WHO Grade III Mixed Glioma

Other names
Types
Causes and risk factors
Common symptoms
Diagnostic tests
Non-pharmacological treatments (therapies & other measures)
Drug treatments
Dietary “molecular” supplements
Immunity booster / regenerative / stem-cell” drugs
Surgeries
Prevention points
When to see a doctor urgently
What to eat and what to avoid
Frequently asked questions

WHO grade III mixed glioma” is an older name used when a brain tumor looked like a mix of two cell types: astrocytes and oligodendrocytes. “Mixed” means both parts were present under the microscope. “WHO grade III” (also called anaplastic) means the tumor cells looked very abnormal and grew faster than low-grade tumors.

Today, doctors rarely use “mixed glioma” because modern tests look at the genes inside the tumor. These tests show that most “mixed” tumors actually belong to one of two main groups:

Astrocytoma, IDH-mutant, CNS WHO grade 3, or
Oligodendroglioma, IDH-mutant and 1p/19q-codeleted, CNS WHO grade 3.

So, the new system focuses on molecular markers (for example, IDH mutations and 1p/19q codeletion) rather than only the look under a microscope. Because of this, the term “mixed glioma” (or “oligoastrocytoma”) has mostly been retired and is reserved only when full molecular testing is not available and the tumor truly shows both components (sometimes labeled NOS—“not otherwise specified”). PMC+2PubMed+2

In daily life, this tumor is a type of diffuse brain cancer. “Diffuse” means the cells infiltrate normal brain, so the edges are not sharp. That is why surgery aims to remove as much as is safe, but microscopic cells can remain. Symptoms depend on the brain area affected and may include seizures, headaches, and weakness. Modern care uses surgery, radiation, and drugs, but this article focuses on definitions, causes, symptoms, and tests.

Other names

Mixed glioma
Oligoastrocytoma (historical)
Anaplastic oligoastrocytoma (AOA; historical WHO grade III name)
WHO grade III mixed glioma (older wording)
Oligoastrocytoma, NOS (used only when molecular tests are missing)
These older terms are now usually re-named as either astrocytoma, IDH-mutant (grade 3) or oligodendroglioma, IDH-mutant and 1p/19q-codeleted (grade 3) after molecular testing. PMC+1

Types

Type A: Astrocytoma, IDH-mutant, CNS WHO grade 3.
This is an infiltrating astrocytic tumor with an IDH1 or IDH2 mutation. Grade 3 means faster growth and more aggressive behavior than grade 2. Pathology often shows increased cell density, nuclear atypia, and more cell division. Molecular tests often show ATRX loss and TP53 changes; 1p/19q is not codeleted in this type. Many tumors once called “anaplastic oligoastrocytoma” reclassify here after testing. PMC

Type B: Oligodendroglioma, IDH-mutant and 1p/19q-codeleted, CNS WHO grade 3.
This infiltrating tumor has both an IDH mutation and 1p/19q codeletion. These two markers define the entity. Grade 3 shows higher aggressiveness than grade 2. These tumors often have a more chemosensitive profile (for example, to PCV chemotherapy) and sometimes distinct imaging features. Many “mixed” cases reassign to this group once 1p/19q codeletion is confirmed. PMC+1

Type C: Oligoastrocytoma, NOS (historical/rare use).
This label is used only when molecular tests are incomplete or not possible, and the tumor truly shows both astrocytic and oligodendroglial parts. Modern guidelines recommend avoiding this label when molecular testing is available. PMC+1

Causes and risk factors

Note: For most people, there is no single clear cause. Scientists talk about risk factors and molecular changes that drive tumor growth. Some items below are biologic events inside the tumor, and others are patient-level risk factors.

Prior ionizing radiation to the head.
This is the strongest proven environmental risk. People who received head radiation in childhood or for other diseases have a higher chance of developing glioma years later. ResearchGate
Inherited cancer syndromes (Li-Fraumeni; TP53).
Some families carry TP53 changes that increase brain tumor risk, including gliomas. PubMed
Neurofibromatosis type 1 (NF1).
A genetic condition that raises risk for several nervous system tumors, including gliomas. PubMed
Turcot syndrome (APC or mismatch repair genes).
This rare syndrome can link colon polyps/cancer with brain tumors, including gliomas. PubMed
Lynch syndrome (mismatch repair).
Another hereditary condition that can be associated with brain tumors in rare cases. PubMed
PTEN/Cowden syndrome.
PTEN pathway problems can raise risks for certain tumors, sometimes including gliomas. PMC
Family history of glioma (polygenic risk).
About 5% of gliomas occur in families, suggesting shared genetic risk. ResearchGate
IDH1 or IDH2 mutation (tumor-intrinsic).
These are very common drivers in grade 2–3 diffuse gliomas and shape the tumor’s biology. They are not inherited in the tumor; they arise within the cancer cells. PMC
1p/19q codeletion (tumor-intrinsic).
Defines oligodendroglioma when combined with an IDH mutation and influences behavior and treatment sensitivity. PMC
ATRX loss and TP53 mutation (tumor-intrinsic).
Common in IDH-mutant astrocytomas and help distinguish them from oligodendrogliomas. PMC
TERT promoter mutation (tumor-intrinsic).
Often co-occurs in oligodendrogliomas and can affect growth and prognosis. ScienceDirect
CDKN2A/B homozygous deletion (tumor-intrinsic).
Loss of these cell-cycle regulators is linked with more aggressive behavior and up-grading in IDH-mutant astrocytoma. PMC
Age (usually young to middle-aged adults).
Grade 3 diffuse gliomas often present in adults around their 30s–50s; age patterns reflect underlying biology. (General epidemiology; background knowledge.)
Male sex (slightly higher risk).
Many gliomas show a small male predominance; reasons are not fully clear. (General epidemiology.)
History of a lower-grade glioma that progressed.
Some grade 3 tumors arise by stepwise progression from a prior grade 2 diffuse glioma. PMC
Immune and inflammatory factors.
Population studies suggest complex links; for example, a history of allergies may be associated with lower glioma risk, but this is not used clinically.
Possible occupational exposures (still uncertain).
Studies have looked at solvents, pesticides, and other exposures; firm conclusions are limited.
Head trauma (not proven cause).
Most data do not support trauma as a direct cause of glioma.
Lifestyle factors (uncertain).
Smoking, alcohol, and diet show no strong, consistent links as direct causes in current evidence.
Environmental fields (cell phones and EMF).
Large studies have not confirmed a consistent causal link with glioma.

(Items 16–20 reflect areas where research has mixed or weak evidence; clinicians emphasize the proven factors above, especially ionizing radiation and hereditary syndromes.) ResearchGate

Common symptoms

Seizures.
Sudden shaking or staring spells can be the first sign, especially in tumors of the brain’s outer areas (cortex).
Headache.
Often dull and pressure-like. It may worsen in the morning or with coughing because pressure in the skull changes.
Weakness of an arm or leg.
The tumor can disturb motor pathways, making movements slow or clumsy.
Numbness or tingling.
Sensation can feel “off,” patchy, or reduced on one side.
Speech problems.
Trouble finding words, slurred speech, or not understanding language if language areas are affected.
Vision problems.
Blurred vision, loss of part of the visual field, or double vision if the tumor affects visual pathways.
Personality or behavior change.
Irritability, apathy, or disinhibition can appear when the frontal lobes are involved.
Memory and thinking difficulty.
Poor short-term memory, attention lapses, or slower processing can occur.
Balance and coordination issues.
Staggering or clumsiness, especially with cerebellar or pathway involvement.
Nausea and vomiting.
Can be related to raised pressure in the head.
Fatigue.
Low energy is common and may reflect the illness itself or seizures/medications.
Sensitivity to light or sound during headaches.
Sometimes imitates migraine-like features.
Confusion or changes in alertness.
Occurs with swelling, seizures, or if large areas are affected.
Smell or taste changes.
Temporal lobe involvement may cause odd smells (phantosmias) or taste changes.
Endocrine or sleep problems (less common).
If deep midline structures are involved, hormones or sleep-wake cycles can be affected.

Diagnostic tests

Physical examination

General neurologic exam.
The doctor checks strength, sensation, reflexes, coordination, vision, and gait. This helps locate the area of the brain that may be affected.
Mental status and cognition.
Simple bedside tasks (orientation, memory, attention) show how thinking is working and guide further testing.
Cranial nerve exam.
Eye movements, face strength, facial feeling, hearing, swallow, and tongue movement are checked to map brainstem and skull-base function.

Manual bedside tests

Pronator drift test.
You hold both arms out with palms up; a slow downward turn suggests subtle weakness in the opposite brain hemisphere.
Finger-to-nose and heel-to-shin.
These check coordination and can reveal cerebellar or pathway problems.
Romberg test.
Standing with feet together and eyes closed checks balance and position sense; sway suggests sensory or cerebellar issues.
Tandem gait (heel-to-toe walking).
This stresses balance and coordination; difficulty suggests cerebellar or frontal lobe involvement.

Lab and pathology (molecular and tissue)

Basic blood tests (CBC, electrolytes, kidney and liver tests).
These do not diagnose the tumor but are important for safe surgery, imaging with contrast, and planning medicines like chemotherapy.
IDH1/IDH2 mutation testing (IHC/NGS).
Finding an IDH mutation helps classify the tumor and guide prognosis; it separates diffuse gliomas into major groups. PMC
1p/19q codeletion testing (FISH/NGS).
If both 1p and 19q are deleted and IDH is mutated, the tumor is an oligodendroglioma. This marker set is required for that diagnosis. PMC
ATRX immunohistochemistry and TP53 testing.
ATRX loss and TP53 changes support the diagnosis of astrocytoma, IDH-mutant when 1p/19q is intact. PMC
TERT promoter mutation testing.
Common in oligodendroglioma and can add prognostic information. ScienceDirect
MGMT promoter methylation.
This is a predictive marker for response to the drug temozolomide and is recommended in diffuse gliomas. PMC
CDKN2A/B homozygous deletion analysis.
Loss here can “up-grade” an IDH-mutant astrocytoma and usually signals more aggressive behavior. PMC
DNA methylation profiling (classifier).
When the diagnosis is unclear, methylation fingerprints can sort the tumor into the most likely class. This helps avoid the vague “mixed” label. PMC

Electrodiagnostic

EEG (electroencephalogram).
Used when seizures are suspected. It shows abnormal electrical activity and helps with seizure care.
Intraoperative mapping and evoked potentials.
During surgery near language or motor areas, doctors stimulate brain tissue and watch responses to protect function while removing tumor.

Imaging

MRI brain with and without gadolinium (core test).
MRI is the main imaging study. It shows the tumor, swelling, and involvement of critical areas. Contrast helps highlight abnormal tissue, but enhancement alone is not specific. PMC
Advanced MRI (diffusion, perfusion, spectroscopy, tractography).
These add detail: diffusion shows cell density; perfusion shows blood volume; spectroscopy shows chemical peaks; DTI/tractography maps white-matter tracts for surgical planning. These tools improve assessment beyond standard MRI. PubMed
Amino-acid PET (for example, 18F-FET) when MRI is unclear.
Amino-acid PET can help separate tumor from treatment change, define active regions, and guide biopsy or radiation planning better than FDG in many cases. Evidence supports its value when MRI findings are uncertain. MDPI+1

A “grade 3 diffuse glioma” (today’s term) is a faster-growing brain tumor that spreads through normal brain tissue like thin roots. It is not the most aggressive type (that is grade 4), but it does grow and return if not treated. Doctors must check the tumor’s genes: an IDH mutation helps confirm the main tumor family; 1p/19q codeletion proves the oligodendroglioma type; and markers like ATRX loss, TP53, and MGMT promoter methylation help with naming, treatment planning, and predicting outcomes. MedNexus+3PMC+3PMC+3

Non-pharmacological treatments (therapies & other measures)

1) Maximal safe surgical resection (often with awake brain mapping).
Goal: remove as much tumor as possible while protecting speech and movement. Mapping and modern navigation reduce deficits and improve the extent of removal, which is linked to better outcomes. BTRT+1

2) Awake language/motor mapping during surgery.
Purpose: protect critical brain areas by testing speech and movement in real time. Mechanism: electrical stimulation identifies “eloquent” cortex so surgeons can stop at safe borders. BTRT

3) Early post-op rehabilitation (physiotherapy/occupational therapy).
Purpose: speed recovery, balance, strength, and daily function. Mechanism: task-specific, neuroplasticity-based training to retrain pathways around surgical areas. PMC

4) Speech and cognitive therapy.
Purpose: improve language, memory, attention after surgery/radiation. Mechanism: structured drills and compensatory strategies that leverage neuroplasticity. PMC

5) Evidence-based exercise program.
Purpose: reduce fatigue and improve quality of life. Mechanism: graded aerobic/resistance activity improves cardiorespiratory fitness and counters treatment-related fatigue. PMC

6) Fatigue management education.
Purpose: pacing, sleep hygiene, and energy conservation lessen daily exhaustion common with radiotherapy/chemo. Mechanism: behavioral strategies and routine optimization. PMC

7) Headache management without overuse.
Purpose: treat tumor-related headaches safely. Mechanism: choose non-opioids first, manage triggers, and avoid medication-overuse headaches; escalate medically as needed. Cancer.gov

8) Seizure self-care plan (with medical team).
Purpose: safety during and after a first seizure; prevent injuries and driving risks. Mechanism: trigger avoidance, adherence to prescribed anti-seizure meds when indicated. (Note: routine drug prophylaxis in seizure-naïve patients is not recommended.) PubMed+1

9) Nutrition counseling focused on general cancer guidance.
Purpose: maintain strength and healthy weight. Mechanism: follow cancer-society dietary advice (plant-forward, whole grains, lean proteins) rather than strict “anti-cancer” fads; high-quality evidence for special glioma diets is limited. PMC

10) Psychological support & mindfulness-based strategies.
Purpose: lower anxiety/depression, improve coping. Mechanism: CBT and mindfulness reduce stress reactivity and improve sleep and mood. PMC

11) Social work & financial counseling.
Purpose: help with work leave, transport, and treatment costs. Mechanism: navigation and benefits counseling integrated with oncology services. Cancer.gov

12) Return-to-work planning.
Purpose: safe, stepwise return to study/work. Mechanism: graded schedules and cognitive accommodations shaped by neuropsychology. PMC

13) Smoking cessation.
Purpose: improve overall survival and wound healing; reduce vascular risk. Mechanism: behavioral + pharmacologic support programs. Cancer.gov

14) Alcohol moderation.
Purpose: reduce seizure risk and interaction with medicines. Mechanism: limit intake and avoid binge drinking during active therapy. Cancer.gov

15) Vaccination review (e.g., flu/COVID).
Purpose: reduce infection risk during chemo/steroids. Mechanism: coordinate timing around chemotherapy for best response. Cancer.gov

16) VTE (blood-clot) prevention education.
Purpose: brain-tumor patients have high clot risk, especially early after diagnosis. Mechanism: early mobility and prompt evaluation for leg swelling/chest pain; drug prophylaxis is individualized. medicaljournalssweden.se

17) Steroid-sparing edema care where possible.
Purpose: minimize long-term steroid side effects. Mechanism: taper dexamethasone carefully, use PPI, glucose monitoring, bone protection as needed. Cancer.gov

18) Sleep optimization.
Purpose: better fatigue, cognition, mood. Mechanism: consistent schedule, light exposure, caffeine timing, and treatment of sleep apnea when present. Cancer.gov

19) Driving and safety counseling.
Purpose: legal and safety compliance after seizures or neurological deficits. Mechanism: follow local rules; clinician letters when seizure-free to return. Cancer.gov

20) Clinical-trials counseling.
Purpose: access to newer therapies when appropriate. Mechanism: screening for trials in adjuvant or recurrent settings. Cancer.gov

Drug treatments

1) Temozolomide (TMZ).
Class & purpose: Oral alkylating agent; standard after radiotherapy for astrocytoma, IDH-mutant, grade 3 (adjuvant setting). Dose/time: 150–200 mg/m² daily on days 1–5 of a 28-day cycle for up to 12 cycles after RT. Mechanism: adds methyl groups to tumor DNA (O6-guanine), causing mismatches; tumors with silenced MGMT are more sensitive. Benefits: In CATNON, adjuvant TMZ significantly improved overall survival for IDH-mutant anaplastic gliomas; concurrent TMZ did not add survival benefit. Side effects: fatigue, nausea, low blood counts, rare PJP infection (prophylaxis may be used during concurrent chemoradiation), and fertility effects; check blood counts before each cycle. eviQ+3PubMed+3ecancer+3

2) PCV regimen (Procarbazine + Lomustine/CCNU + Vincristine).
Class & purpose: Combination cytotoxic chemo; standard with RT for oligodendroglioma, IDH-mutant, 1p/19q-codeleted, grade 3. Dose/time (typical EORTC 26951 style): CCNU ~110 mg/m² PO day 1; Procarbazine 60 mg/m² PO days 8–21; Vincristine 1.4 mg/m² IV (max 2 mg) days 8 & 29; cycles every 6 weeks for up to 6 cycles after RT. Mechanism: multi-agent DNA damage and microtubule inhibition. Benefits: Long-term randomized trials (RTOG 9402, EORTC 26951) show longer survival with RT+PCV vs RT alone, especially in 1p/19q-codeleted tumors. Side effects: myelosuppression, nausea, neuropathy (vincristine), and procarbazine food/drug interactions (MAO-like). eviQ+3PubMed+3PMC+3

3) Dexamethasone.
Class & purpose: Corticosteroid for brain swelling and headache relief. Dose/time: Often 2–4 mg twice daily, titrated to the lowest effective dose, and tapered. Mechanism: reduces vasogenic edema around tumor. Side effects: high sugar, mood change, infection risk, muscle weakness, bone loss; use stomach and bone protection as needed. Cancer.gov

4) Levetiracetam.
Class & purpose: Anti-seizure medicine to treat (not routinely prevent) seizures. Dose/time: Commonly 500–1,000 mg twice daily; adjust by kidney function and response. Mechanism: modulates synaptic vesicle protein SV2A. Notes: Do not start routine prophylaxis in seizure-naïve patients; treat if seizures occur or if surgeon/epileptologist advises. Side effects: sleepiness, mood changes, dizziness. PubMed

5) Ondansetron or other 5-HT3 antiemetics.
Class & purpose: Nausea control during chemo. Dose/time: Before and after TMZ or CCNU per protocol. Mechanism: blocks serotonin receptors in the gut/brain. Side effects: constipation, headache; rare QT prolongation. Cancer.gov

6) Trimethoprim-sulfamethoxazole (PJP prophylaxis when indicated).
Class & purpose: Antibiotic to prevent Pneumocystis jirovecii pneumonia during concurrent TMZ-RT or prolonged high-dose steroids. Dose/time: Commonly 1 DS tablet three times weekly (or per local protocol); alternatives if allergic. Mechanism: blocks folate pathways in Pneumocystis. Side effects: rash, low counts; weigh risks/benefits as newer data question universal prophylaxis in all settings. eviQ+2PMC+2

7) Proton-pump inhibitor (e.g., omeprazole) when on steroids.
Purpose: reduce stomach irritation/ulcer risk. Mechanism: acid suppression. Side effects: headache, rare low magnesium with long use. Cancer.gov

8) Apixaban/Rivaroxaban (for cancer-associated VTE, if occurs; individualized).
Class & purpose: Oral anticoagulants for blood clots when benefits outweigh brain-tumor bleeding risk. Dose/time: per ASCO guidance. Mechanism: Factor Xa inhibition. Side effects: bleeding; specialist input is essential in primary brain tumors. ASCO Publications+1

9) Acetaminophen (paracetamol).
Purpose: headache or post-op pain with fewer bleeding risks than NSAIDs right after surgery. Dose/time: per label; avoid overdose. Side effects: liver toxicity if excessive. Cancer.gov

10) Proton therapy or IMRT planning aids (medication adjuncts).
Purpose: while not a drug, pre-meds (antiemetics, steroids) make RT more tolerable; modern IMRT/IGRT reduces dose to normal brain. Mechanism: precise shaping and daily imaging. Side effects: fewer late effects compared with older techniques. ASTRO+1

11) Bevacizumab (select recurrent cases for symptom relief).
Class & purpose: Anti-VEGF antibody; can reduce edema and steroid needs in recurrent high-grade gliomas; no OS gain proven. Dose/time: IV every 2–3 weeks as per protocol. Mechanism: reduces abnormal tumor vessels and leakage. Side effects: hypertension, bleeding, clots, wound-healing issues; not routine first-line for grade 3. PubMed

12) Lomustine (single-agent in some recurrent settings).
Class: nitrosourea alkylator. Dose/time: e.g., 110 mg/m² PO once every 6 weeks; counts limit dosing. Use: option at recurrence when PCV not appropriate or previously used. Side effects: delayed low counts, nausea. PMC

13) Procarbazine (single-agent in select settings).
Class: alkylator/MAO-like. Dose: varies; often part of PCV. Notes: strict food/drug interaction counseling. Side effects: nausea, marrow suppression. PMC

14) Vincristine (component of PCV).
Class: microtubule inhibitor. Dose: 1.4 mg/m² IV (max 2 mg) on days 8 & 29 in PCV cycles. Side effects: neuropathy/constipation; careful dosing. eviQ

15) Antacid/anti-reflux care during steroids/chemo.
Purpose: comfort and adherence. Mechanism: symptom control to keep nutrition adequate. Cancer.gov

16) Growth-factor support (e.g., G-CSF) when needed.
Purpose: treat significant chemo-related neutropenia. Mechanism: stimulates white cell production. Side effects: bone pain; use per oncology protocol. Cancer.gov

17) Anti-depressants/anxiolytics when indicated.
Purpose: manage mood/anxiety that affect quality of life and adherence. Mechanism: neurotransmitter modulation; check interactions with procarbazine. Cancer.gov

18) Pain-control ladder (start simple).
Purpose: control persistent pain. Mechanism: stepwise from acetaminophen to, if required, carefully monitored opioids. Cancer.gov

19) Bowel regimen with opioids/vincristine.
Purpose: prevent constipation. Mechanism: stimulant/osmotic laxatives, hydration, fiber as tolerated. eviQ

20) Anticoagulation prophylaxis after tumor surgery (selected cases).
Purpose: prevent post-op clots; choice individualized. Mechanism: pharmacologic or mechanical prophylaxis per guidelines. Portail Vasculaire

Dietary “molecular” supplements

There is no high-quality evidence that specific supplements cure or control grade 3 gliomas. Most data are preclinical or small, mixed studies. Focus should remain on balanced nutrition (plant-forward, whole grains, lean proteins) and adequate calories/protein during therapy. If you still consider supplements, discuss each one with your oncology team to avoid drug interactions (especially with procarbazine, which has MAO-like interactions). PMC

Vitamin D (only if deficient).
Dose: individualized to correct deficiency. Function/mechanism: bone and immune support; no proven anti-glioma effect; avoid excess. PMC
Omega-3 fatty acids (food-first).
Dose: diet or modest supplements. Function: general anti-inflammatory nutrition; no direct glioma control proven. PMC
Multivitamin (standard dose).
Dose: one daily if intake is poor. Function: covers gaps; avoid high-dose antioxidants during RT/chemo unless advised. PMC
Probiotic/fermented foods (food-first).
Function: gut comfort during treatment; choose safe products; immunosuppressed patients should ask first. PMC
Protein supplements (whey/plant) if intake low.
Function: maintain muscle mass and healing when appetite is poor. PMC
Fiber supplements (as needed).
Function: stool regularity, especially with vincristine/opioids; increase fluids. PMC
Electrolyte solutions.
Function: prevent dehydration on tough days; watch sugar content. PMC
Caffeine (moderation).
Function: fatigue help; avoid near bedtime and if it triggers headaches/anxiety. PMC
Curcumin, green tea extracts, etc.
Note: promising lab data but no reliable clinical benefit in grade 3 glioma; potential drug interactions—avoid without team approval. PMC
Ketogenic/very low-carb diets
Note: studied mostly in small/early studies; adherence is hard and benefits unproven; risk of weight loss/malnutrition—not routine. PMC

Immunity booster / regenerative / stem-cell” drugs

There are no approved “stem-cell drugs” that cure grade 3 diffuse gliomas. Some experimental options exist only in clinical trials, mostly for recurrent disease. Always discuss risks carefully.

Tumor vaccines (e.g., dendritic-cell vaccines).
Idea: train the immune system to recognize tumor antigens. Status: investigational in trials; not standard for grade 3. Cancer.gov
Oncolytic viruses (e.g., DNX-2401 in trials).
Idea: engineered viruses infect and kill tumor cells, then stimulate immunity. Evidence: early-phase signals; still experimental. PMC
CAR-T cell therapies (e.g., IL13Rα2 targets).
Idea: patient T-cells engineered to attack tumor antigens. Evidence: small studies show feasibility; safety and durability still under study. PMC
Checkpoint inhibitors (PD-1/PD-L1).
Idea: release immune “brakes.” Evidence: limited benefit in most diffuse gliomas; select trials continue. Cancer.gov
IDH inhibitors (e.g., vorasidenib).
Idea: block mutant IDH metabolism. Evidence: benefit shown in grade 2 IDH-mutant gliomas; role in grade 3 under investigation; not current standard. Cochrane Library
TTFields (Tumor Treating Fields).
Idea: alternating electric fields disrupt cancer cell division. Approved for GBM; routine use in grade 3 diffuse gliomas is not established. Frontiers

Surgeries

1) Maximal safe resection (first operation).
Procedure: remove as much tumor as safely possible, often with awake mapping. Why: more removal usually links to better control and longer survival. BTRT

2) Awake craniotomy with brain mapping.
Procedure: patient helps test speech/movement as surgeon stimulates areas. Why: preserves vital functions while allowing wider resection. ScienceDirect

3) Re-operation at recurrence (selected patients).
Procedure: second surgery if tumor regrows and location is operable. Why: can improve symptoms and may prolong survival in carefully chosen cases. SpringerOpen+1

4) Stereotactic biopsy (when resection isn’t safe).
Procedure: small tissue sample via narrow path. Why: confirms diagnosis and allows modern molecular testing. Cancer.gov

5) Ventriculoperitoneal shunt (for hydrocephalus).
Procedure: a thin tube drains extra cerebrospinal fluid to the abdomen. Why: relieves pressure, headaches, gait problems if fluid builds up. MedlinePlus+1

Prevention points

There is no proven way to prevent grade 3 diffuse glioma. The only well-established environmental risk is ionizing radiation (usually at high therapeutic doses in childhood). For radiofrequency (mobile-phone) exposure, IARC lists it as “possibly carcinogenic” (Group 2B)—evidence remains limited and mixed. Focus on general cancer-prevention habits. NIEHS+3Nature+3jpatholtm.org+3

Avoid unnecessary ionizing radiation to the head. Nature
Use hands-free or speaker for long mobile calls if concerned (prudent avoidance). IARC
Don’t smoke; keep alcohol low. Cancer.gov
Maintain healthy weight, physical activity, and a plant-forward diet. PMC
Use helmets and prevent head injury (not a known cause, but safety matters). Cancer.gov
Reduce exposure to known carcinogens at work; follow safety rules. monographs.iarc.who.int
Manage other illnesses (diabetes, hypertension) to tolerate therapy better. Cancer.gov
Keep vaccinations current to avoid infections during therapy. Cancer.gov
Seek genetic counseling if strong family cancer syndromes exist. Nature
Regular checkups and prompt evaluation of persistent new neurological symptoms. Cancer.gov

When to see a doctor urgently

See a doctor immediately for new or worsening headaches, seizures, weakness or numbness on one side, trouble speaking, vision loss, confusion, severe vomiting, or any rapid decline after a change in steroids or chemotherapy. New leg swelling or chest pain needs urgent evaluation for possible blood clots. Cancer.gov+1

What to eat and what to avoid

Eat more: soft fruits/vegetables, whole grains, legumes, fish/lean meats, yogurt/fermented foods, nuts/seeds, olive oil, eggs (if tolerated), ample fluids, and small frequent meals during treatment “down days.” Avoid/limit: very salty/ultra-processed foods, high-sugar drinks, raw/unpasteurized items when counts are low, heavy alcohol, large high-dose antioxidant supplements during radiotherapy/chemo (unless your team advises), and any supplement that interacts with procarbazine (MAO effects)—this includes certain aged cheeses, cured meats, some fermented products, and many over-the-counter pills. PMC

Frequently asked questions

1) Is “mixed glioma” still my diagnosis?
No. Your care team should re-label the tumor using IDH mutation and 1p/19q codeletion status (astrocytoma vs oligodendroglioma). PMC

2) Why did my doctor order molecular tests?
Because treatment and prognosis depend on genes like IDH, 1p/19q, ATRX, and MGMT. PMC+2PMC+2

3) What radiation dose is standard for grade 3?
About 59.4 Gy in 33 fractions (1.8 Gy/fraction). PubMed

4) What’s standard chemo for grade 3 astrocytoma (IDH-mutant)?
Radiotherapy followed by adjuvant temozolomide (12 cycles). ecancer

5) What’s standard chemo for grade 3 oligodendroglioma (IDH-mutant, 1p/19q-codeleted)?
Radiotherapy plus PCV. PubMed

6) Does giving temozolomide during radiation help in this setting?
Not for overall survival in IDH-mutant anaplastic gliomas (CATNON). PubMed

7) Do I need anti-seizure medicine if I’ve never had a seizure?
Routine preventive AEDs are not recommended; treat if seizures occur. PubMed

8) Do I need PJP pneumonia prevention?
Often considered during concurrent TMZ + RT or with prolonged high-dose steroids; practices vary with evolving data. eviQ+1

9) Are special anti-cancer diets proven to help?
No strong evidence; focus on balanced cancer-society nutrition and weight maintenance. PMC

10) What is MGMT and why test it?
MGMT methylation is a biomarker linked to sensitivity to alkylating agents like TMZ and overall prognosis. PMC+1

11) Is TTFields standard for grade 3?
No; it’s established for GBM, not routine for grade 3 diffuse glioma. Frontiers

12) Will re-operation help if my tumor grows back?
Sometimes. In selected patients it can improve symptoms and may extend survival. SpringerOpen

13) Are there targeted drugs for IDH mutation now?
Vorasidenib showed benefit in grade 2 IDH-mutant glioma; role in grade 3 is still under study. Cochrane Library

14) What about bevacizumab?
It can reduce swelling and steroid use in recurrence but does not clearly extend life. PubMed

15) Where can I read a current overview for clinicians and patients?
See the NCI PDQ pages (regularly updated). Cancer.gov+1

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