult glioma classification is now molecular by definition: a diagnosis cannot be made properly without IDH and 1p/19q status, so molecular testing is part of naming the disease rather than an addition to it.
The classification of adult diffuse glioma was rebuilt around molecular features. IDH status and 1p/19q codeletion define the three main adult types, and a tumour that looks like one entity under a microscope may be classified as another once molecular results arrive. MGMT promoter methylation is a separate, treatment-relevant test.
01Before any molecular question
Usually established first: imaging characteristics, tumour location and the extent of any resection. Neurological function and its likely trajectory are central to every decision in this disease, and sit alongside the oncological discussion rather than after it.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Astrocytoma, IDH-mutant
Graded 2 to 4. A distinct entity from IDH-wildtype glioblastoma despite overlapping appearances.
Oligodendroglioma, IDH-mutant and 1p/19q codeleted
Defined by both features together. Neither alone is sufficient for the diagnosis.
Glioblastoma, IDH-wildtype
Grade 4 by definition. The most common and most aggressive adult glioma.
Paediatric-type gliomas
Classified separately, with distinct alterations including BRAF fusions and histone alterations. Can occur in young adults.
Other CNS tumours
Meningioma, ependymoma, medulloblastoma and CNS lymphoma are separate diseases with their own molecular classifications.
03What is discussed
IDH1 and IDH2 mutation status is the first branch point in adult glioma classification. 1p/19q codeletion, together with IDH mutation, defines oligodendroglioma. ATRX loss and TP53 alteration support the astrocytoma designation. MGMT promoter methylation is a separate epigenetic test that carries treatment relevance in glioblastoma. EGFR amplification, TERT promoter alteration and chromosome 7 gain with chromosome 10 loss are features that can establish a glioblastoma diagnosis even in a tumour that looks lower grade. BRAF V600E and BRAF fusions appear in specific glioma types, and NTRK and FGFR alterations occur less commonly.
IDH1 and IDH2
The first branch point in adult glioma classification, and now a treatment target in lower-grade disease.
1p/19q codeletion
Together with IDH mutation, defines oligodendroglioma. Both are required.
MGMT promoter methylation
An epigenetic marker, not a mutation. Treatment-relevant in glioblastoma.
ATRX and TP53
Support the astrocytoma designation.
EGFR amplification, TERT, +7/-10
Molecular features that can establish glioblastoma even where the histology looks lower grade.
BRAF
V600E and fusions, in specific glioma types and more often in younger patients.
This is not an exhaustive list, and which markers are relevant depends on the individual case. Not every marker listed is assessed in every patient.
04What is tested, and from what
Molecular testing in glioma is part of making the diagnosis, not an optional extra, and current classification cannot be applied without it. Tissue comes from surgery or biopsy. Methylation profiling is increasingly used in difficult cases and in paediatric-type tumours to resolve diagnoses that histology alone cannot. Because the blood-brain barrier limits shedding, plasma-based testing is much less useful here than in other cancers.
Most glioma is sporadic. Inherited syndromes including Li-Fraumeni (TP53), neurofibromatosis types 1 and 2, Lynch syndrome and constitutional mismatch repair deficiency are recognised. Very young onset, multiple primary tumours, or a striking family history are the usual prompts. Constitutional mismatch repair deficiency in particular is worth considering in a child or young adult with a high-grade glioma and characteristic skin findings.
Cancer genetics and hereditary riskPlasma ctDNA is much less informative in brain tumours because the blood-brain barrier limits how much tumour DNA reaches the circulation. Cerebrospinal fluid is a more informative compartment and is under active study, particularly for CNS lymphoma and leptomeningeal disease.
More on ctDNA monitoring05The timing question
Testing that arrives after the decision it was meant to inform has already been made is a common and avoidable problem. This is the sequence in which molecular information tends to become relevant.
06Take these to your team
When a decision is being made
Questions worth raising with a treating team.
At progression, recurrence or resistance
The molecular picture at diagnosis is not always the molecular picture later.
07What shapes eligibility
Eligibility is written almost entirely in molecular terms: IDH status, 1p/19q status, MGMT methylation, grade and prior therapy. An incomplete molecular diagnosis prevents assessment against most glioma trials.
| Term | What it means |
|---|---|
| IDH | A metabolic enzyme. Mutations in it define a distinct and generally slower-growing group of gliomas. |
| 1p/19q codeletion | Loss of parts of two chromosomes together. Required, with IDH mutation, to diagnose oligodendroglioma. |
| MGMT promoter methylation | A chemical modification that switches off a DNA repair gene, making certain treatment more effective. |
| Pseudoprogression | Imaging changes after treatment that look like tumour growth but are not. |
| Methylation profiling | A test that classifies tumours by their pattern of chemical DNA modifications rather than by mutations. |
These are the services most often relevant to this cancer. Which of them applies is a clinical question, not an automatic one.
This entry is educational. It describes what is commonly discussed in this cancer, not what should happen for any individual. Which of it applies depends on the specific diagnosis, stage, prior treatment and the person themselves. Nothing here is a recommendation, and no list of biomarkers here is exhaustive. Decisions belong with a treating team who know the whole case.
Take the next step
A no-obligation conversation with our care team, arranged through KPCIRC.
Book a consultationCommission your decision report and a dedicated clinical team.
Explore Blueprint CareSignal replies to your first question within four hours, at no cost.
Start with Signal