Anaplastic Mixed Glioma

Anaplastic mixed glioma” (also called anaplastic oligoastrocytoma) was an older name for a fast-growing brain tumor that looked like a mix of two cell types under the microscope: astrocytes and oligodendrocytes. Today, experts do not use this mixed label. Modern diagnosis uses molecular tests (genes and chromosomes) to sort these tumors into one of three precise groups: (1) astrocytoma, IDH-mutant; (2) oligodendroglioma, IDH-mutant and 1p/19q-codeleted; or, if IDH-wildtype with certain changes, (3) glioblastoma. The term “anaplastic” is also rarely used now; grading (2, 3, or 4) sits inside each tumor type. In practice, almost all tumors once called “anaplastic mixed glioma” are re-classified as either astrocytoma, IDH-mutant (grade 3) or oligodendroglioma, IDH-mutant, 1p/19q-codeleted (grade 3) after molecular testing. Radiopaedia+3PMC+3PMC+3

Anaplastic mixed glioma” (also called oligoastrocytoma or anaplastic oligoastrocytoma) was a label used when a tumor looked like a mix of astrocytoma and oligodendroglioma under the microscope. Modern testing shows these “mixed” tumors can almost always be sorted into one of two groups using gene tests. Because of that, the World Health Organization (WHO) removed “oligoastrocytoma/mixed glioma” from the official list in 2016 and confirmed this in the 2021/2024 WHO classification. Today, doctors diagnose these tumors as either astrocytoma, IDH-mutant (CNS WHO grade 2–4) or oligodendroglioma, IDH-mutant and 1p/19q-codeleted (CNS WHO grade 2–3). So when someone says “anaplastic mixed glioma,” it usually maps to one of those two modern diagnoses at grade 3. PMC+2PMC+2

Other names

You might still find older or historical names in reports, textbooks, or online:

• Anaplastic oligoastrocytoma (AOA)

• Mixed oligoastrocytoma

• Oligoastrocytoma, NOS / NOS (obsolete)

• Anaplastic mixed glioma (umbrella term that is no longer recommended)

These terms are now considered historical and should be replaced with the integrated (molecular) diagnoses above. Radiopaedia+1

Types

Because “mixed” tumors are no longer a category, the “types” relevant to a case once labeled anaplastic mixed glioma are:

1. Astrocytoma, IDH-mutant, CNS WHO grade 3
   This is an adult-type diffuse glioma with a mutation in IDH1/IDH2 and astrocytic features. Grades 2–4 exist within this single tumor type; grade 3 indicates more aggressive behavior but not the same as glioblastoma. Loss of ATRX and TP53 mutation are common. PMC+2PubMed+2

2. Oligodendroglioma, IDH-mutant and 1p/19q-codeleted, CNS WHO grade 3
   This tumor must have both an IDH mutation and combined 1p/19q codeletion. Grade 3 means higher mitotic activity and other malignant features compared with grade 2. PMC+1

3. Glioblastoma (IDH-wildtype) with defining molecular features
   A minority of cases once called “anaplastic” are actually IDH-wildtype gliomas that qualify as glioblastoma by certain molecular markers (e.g., TERT promoter mutation, EGFR amplification, +7/−10 signature). Nature

Causes and risk factors

For most patients, the exact cause is unknown. Scientists do know some factors that can raise risk or are linked to how these tumors start or grow. Not all are strong or proven; many are rare. Think of this list as possible contributors rather than guarantees.

1. Ionizing radiation to the head (past medical radiation): Prior therapeutic radiation can increase the risk of developing a glioma years later. Cancer.gov+1

2. Getting older: Adult diffuse gliomas are more common in middle-aged and older adults. Mayo Clinic

3. Family history of glioma: A small number of families show clustering of gliomas. Cancer.gov

4. Li-Fraumeni syndrome (TP53): A rare inherited condition that increases risk for several cancers, including certain brain tumors. Cancer.gov

5. Neurofibromatosis type 1 (NF1): Raises risk of some CNS tumors; gliomas can occur in NF1. Cancer.gov

6. Turcot syndrome (mismatch repair/APC variants): Rare inherited syndrome that can include brain tumors. Cancer.gov

7. Tuberous sclerosis complex (TSC1/TSC2): Increases risk for specific CNS tumors; indicates glial pathway dysregulation. Cancer.gov

8. Cowden syndrome (PTEN): A hamartoma syndrome that raises risk for several tumors; CNS neoplasms are part of the spectrum. Cancer.gov

9. Neurofibromatosis type 2 (NF2): Predisposes to multiple CNS tumors; while best known for vestibular schwannomas/meningiomas, CNS tumor risk is elevated. Cancer.gov

10. Vinyl chloride exposure (possible): Evidence suggests it may be a risk factor for glioma, though data are limited. Cancer.gov+1

11. Male sex (slight predominance in many gliomas): Some diffuse gliomas are a bit more common in males. Mayo Clinic

12. IDH1/IDH2 gene mutations (tumor-initiating biology): These mutations are early events in many adult diffuse gliomas and help define modern types. (This explains tumor biology rather than a lifestyle “cause.”) PMC

13. 1p/19q codeletion (defining oligodendroglioma biology): A hallmark change that drives tumor behavior in oligodendroglioma. (Again, a defining alteration, not a preventable exposure.) PMC

14. ATRX loss and TP53 mutation (astrocytoma biology): Common in IDH-mutant astrocytoma and shape growth patterns. PubMed

15. TERT promoter mutation, EGFR amplification, +7/−10 (IDH-wildtype pathway): Molecular features that define glioblastoma biology in IDH-wildtype tumors. Nature

16. High-dose diagnostic/occupational radiation (rare now): Historically linked to increased brain tumor risk. Cancer.gov

17. Race/ethnicity and geography (epidemiology varies): Observed differences exist across populations, but reasons are not fully known. (General PDQ context.) Cancer.gov

18. Immune and inflammatory pathways: Not classic “causes,” but immune microenvironment influences glioma biology and treatment response. (Guideline/consensus context.) Nature

19. Epigenetic patterns/methylation classes: Genome-wide methylation profiles can define glioma classes and reflect underlying causes. PMC+1

20. Most lifestyle factors (like phones, routine chemicals) lack strong proof: Large studies have not confirmed clear links for many everyday exposures. (General PDQ overview.) Cancer.gov

Bottom line: for a person, you usually did nothing to cause it. The most important “causes” here are molecular alterations that pathologists test for to give the correct diagnosis and plan. PMC

Symptoms

Symptoms depend on tumor size and location. They can be slow or fast to appear.

1. Headache: Often worse in the morning or with strain, due to pressure changes. Cancer.gov+1

2. Seizures: New-onset seizures are common in diffuse gliomas, especially lower-grade/IDH-mutant tumors. Cancer.gov

3. Weakness on one side (arm/leg): Tumor pressure in the motor cortex can cause focal weakness. Cancer.gov

4. Speech problems (aphasia): Trouble finding words or understanding speech when the dominant temporal/frontal lobes are involved. Cancer.gov

5. Vision loss or field cuts: Occurs when the occipital lobe or pathways are affected. Cancer.gov

6. Nausea/vomiting: Often related to raised intracranial pressure. Cancer.gov

7. Balance or walking problems (ataxia): Cerebellar or frontal pathway involvement can disturb coordination. Cancer.gov

8. Numbness or tingling: Sensory cortex or pathways irritated by the tumor. Cancer.gov

9. Memory and thinking changes: Frontal/temporal lobe tumors can affect attention and memory. Cancer.gov

10. Personality or mood change: Irritation of frontal networks can cause apathy, disinhibition, or mood shifts. Cancer.gov

11. Fatigue and sleepiness: Common in brain tumor patients from the tumor, seizures, or medications. Cancer.gov

12. Hearing problems or tinnitus: If auditory pathways are involved. Cancer.gov

13. Endocrine symptoms (rare in these): If deep midline structures/hypothalamus are affected. Cancer.gov

14. Double vision: When cranial nerve pathways or brainstem tracts are involved. Cancer.gov

15. Papilledema (optic disc swelling): A sign of raised intracranial pressure seen on eye exam. Cancer.gov

Diagnostic tests

Modern diagnosis blends clinical exam + imaging + surgical pathology + molecular testing. This combination is essential because the old “mixed” label disappears once molecular tests are done.

A) Physical examination

1. General neurological exam: Doctor checks mental status, cranial nerves, strength, sensation, reflexes, and coordination to map which brain areas may be involved. This guides what imaging to order. Cancer.gov

2. Vital signs and overall exam: Looks for signs of raised pressure (e.g., blood pressure changes, vomiting) and general health to plan safe imaging and surgery. Cancer.gov

3. Ophthalmoscopy for papilledema: The eye doctor or neurologist looks for optic disc swelling, which suggests raised intracranial pressure and need for urgent imaging. Cancer.gov

4. Cognitive and language screening at bedside: Simple tasks (orientation, naming, repetition) localize dysfunction and track change over time. Cancer.gov

B) Manual (bedside) neurological tests

5. Motor strength testing (manual muscle testing): Push/pull against resistance to grade strength and detect focal weakness. Cancer.gov

6. Reflex testing and plantar responses: Asymmetry or pathologic reflexes (e.g., Babinski) can point to corticospinal tract involvement. Cancer.gov

7. Coordination tests: Finger-to-nose, heel-to-shin, and rapid alternating movements reveal cerebellar or frontal pathway issues. Cancer.gov

8. Gait and balance tests (e.g., Romberg): Unsteady stance or falls suggest proprioceptive or cerebellar involvement. Cancer.gov

C) Laboratory and pathological tests

9. Stereotactic biopsy or surgical resection for tissue: Getting tumor tissue is the gold standard for diagnosis and enables all molecular testing. Nature

10. Histopathology (H&E): A pathologist examines cells to see diffuse glioma features (infiltration) and anaplastic signs (mitoses, cellularity, microvascular proliferation, necrosis). Grading now occurs within tumor types. PMC

11. IDH1 R132H immunohistochemistry / sequencing: Detects IDH mutations, which define adult-type diffuse glioma categories and correlate with prognosis. PMC

12. 1p/19q codeletion testing (FISH/array/NGS): Confirms oligodendroglioma when both 1p and 19q arms are deleted along with an IDH mutation. PMC

13. ATRX immunohistochemistry and TP53 testing: Helps separate astrocytoma (often ATRX loss and TP53 mutation) from oligodendroglioma (ATRX retained, TP53 usually wild-type). PubMed

14. MGMT promoter methylation & broader sequencing/methylation profiling: Used for prognostic/therapeutic planning and, increasingly, for classification; genome-wide DNA methylation can refine difficult cases. PMC+1

D) Electrodiagnostic tests

15. EEG (electroencephalogram): Records brain waves to confirm and characterize seizures, which are common in diffuse gliomas. Cancer.gov

16. Evoked potentials (as needed): Visual or somatosensory evoked potentials can help in selected cases to assess pathway integrity, especially around surgery. Nature

17. Intraoperative neurophysiologic monitoring and awake cortical mapping: During surgery, mapping speech and motor areas helps remove tumor safely while protecting function. Nature

E) Imaging tests

18. MRI of the brain with and without gadolinium (core test): Best first test for a suspected glioma. T1/T2/FLAIR sequences show the infiltrating nature; contrast highlights leaky vessels. Nature

19. Advanced MRI (perfusion, diffusion, MR spectroscopy): Perfusion (rCBV) suggests tumor grade/vascularity; diffusion reflects cell density; spectroscopy shows metabolites (e.g., high choline). These help plan surgery and track treatment. Wiley Online Library

20. Functional MRI (fMRI): Maps language and motor areas before surgery to reduce postoperative deficits. Nature

21. CT head (often first in emergencies): Faster and widely available to detect mass effect or bleeding; MRI still provides more detail. Cancer.gov

22. Amino-acid PET (e.g., FET-PET) or FDG-PET (selected centers): Helps distinguish tumor from treatment effects and can guide biopsy; used per regional practice/guidelines. Nature

23. Spine MRI (when indicated): Only if symptoms suggest spread along CSF pathways, which is uncommon for these tumors. Nature

24. Post-operative MRI within 24–48 hours: Establishes the “new baseline” and checks the extent of resection. Nature

Non-pharmacological treatments (therapies & “other” supports)

1. Maximal safe resection with brain mapping
   Surgeons aim to remove as much tumor as possible without harming speech or movement. Awake mapping or tractography helps protect critical brain areas. Greater “extent of resection” is linked to better outcomes in diffuse glioma, so surgery is both diagnostic and therapeutic. Purpose: lower tumor burden, improve seizures, and enable precise diagnosis. Mechanism: immediate reduction of tumor cells and pressure. PMC

2. Fluorescence-guided surgery (5-ALA)
   Before surgery, a special dye (5-ALA) makes tumor cells glow pink under blue light, helping surgeons see tumor borders. Purpose: remove more tumor safely. Mechanism: tumor cells take up the dye and fluoresce, improving visual contrast during resection. cns.org

3. Intraoperative MRI or ultrasound
   Real-time imaging during surgery checks how much tumor remains. Purpose: maximize safe removal. Mechanism: updates the surgeon as the brain shifts, guiding further resection when safe. PMC

4. Precision radiotherapy planning (IMRT/protons)
   Modern planning shapes the dose around the target while sparing normal brain. Purpose: control microscopic disease after surgery. Mechanism: accurately deposits ~59.4 Gy to the tumor bed and margin while limiting exposure to healthy tissue. PubMed+1

5. Neuro-rehabilitation (PT/OT/speech-language)
   Targeted exercises and training rebuild strength, balance, speech, and daily living skills after surgery or during therapy. Purpose: maintain independence and quality of life. Mechanism: neuroplasticity—repeated practice helps remaining brain circuits take over functions. PubMed

6. Cognitive rehabilitation
   Structured memory, attention, and executive-function training can improve everyday thinking skills. Purpose: reduce “chemo-brain” and tumor-/treatment-related cognitive issues. Mechanism: task-specific drills and compensatory strategies (planners, cues). soc-neuro-onc.org

7. Psychological support & mindfulness
   Mindfulness-based interventions, relaxation training, and counseling can reduce anxiety and distress. Purpose: improve coping and sleep. Mechanism: down-regulates stress pathways and improves emotional regulation. PubMed

8. Yoga/tai chi & safe exercise
   Gentle activity helps fatigue, mood, and fitness. Purpose: increase energy and function. Mechanism: improves cardiorespiratory fitness and reduces inflammation; oncology guidelines recommend regular activity tailored to tolerance. ACS Publications+1

9. Acupuncture for pain or nausea (selected cases)
   Used as a complement to standard care. Purpose: lessen pain or chemotherapy-related symptoms. Mechanism: neuromodulation and endogenous opioid release; evidence is moderate for some pain indications in cancer care. AMA End the Epidemic

10. Nutrition counseling
    Focus on vegetables, fruits, whole grains, legumes; adequate protein; limit highly processed foods and sugary drinks. Purpose: maintain weight and strength during treatment and recovery. Mechanism: supports immune function and helps manage treatment side effects. American Cancer Society

11. Seizure-safety education
    Household precautions, driving/height/sleep/heat safety, medication adherence, and triggers. Purpose: injury prevention and better seizure control. Mechanism: risk-reduction behaviors paired with correct antiseizure treatment. PubMed

12. Steroid-sparing edema strategies
    Elevation, careful fluid/salt balance, and gradual steroid taper when possible. Purpose: reduce steroid side effects. Mechanism: non-drug measures plus timely imaging and oncology input to keep edema controlled. PMC

13. Fatigue management plan
    Scheduled rest, activity pacing, sleep hygiene, and light-to-moderate exercise. Purpose: reduce cancer-related fatigue. Mechanism: circadian support, de-conditioning reversal. Integrative Oncology

14. Headache self-management
    Hydration, trigger tracking, and appropriate non-opioid pain strategies alongside medical care. Purpose: comfort and function. Mechanism: behavioral plus medical synergy. PMC

15. Palliative care early integration
    Symptom control and goal-setting added to active tumor care—not “giving up.” Purpose: better quality of life and sometimes better outcomes. Mechanism: proactive symptom relief and support for patients and families. Integrative Oncology

16. Social work & caregiver training
    Navigating work, transport, finances, and caregiver stress. Purpose: sustain treatment adherence and safety at home. Mechanism: practical problem-solving and respite planning. Integrative Oncology

17. Vocational & driving counseling
    Return-to-work planning and legal/safety requirements for driving after seizures. Purpose: safe independence. Mechanism: staged return with medical clearance. PubMed

18. Falls-prevention at home
    Remove tripping hazards, install grab bars, and use assistive devices when advised. Purpose: prevent injuries. Mechanism: environmental modification. PubMed

19. Infection-prevention habits
    Hand hygiene, vaccines per oncology guidance, food safety during neutropenic windows. Purpose: avoid treatment interruptions. Mechanism: barrier and vaccine protection. American Cancer Society

20. Smoking & alcohol reduction support
    Behavioral support to quit smoking; limit alcohol. Purpose: better overall outcomes. Mechanism: reduces vascular and metabolic risks during therapy. American Cancer Society MediaRoom

Drug treatments

Doses are typical references; individual plans vary and must be set by the treating team.) *

1. Temozolomide (TMZ)
   What it is: an oral alkylating chemotherapy used for IDH-mutant grade 3 astrocytoma after radiotherapy (benefit shown in CATNON). Class: alkylating agent. Dose/time: adjuvant 150–200 mg/m² once daily on days 1–5 every 28 days, typically up to 12 cycles if tolerated; concurrent use during RT did not add benefit in CATNON for this population. Purpose: improve survival and delay progression. How it works: adds methyl groups to DNA (O6-guanine), causing tumor-cell death; benefit is influenced by tumor biology (e.g., MGMT status in GBM). Key side effects: low blood counts, nausea, fatigue, rare pneumocystis risk during prolonged concurrent dosing. PubMed+2NCBI+2

2. PCV regimen (Procarbazine + Lomustine/CCNU + Vincristine)
   What it is: the standard chemo partner with radiotherapy for 1p/19q-codeleted oligodendroglioma (grade 3), with long-term survival gains in two phase-III trials. Class: combination alkylating (procarbazine, lomustine) + antimicrotubule (vincristine). Dose/time: classic PCV every 6 weeks × 4–6 cycles—lomustine 110 mg/m² day 1; procarbazine 60 mg/m² days 8–21; vincristine 1.4 mg/m² (max 2 mg) days 8 and 29. Purpose: extend overall survival when added to RT. How it works: multi-agent DNA damage and mitotic arrest. Key side effects: myelosuppression, neuropathy (vincristine), nausea; requires monitoring. Cancer Care Ontario+2eviQ+2

3. Lomustine (CCNU) single-agent (select recurrences)
   Class: nitrosourea alkylator. Dose/time: 110–130 mg/m² orally every 6–8 weeks as tolerated. Purpose: salvage at recurrence when PCV is not suitable. Mechanism: cross-links DNA; penetrates the blood–brain barrier. Side effects: delayed low blood counts, nausea (premedication needed), rare lung/liver toxicity. ScienceDirect

4. Procarbazine (component of PCV; sometimes alone in salvage)
   Class: alkylating/methylating agent. Dose/time: often 60 mg/m² daily for 14 days within the PCV 6-week cycle. Purpose: part of proven survival-benefit combo in codeleted oligodendroglioma. Mechanism: DNA damage; MAO-inhibitor activity means diet/drug interactions. Side effects: myelosuppression, nausea, interactions with tyramine-rich foods. Cancer Care Ontario

5. Vincristine (component of PCV)
   Class: vinca alkaloid (microtubule inhibitor). Dose/time: 1.4 mg/m² IV (cap 2 mg) on days 8 & 29 in each 6-week PCV cycle. Purpose: adds a second mechanism to PCV. Mechanism: blocks mitosis. Side effects: neuropathy/constipation; dose-capped to reduce neurotoxicity. Cancer Care Ontario

6. Bevacizumab (selected situations)
   Class: anti-VEGF monoclonal antibody. Dose/time: common dosing 10 mg/kg IV q2 weeks or 15 mg/kg q3 weeks. Purpose: not shown to extend survival in grade 2–3 gliomas; may reduce edema and steroid need at symptomatic recurrence or treat radiation necrosis. Mechanism: reduces abnormal tumor/peri-necrosis blood-vessel leakiness. Side effects: hypertension, bleeding, clotting, wound-healing problems. Nature+1

7. Anti-seizure medicines (e.g., Levetiracetam)
   Class: antiepileptics. Dose/time: individualized; levetiracetam commonly 500–1500 mg twice daily. Purpose: treat (not prevent) seizures—routine preventive use is not recommended in patients who have never had a seizure. Mechanism: stabilizes neuronal firing. Side effects: mood/irritability (levetiracetam), dizziness; monitor interactions with chemo. PubMed

8. Dexamethasone (for brain swelling)
   Class: corticosteroid. Dose/time: lowest effective dose for shortest time (e.g., 2–4 mg q6–12h), then gradual taper. Purpose: reduce tumor-related edema and headache. Mechanism: decreases capillary permeability. Side effects: sleep problems, mood changes, sugar rise, infection risk, muscle weakness—hence “steroid-sparing” plans when possible. PMC

9. Antiemetics (e.g., ondansetron, palonosetron) with chemo
   Class: 5-HT3 antagonists ± dexamethasone, NK1 blockers. Dose/time: per regimen day(s). Purpose: prevent nausea with PCV/CCNU/TMZ. Mechanism: blocks serotonin pathways. Side effects: constipation, headache. PMC

10. PCP prophylaxis when indicated (e.g., TMP-SMX)
    Class: antimicrobial prophylaxis. Dose/time: e.g., trimethoprim-sulfamethoxazole 3x/week during prolonged high-dose steroids or concurrent chemoradiation if risk is high. Purpose: prevent Pneumocystis pneumonia. Mechanism: inhibits folate pathway in the organism. Side effects: rash, cytopenias—clinician-specific decision. PMC

11. Lacosamide / Lamotrigine (seizure options)
    Used if levetiracetam not tolerated or seizures persist. Purpose/mechanism: stabilize neuronal membranes and reduce excitability; dosing individualized; monitor interactions and skin rash risk (lamotrigine). PubMed

12. Proton-pump inhibitor during steroids (select patients)
    Purpose: protect stomach from steroid-related irritation/ulcer risk; dosing per standard gastro-protection protocols. Mechanism: reduces acid secretion. PMC

13. Mannitol or hypertonic saline (acute intracranial pressure)
    Hospital-based for acute spikes in pressure. Purpose: emergency symptom control. Mechanism: osmotic fluid shift. Side effects: electrolyte shifts—monitoring required. PMC

14. Lomustine-temozolomide alternation (select salvage)
    Occasional off-protocol strategies use alternating alkylators; evidence is limited and individualized. Side effects: cumulative myelosuppression. Purpose: disease control after standard options. PMC

15. Irinotecan with bevacizumab (select salvage)
    Small studies/real-world series only. Purpose: symptom and radiographic control in some recurrences; no proven OS gain. Side effects: diarrhea, cytopenias. PMC

16. Topotecan/fotemustine/carmustine wafers (specialty cases)
    Niche agents or local therapies; benefits are uncertain and toxicity can be significant; considered case-by-case. PMC

17. Clinical-trial targeted agents (e.g., IDH inhibitors)
    Oral IDH inhibitors are approved for lower-grade IDH-mutant gliomas and are being studied in higher grades; discuss trials if available. Purpose: targeted pathway blockade. Side effects vary by agent. PMC

18. Antidepressants/anxiolytics (when needed)
    Purpose: treat depression/anxiety that can accompany brain tumors. Mechanism: neurotransmitter modulation; watch for drug–drug interactions with chemo/anticonvulsants. PubMed

19. Sleep medicines or melatonin (short course, selected cases)
    Purpose: insomnia management alongside sleep hygiene; evidence for melatonin in cancer symptoms is mixed—use prudently. PubMed

20. Pain control ladder (acetaminophen → opioids if needed)
    Use multimodal non-opioids first; integrate integrative therapies where evidence exists. Purpose: safe, stepwise pain relief. Mechanism: peripheral/central modulation. AMA End the Epidemic

Dietary molecular supplements

There’s no supplement proven to shrink these tumors. Use supplements only to correct a deficiency or help a specific symptom, and always clear with the oncology team (interactions are common). General nutrition patterns help more than pills.

1. Vitamin D (if deficient): Correcting low vitamin D supports bone and muscle during steroids/less activity. Typical: individualized repletion then maintenance. Mechanism: bone mineral support; immune modulation is theoretical. American Cancer Society

2. Omega-3 (EPA/DHA): May help triglycerides/inflammation and appetite in some cancer settings; avoid high doses around surgeries due to bleeding risk. American Cancer Society

3. Oral nutrition supplements (protein-calorie shakes): Maintain weight and strength when intake is poor. American Cancer Society

4. Multivitamin at RDA levels: Covers gaps when appetite is low; avoid mega-doses. American Cancer Society

5. Fiber (as tolerated): Helps constipation from opioids/antiepileptics; increase slowly. American Cancer Society

6. Probiotics (select patients only): May reduce antibiotic-associated diarrhea; avoid when severely immunosuppressed. American Cancer Society

7. Magnesium (if low): Some antiseizure meds/steroids can affect levels; correct deficits to reduce cramps/weakness. American Cancer Society

8. Iron (only if iron-deficiency anemia): Consider with ESAs per guideline; monitor ferritin and transferrin saturation. PubMed

9. B12/folate (if deficient): Replace after lab confirmation to support red-cell production and nerve function. American Cancer Society

10. Caution with herbs/antioxidants: Many interact with chemo or affect bleeding; SIO-ASCO guidelines advise selective, evidence-based use only. PubMed

Immunity-booster / regenerative / stem-cell drugs

There are no proven “immune-boosting” or stem-cell drugs that treat anaplastic gliomas. The items below are supportive—used to keep treatment on track or manage side effects:

1. Filgrastim (G-CSF): boosts white cells to lower febrile neutropenia risk during chemo; typical dosing daily for several days after chemotherapy cycles. PMC

2. Pegfilgrastim (long-acting G-CSF): single shot per cycle to prevent neutropenia in higher-risk regimens. NCBI

3. Epoetin alfa / Darbepoetin (ESAs): used only for chemotherapy-related anemia in non-curative settings to reduce transfusions; careful risk–benefit discussion. ASCO Publications

4. Seasonal vaccines (e.g., influenza): recommended timing around therapy to reduce infections; coordinate with oncology team. American Cancer Society

5. Bevacizumab for radiation necrosis: not a tumor “cure,” but can reduce edema and steroid needs in confirmed radionecrosis. PMC

6. Clinical-trial cellular/immune therapies: vaccines or T-cell approaches are experimental; ask about trials at major centers. PMC

Surgeries

1. Maximal safe craniotomy with mapping
   Procedure: tailored skull opening; remove tumor using navigation, awake mapping if near speech/motor. Why: more removal → better control and often better survival while protecting function. PMC

2. Fluorescence-guided resection (5-ALA)
   Procedure: drink 5-ALA pre-op; tumor glows under blue light. Why: helps surgeons see residual tumor to improve extent of resection. cns.org

3. Intraoperative MRI-guided resection
   Procedure: MRI during surgery; re-image as needed. Why: detects hidden tumor left behind due to brain shift. PMC

4. Stereotactic biopsy
   Procedure: small burr-hole with needle to sample tumor when resection is unsafe. Why: obtain tissue for IDH/1p19q/MGMT testing to choose the right plan. PMC

5. Laser interstitial thermal therapy (LITT) (select cases)
   Procedure: MRI-guided laser heats and ablates a small target. Why: used in deep or previously treated sites, or for radiation necrosis in select patients. Oxford Academic

Prevention tips

1. Keep follow-up MRIs and blood tests on schedule to catch problems early. PMC

2. Use seizure-safety rules (sleep, meds, avoid heights/solo swimming) if you have seizures. PubMed

3. Vaccinations and hand hygiene to lower infection risk during chemo/steroids. American Cancer Society

4. Follow steroid taper plans to avoid withdrawal and side effects. PMC

5. Stay physically active within limits to reduce fatigue, clots, and deconditioning. ACS Publications

6. Nutrition pattern: plant-forward, whole-grain, lean protein; limit highly processed foods. American Cancer Society MediaRoom

7. Avoid smoking and limit alcohol; both worsen outcomes and interactions. American Cancer Society MediaRoom

8. Fall-proof your home and use aids if balance is poor. PubMed

9. Sun- and wound-care when on bevacizumab or post-op to lower bleeding/healing issues. Nature

10. Ask about growth-factor support (G-CSF) if your chemo carries high neutropenia risk. PMC

When to see a doctor urgently

Go now (ER or urgent call) for: a first-ever seizure or a cluster of seizures; sudden severe headache with vomiting; new weakness or speech trouble; high fever or shaking chills during chemo; confusion, drowsiness, or abrupt vision change; a rapidly worsening steroid side effect (e.g., severe high blood sugar). These can be emergencies related to swelling, bleeding, seizure, or infection. PMC

What to eat & what to avoid

1. Build your plate around vegetables, fruits, beans, whole grains, nuts/seeds; add lean proteins (fish, eggs, dairy, poultry, soy, or lentils). American Cancer Society MediaRoom

2. Protein at each meal (especially during treatment) to maintain muscle. American Cancer Society

3. Fluids: aim for regular hydration unless restricted; helps headaches/constipation. American Cancer Society

4. Limit red/processed meats, sugar-sweetened drinks, and ultra-processed snacks. American Cancer Society MediaRoom

5. Small, frequent meals if appetite is low; use fortified shakes if needed. American Cancer Society

6. Food safety during low white counts: avoid raw sushi/eggs/unpasteurized dairy; wash produce well. American Cancer Society

7. Alcohol: best to avoid, especially on chemo or seizure medicines. American Cancer Society MediaRoom

8. Salt: moderate intake, especially on steroids (fluid retention). PMC

9. Supplements: only for proven deficiencies or specific needs; avoid high-dose antioxidants or herbs without team approval. PubMed

10. Exercise most days if you can; activity plus nutrition works better than either alone. ACS Publications

Frequently asked questions

1. Is “anaplastic mixed glioma” still a diagnosis?
   No. It has been replaced by molecularly defined astrocytoma, IDH-mutant or oligodendroglioma, IDH-mutant and 1p/19q-codeleted. PMC

2. Which is better—temozolomide or PCV?
   They’re used for different modern tumor types. PCV+RT has the best evidence in 1p/19q-codeleted oligodendroglioma (grade 3). Adjuvant temozolomide after RT helps astrocytoma, IDH-mutant (grade 3). PMC+1

3. How much radiation do people get?
   Commonly 59.4 Gy in 33 treatments for grade 3 disease, planned with IMRT or, in some centers, protons. PubMed

4. Does MGMT methylation matter?
   It predicts benefit from temozolomide in GBM; its role in IDH-mutant grade 3 is less direct, but MGMT is still often reported. New England Journal of Medicine

5. Do I need seizure medicine if I never had a seizure?
   No—guidelines say not to give antiepileptics prophylactically in seizure-naïve brain-tumor patients. PubMed

6. Can bevacizumab cure my tumor?
   No. It may reduce swelling and help symptoms or treat radiation necrosis, but it hasn’t shown a survival benefit in grade 2–3 gliomas. Nature

7. Are there proven supplements for these tumors?
   No supplement has proven tumor-shrinking effects. Focus on diet quality; use supplements only for deficiencies or targeted symptoms. American Cancer Society

8. Is ketogenic diet recommended?
   Not routinely; strong clinical evidence is lacking. Follow mainstream oncology nutrition guidance unless in a supervised study. American Cancer Society

9. What is 5-ALA surgery and do I need it?
   A dye makes tumor tissue glow so surgeons can remove more safely; whether you get it depends on availability and location of your tumor. cns.org

10. What’s the recovery time after radiation?
    Fatigue often peaks near the end of RT and improves over weeks; gentle exercise and sleep hygiene help. ACS Publications

11. How many cycles of temozolomide are typical?
    Often up to 12 cycles if tolerated for IDH-mutant grade 3 astrocytoma after RT (CATNON). Your team tailors this. PubMed

12. Why is PCV so specific about days 1, 8–21, 8 & 29?
    That schedule is how the drugs work together while allowing marrow recovery, and it’s the regimen tested in trials that improved survival. Cancer Care Ontario

13. Are clinical trials important?
    Yes—trials test targeted drugs (including IDH inhibitors), re-irradiation strategies, and novel immunotherapies that might fit your tumor’s biology. PMC

14. Can I exercise during treatment?
    Usually yes, with tailoring. Aim for regular, moderate activity for energy, mood, and function. ACS Publications

15. Who should be on my care team?
    Neurosurgeon, neuro-oncologist, radiation oncologist, neuroradiologist, neuropathologist, rehabilitation, nutrition, psychology/palliative care—multidisciplinary care matters. PMC

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 16, 2025.

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