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← Brain Tumours mini review

Brain Tumours: MCQ bank

127 clinical-vignette questions in three levels: 39 basics, 49 applied and innovative, and 39 challenging (29 Metastases, 70 Glioma, 28 Paediatric; 7 built on schematic imaging, endoscopy or histology drawings). Practise question by question with instant marking, or take a timed mock test with a result summary by topic, level and section. You can also print the page as a booklet.

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Topic

Level 1 · Basics

Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.

Q1MetastasesLevel 1At a glance

In adults over 40, what is the commonest type of intracranial tumour?

  1. APituitary adenoma
  2. BMetastasis from a systemic cancer
  3. CPrimary CNS lymphoma
  4. DGlioblastoma
  5. EMeningioma
Show answer

Answer: B. Metastases outnumber all primary brain tumours combined in middle-aged and older adults; lung and breast cancer and melanoma are the commonest sources.

Review: section 01

Q2GliomaLevel 1At a glance

Which is the commonest malignant primary brain tumour in adults?

  1. AGlioblastoma, IDH-wildtype
  2. BEpendymoma
  3. COligodendroglioma
  4. DPilocytic astrocytoma
  5. EMedulloblastoma
Show answer

Answer: A. Glioblastoma is the commonest malignant primary brain tumour in adults, with a median age near 64. Meningioma is the commonest primary tumour overall but is usually benign.

Review: section 01

Q3GliomaLevel 1Presentation, traps & genetics

Which is the only firmly established environmental risk factor for glioma and meningioma?

  1. AMobile phone use
  2. BIonising radiation to the head
  3. CLiving near power lines
  4. DProcessed meat
  5. EHead injury
Show answer

Answer: B. Cranial irradiation (for example childhood leukaemia treatment) raises the risk of meningioma, glioma and nerve sheath tumours decades later. Mobile phones and power lines have not been shown to cause brain tumours.

Review: section 02

Q4GliomaLevel 1Presentation, traps & genetics

What is the commonest presenting symptom of a low-grade (IDH-mutant) glioma in a young adult?

  1. AHemiplegia
  2. BSeizure
  3. CComa
  4. DPapilloedema
  5. ESevere morning headache
Show answer

Answer: B. Seizures affect most patients with low-grade and IDH-mutant gliomas and are often the first symptom; focal deficits and raised pressure are uncommon at diagnosis.

Review: section 02

Q5GliomaLevel 1Presentation, traps & genetics

Which statement about brain tumour headache is correct?

  1. AIt is usually tension-type and rarely occurs without other symptoms
  2. BHeadache alone for 6 months is typical
  3. CMost patients have the classic early-morning headache with vomiting
  4. DIt is always on the side of the tumour
  5. EIt is relieved by lying flat
Show answer

Answer: A. The classic triad (morning, vomiting, severe) is seen in only about 5%. Tumour headache is usually tension-like and accompanied by other neurological features; isolated long-standing headache is seldom a tumour.

Review: section 02

Q6GliomaLevel 1Presentation, traps & genetics

Which headache feature is a red flag that warrants brain imaging?

  1. AHeadache after missing a meal
  2. BLifelong episodic migraine unchanged in pattern
  3. CNew headache after age 50, or a change in pattern
  4. DBilateral pressing headache relieved by paracetamol
  5. EHeadache with neck stiffness after exercise that settles in an hour
Show answer

Answer: C. New or changed headache, especially over 50, and headache with neurological signs, worsening on Valsalva or lying down, fever or a cancer history are red flags.

Review: section 02

Q7GliomaLevel 1Screening, workup & staging

Which investigation is best for a suspected brain tumour?

  1. APlain CT head
  2. BLumbar puncture
  3. CMRI brain with and without contrast
  4. DSkull X-ray
  5. EEEG
Show answer

Answer: C. Contrast MRI (with FLAIR, diffusion and susceptibility sequences) is the test of choice. CT is used in emergencies or when MRI is contraindicated; lumbar puncture is dangerous with mass effect.

Review: section 03

Q8GliomaLevel 1Biomarkers

Which molecular pair defines oligodendroglioma in the 2021 WHO classification?

  1. ABRAF V600E with CDKN2A deletion
  2. BH3 K27M mutation
  3. CIDH-wildtype with EGFR amplification
  4. DATRX loss with TP53 mutation
  5. EIDH mutation with 1p/19q codeletion
Show answer

Answer: E. Oligodendroglioma needs both an IDH1/2 mutation and whole-arm 1p/19q codeletion. ATRX loss and TP53 mutation mark IDH-mutant astrocytoma.

Review: section 04

Q9GliomaLevel 1Biomarkers

Methylation of which gene promoter predicts benefit from temozolomide in glioblastoma?

  1. AIDH1
  2. BMGMT
  3. CPTEN
  4. DTERT
  5. EEGFR
Show answer

Answer: B. MGMT repairs alkylator damage; when its promoter is methylated the gene is silenced and temozolomide works better (Hegi 2005).

Review: section 04

Q10GliomaLevel 1Systemic therapy

What is the standard first-line treatment for a fit 55-year-old after resection of glioblastoma?

  1. ATemozolomide alone
  2. BRadiotherapy alone
  3. CRadiotherapy 60 Gy with daily temozolomide, then 6 monthly cycles of temozolomide
  4. DWhole-brain radiotherapy
  5. EBevacizumab with radiotherapy
Show answer

Answer: C. The EORTC/NCIC trial established chemoradiation with temozolomide followed by adjuvant temozolomide: median 14.6 vs 12.1 months and 5-year survival 10 vs 2%.

Review: section 06

Q11GliomaLevel 1Biomarkers

The classic "fried egg" cells with chicken-wire capillaries and calcification describe:

  1. AMedulloblastoma
  2. BGlioblastoma
  3. CMeningioma
  4. DOligodendroglioma
  5. EPilocytic astrocytoma
Show answer

Answer: D. Rounded nuclei with clear perinuclear haloes, delicate branching capillaries and microcalcifications are the classic histology of oligodendroglioma; the diagnosis is confirmed molecularly.

Review: section 04

Q12GliomaLevel 1ImageBiomarkers

A biopsy shows a highly cellular astrocytic tumour with a band of crowded nuclei around necrosis (schematic shown). In an adult with an IDH-wildtype tumour this is:

Schematic drawing · not a patient image
  1. APilocytic astrocytoma
  2. BMeningioma
  3. CGlioblastoma
  4. DEpendymoma
  5. EOligodendroglioma
Show answer

Answer: C. Pseudopalisading necrosis and microvascular proliferation are the histological hallmarks of glioblastoma.

Review: section 04

Q13MetastasesLevel 1Systemic therapy

A patient with a brain tumour has never had a seizure. What should be done about antiseizure medication?

  1. AStart phenytoin for life
  2. BNo prophylactic antiseizure drug
  3. CStart carbamazepine during radiotherapy
  4. DStart valproate and check levels
  5. EStart levetiracetam for 1 year
Show answer

Answer: B. Prophylaxis does not prevent first seizures and adds side effects; SNO/EANO guidance recommends against it outside the perioperative period in high-risk cases.

Review: section 06

Q14MetastasesLevel 1Systemic therapy

Which antiseizure drug is preferred for a patient with a brain tumour who has had a seizure and is receiving chemotherapy?

  1. ACarbamazepine
  2. BLevetiracetam
  3. CPhenytoin
  4. DPhenobarbital
  5. EOxcarbazepine with rifampicin
Show answer

Answer: B. Levetiracetam does not induce liver enzymes, so it avoids interactions with chemotherapy, targeted drugs and steroids; it can be titrated quickly.

Review: section 06

Q15MetastasesLevel 1Systemic therapy

Dexamethasone is preferred over other steroids for brain tumour oedema mainly because:

  1. AIt prevents seizures
  2. BIt crosses into tumour but not normal brain
  3. CIt shrinks the tumour cells directly
  4. DIt is potent with almost no mineralocorticoid effect
  5. EIt has no effect on glucose
Show answer

Answer: D. Dexamethasone reduces vasogenic oedema with minimal salt retention. It does not treat the tumour (except lymphoma) and causes hyperglycaemia, myopathy and infection.

Review: section 06

Q16MetastasesLevel 1ImageScreening, workup & staging

A 60-year-old smoker has three ring-enhancing lesions at the grey–white junction with extensive oedema. Which is the most useful next test?

Schematic drawing · not a patient image
  1. ALumbar puncture
  2. BRepeat MRI in 6 months
  3. CCT chest, abdomen and pelvis
  4. DEEG
  5. ESerum CEA only
Show answer

Answer: C. Multiple lesions at the grey–white junction in a smoker strongly suggest metastases; look for the primary and biopsy the easiest site.

Review: section 03

Q17MetastasesLevel 1Local therapy

Which treatment is usually preferred for 1–4 small brain metastases in a patient with controlled systemic disease?

  1. AObservation only
  2. BProphylactic phenytoin
  3. CWhole-brain radiotherapy alone
  4. DStereotactic radiosurgery alone
  5. ECraniospinal irradiation
Show answer

Answer: D. SRS controls most treated lesions; adding WBRT reduces new lesions but does not improve survival and harms cognition (N0574, EORTC 22952).

Review: section 05

Q18MetastasesLevel 1Systemic therapy

Patients with brain tumours who develop a deep vein thrombosis should usually:

  1. ABe anticoagulated after a CT shows no bleeding
  2. BNever receive anticoagulants
  3. CReceive an IVC filter routinely
  4. DReceive aspirin only
  5. EReceive anticoagulation only if the tumour is benign
Show answer

Answer: A. Most brain tumours do not prohibit anticoagulation; a non-contrast CT excludes bleeding first. DOACs or LMWH are used.

Review: section 06

Q19PaediatricLevel 1At a glance

What is the commonest group of brain tumours in children?

  1. AGlioblastomas
  2. BLow-grade gliomas
  3. CMeningiomas
  4. DMetastases
  5. EPrimary CNS lymphomas
Show answer

Answer: B. Paediatric low-grade gliomas (pilocytic astrocytoma above all) make up 30–40% of childhood CNS tumours; medulloblastoma is the commonest malignant one.

Review: section 01

Q20PaediatricLevel 1Presentation, traps & genetics

Roughly what proportion of childhood brain tumours arise in the posterior fossa?

  1. AOne-third to one-half
  2. BAbout 90%
  3. CNone in infants
  4. DLess than 5%
  5. EAll medulloblastomas and no gliomas
Show answer

Answer: A. Between a third and a half are infratentorial: pilocytic astrocytoma, medulloblastoma, ependymoma and DIPG.

Review: section 02

Q21PaediatricLevel 1Presentation, traps & genetics

A 5-year-old has early-morning vomiting for 6 weeks, a broad-based gait and a head tilt. The best next step is:

  1. AEye refraction
  2. BStool examination
  3. CUrgent brain MRI (or CT if MRI unavailable)
  4. DAntihelminthic treatment
  5. EProton pump inhibitor trial
Show answer

Answer: C. Morning vomiting, ataxia and head tilt suggest a posterior fossa tumour with raised pressure; image urgently.

Review: section 02

Q22PaediatricLevel 1Biomarkers

The commonest malignant brain tumour of childhood is:

  1. AGlioblastoma
  2. BCraniopharyngioma
  3. CMedulloblastoma
  4. DOligodendroglioma
  5. EMeningioma
Show answer

Answer: C. Medulloblastoma, an embryonal tumour of the cerebellum, is the commonest malignant paediatric brain tumour.

Review: section 04

Q23PaediatricLevel 1Presentation, traps & genetics

Optic pathway glioma is most strongly associated with:

  1. ATuberous sclerosis
  2. BVon Hippel-Lindau disease
  3. CNeurofibromatosis type 1
  4. DLi-Fraumeni syndrome
  5. EDown syndrome
Show answer

Answer: C. About 10–15% of children with NF1 develop optic pathway gliomas; most NF1 patients with OPG need treatment only for visual loss.

Review: section 02

Q24PaediatricLevel 1Presentation, traps & genetics

Subependymal giant cell astrocytoma is associated with:

  1. ANF2-related schwannomatosis
  2. BGorlin syndrome
  3. CLynch syndrome
  4. DTurcot syndrome with APC
  5. ETuberous sclerosis complex
Show answer

Answer: E. SEGA occurs in 6–9% of people with tuberous sclerosis and responds to mTOR inhibitors.

Review: section 02

Q25PaediatricLevel 1Presentation, traps & genetics

Bilateral vestibular schwannomas are diagnostic of:

  1. ANF1
  2. BLi-Fraumeni
  3. CTuberous sclerosis
  4. DNF2-related schwannomatosis
  5. ECowden syndrome
Show answer

Answer: D. Bilateral vestibular schwannomas, seen in 90–95% of NF2-related schwannomatosis, are diagnostic.

Review: section 02

Q26PaediatricLevel 1ImageScreening, workup & staging

A cystic cerebellar mass with an enhancing mural nodule in a child (schematic shown) is most likely:

Schematic drawing · not a patient image
  1. AMedulloblastoma
  2. BMetastasis
  3. CPilocytic astrocytoma
  4. DGlioblastoma
  5. EMeningioma
Show answer

Answer: C. Cyst with a mural nodule in the cerebellum of a child is classic pilocytic astrocytoma; complete resection usually cures it.

Review: section 03

Q27PaediatricLevel 1ImageScreening, workup & staging

DIPG can usually be diagnosed without a biopsy because:

Schematic drawing · not a patient image
  1. ABlood tests are diagnostic
  2. BTypical MRI appearance in the right clinical setting is sufficient
  3. CBiopsy is impossible
  4. DIt never progresses
  5. EIt is always benign
Show answer

Answer: B. An expansile, diffusely infiltrating pontine lesion in a child with a short history of cranial nerve palsies, long tract signs and ataxia allows a clinical diagnosis; biopsy is for atypical cases or trials.

Review: section 03

Q28PaediatricLevel 1Local therapy

The main treatment for DIPG is:

  1. ATemozolomide alone
  2. BSurgical resection
  3. CCraniospinal irradiation
  4. DObservation
  5. EFocal radiotherapy
Show answer

Answer: E. DIPG is inoperable; focal RT relieves symptoms and is the only proven treatment; hypofractionated courses are non-inferior.

Review: section 05

Q29GliomaLevel 1Local therapy

What is the first step in management of most accessible diffuse gliomas?

  1. AWhole-brain radiotherapy
  2. BMaximal safe resection
  3. CTemozolomide alone
  4. DWatch and wait without tissue
  5. ESteroids alone
Show answer

Answer: B. Resection provides tissue for an integrated diagnosis and, when safe, prolongs survival in all molecular groups.

Review: section 05

Q30GliomaLevel 1Screening, workup & staging

After resection of a high-grade glioma, postoperative MRI should be done:

  1. AOnly if symptoms appear
  2. BAfter radiotherapy
  3. CAt 6 weeks
  4. DAt 3 months
  5. EWithin 24–48 hours
Show answer

Answer: E. Early MRI measures the extent of resection before postoperative enhancement confuses the picture.

Review: section 03

Q31GliomaLevel 1Presentation, traps & genetics

Which statement about mobile phones and brain tumours is supported by evidence?

  1. AThey cause most brain metastases
  2. BEarphones increase the risk
  3. CThey cause meningiomas in children
  4. DThey are a proven cause of glioma
  5. ENo causal link has been shown in large studies
Show answer

Answer: E. Large studies and a 2024 WHO-commissioned review found no causal link; incidence has not risen in line with phone use.

Review: section 02

Q32MetastasesLevel 1Local therapy

Whole-brain radiotherapy added to radiosurgery for 1–3 metastases:

  1. AIs required in all patients
  2. BImproves overall survival
  3. CHas no effect on intracranial control
  4. DReduces new brain metastases but worsens cognition without improving survival
  5. EPrevents seizures
Show answer

Answer: D. N0574 and EORTC 22952 showed better intracranial control but more cognitive decline and no survival gain.

Review: section 05

Q33MetastasesLevel 1Systemic therapy

Which side effect is NOT typical of long-term dexamethasone?

  1. AWeight loss and low blood sugar
  2. BHyperglycaemia
  3. CInsomnia and mood change
  4. DProximal myopathy
  5. EOral thrush
Show answer

Answer: A. Steroids cause weight gain and hyperglycaemia, not hypoglycaemia. Plan a taper to the lowest effective dose.

Review: section 06

Q34GliomaLevel 1Systemic therapy

Tumour-treating fields are:

  1. AA form of proton therapy
  2. BA vaccine
  3. CA scalp-worn device delivering alternating electric fields, used with adjuvant temozolomide
  4. DAn implanted chemotherapy wafer
  5. EA radiosurgery technique
Show answer

Answer: C. The device is worn at least 18 hours a day on a shaved scalp; EF-14 showed median survival 20.9 vs 16.0 months.

Review: section 06

Q35GliomaLevel 1ImageScreening, workup & staging

A 61-year-old man has 3 weeks of right-sided weakness. Post-contrast MRI (schematic) shows a large left hemispheric mass with a thick irregular enhancing rim, central necrosis, oedema and midline shift. He has no history of cancer. The most likely diagnosis is:

Schematic drawing · not a patient image
  1. AGlioblastoma
  2. BPilocytic astrocytoma
  3. CMeningioma
  4. DLow-grade oligodendroglioma
  5. EColloid cyst
Show answer

Answer: A. A thick irregular ring with necrosis and mass effect in an older adult is typical of glioblastoma; metastasis, lymphoma and abscess are the main alternatives, and tissue confirms it.

Review: section 03

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, predicted lung function, NNT), CT and fluid findings, reading trial results, sequencing traps.

Q36GliomaLevel 2ImageScreening, workup & staging

A 38-year-old has a non-enhancing right frontal tumour. MRI (schematic) shows a mass bright on T2 but dark in its centre on FLAIR with a bright rim. This sign suggests:

T2FLAIRSchematic drawing · not a patient image
  1. ALymphoma
  2. BIDH-mutant, 1p/19q-intact astrocytoma
  3. CGlioblastoma
  4. DOligodendroglioma
  5. EAbscess
Show answer

Answer: B. The T2–FLAIR mismatch sign is highly specific for IDH-mutant, non-codeleted astrocytoma; oligodendrogliomas lack it.

Review: section 03

Q37GliomaLevel 2ImageScreening, workup & staging

CT of a 42-year-old with a frontal mass shows clumped calcification reaching the cortex (schematic). Which diagnosis is suggested?

Schematic drawing · not a patient image
  1. AOligodendroglioma
  2. BGlioblastoma
  3. CPilocytic astrocytoma
  4. DMeningioma
  5. EMetastasis
Show answer

Answer: A. Calcification and cortical involvement in a frontal glioma suggest oligodendroglioma, though molecular testing confirms it.

Review: section 03

Q38GliomaLevel 2Biomarkers

A histologically grade 2 IDH-wildtype diffuse astrocytoma in a 63-year-old carries a TERT promoter mutation. The WHO 2021 diagnosis is:

  1. AAstrocytoma, IDH-mutant, grade 2
  2. BPleomorphic xanthoastrocytoma
  3. COligodendroglioma
  4. DDiffuse astrocytoma, grade 2
  5. EGlioblastoma, IDH-wildtype, grade 4
Show answer

Answer: E. TERT promoter mutation, EGFR amplification or +7/−10 in an IDH-wildtype adult diffuse astrocytic glioma establishes glioblastoma even without necrosis.

Review: section 04

Q39GliomaLevel 2Biomarkers

An IDH-mutant astrocytoma with no necrosis has homozygous CDKN2A/B deletion. Its CNS WHO grade is:

  1. A4
  2. B1
  3. C2
  4. D3
  5. EGrade not assigned
Show answer

Answer: A. CDKN2A/B homozygous deletion makes an IDH-mutant astrocytoma grade 4 regardless of histology.

Review: section 04

Q40GliomaLevel 2Biomarkers

Immunohistochemistry for IDH1 R132H is negative in a grade 2 diffuse glioma in a 35-year-old. What next?

  1. ATreat as glioblastoma
  2. BTest MGMT and stop
  3. CRepeat IHC on the same block
  4. DDiagnose IDH-wildtype glioma
  5. ESequence IDH1 codon 132 and IDH2 codon 172
Show answer

Answer: E. IHC finds about 90% of IDH mutations; non-canonical IDH1 and IDH2 mutations need sequencing, especially under 55 or in grade 2–3 tumours.

Review: section 04

Q41GliomaLevel 2Biomarkers

In an IDH-mutant glioma, retained ATRX expression and no p53 overexpression suggest:

  1. AEpendymoma
  2. BH3 K27M glioma
  3. CGlioblastoma
  4. DIDH-mutant astrocytoma
  5. E1p/19q codeletion (oligodendroglioma)
Show answer

Answer: E. ATRX loss and p53 mutation are typical of astrocytoma and mutually exclusive with 1p/19q codeletion; confirm codeletion when possible.

Review: section 04

Q42GliomaLevel 2Systemic therapy

In the EORTC/NCIC trial, about how much did temozolomide improve 2-year survival in glioblastoma?

  1. AFrom 1% to 2%
  2. BFrom 50% to 90%
  3. CNo difference
  4. DFrom 27% to 11%
  5. EFrom about 11% to 27%
Show answer

Answer: E. 2-year survival 27 vs 11%, and 5-year 10 vs 2%: modest median gains but a meaningful tail.

Review: section 06

Q43GliomaLevel 2Systemic therapy

In MGMT-methylated glioblastoma (Hegi analysis), median survival with RT + temozolomide versus RT alone was about:

  1. A21.7 vs 15.3 months
  2. B48 vs 31 months
  3. C9 vs 8 months
  4. D12.7 vs 11.8 months
  5. E60 vs 15 months
Show answer

Answer: A. Methylated tumours gained substantially; unmethylated tumours only 12.7 vs 11.8 months.

Review: section 06

Q44GliomaLevel 2Systemic therapy

A 74-year-old with glioblastoma, KPS 80, MGMT methylated. Which first-line option has randomised support?

  1. ABevacizumab alone
  2. BNivolumab with RT
  3. CRT 60 Gy alone only
  4. DShort-course RT (40 Gy in 15) with temozolomide
  5. EWhole-brain RT
Show answer

Answer: D. Perry 2017: adding temozolomide to short-course RT in patients ≥65 improved survival, most clearly if methylated; temozolomide alone is also reasonable for methylated frail patients.

Review: section 06

Q45GliomaLevel 2Systemic therapy

A 78-year-old with unmethylated glioblastoma, KPS 60, lives far away. A reasonable plan is:

  1. ART 60 Gy with temozolomide and lomustine
  2. BBevacizumab first line
  3. CTemozolomide alone
  4. DShort-course RT alone (25 Gy in 5 or 40 Gy in 15) or best supportive care
  5. ETumour-treating fields alone
Show answer

Answer: D. Temozolomide adds little when unmethylated; short RT or supportive care respects function and travel burden.

Review: section 06

Q46GliomaLevel 2Systemic therapy

Bevacizumab in newly diagnosed glioblastoma (AVAglio, RTOG 0825):

  1. AProlonged overall survival by 6 months
  2. BProlonged PFS but not overall survival
  3. CWas better tolerated than placebo
  4. DHad no effect on any endpoint
  5. EIs the standard of care
Show answer

Answer: B. A classic lesson: an imaging-based PFS gain from an antiangiogenic drug did not translate into longer life and added toxicity.

Review: section 06

Q47GliomaLevel 2Systemic therapy

A patient on daily temozolomide during RT is taking dexamethasone and has lymphopenia. What prophylaxis is suggested?

  1. AProphylactic antifungal fluconazole
  2. BPneumocystis jirovecii prophylaxis
  3. CRoutine G-CSF
  4. DRoutine antibacterial ciprofloxacin
  5. EAntiviral acyclovir for all
Show answer

Answer: B. PJP risk rises with steroids and lymphopenia; prophylaxis is suggested in these patients (labelling recommends it for all during concurrent RT).

Review: section 06

Q48GliomaLevel 2Survivorship

Ten weeks after chemoradiation for MGMT-methylated glioblastoma, MRI shows new enhancement at the cavity rim. The patient is well. Best approach?

  1. AUrgent re-resection
  2. BHospice referral
  3. CStart whole-brain RT
  4. DStop temozolomide and start bevacizumab
  5. EContinue adjuvant temozolomide and repeat MRI in 4–8 weeks
Show answer

Answer: E. Early in-field enhancement within 3–6 months, especially with MGMT methylation, is often pseudoprogression; continue and re-image.

Review: section 08

Q49GliomaLevel 2Systemic therapy

A 32-year-old has a residual, non-enhancing IDH-mutant astrocytoma (grade 2) after surgery; seizures are controlled. Which option has phase 3 evidence of delaying progression?

  1. AVorasidenib
  2. BBevacizumab
  3. CLomustine alone
  4. DWhole-brain radiotherapy
  5. ENivolumab
Show answer

Answer: A. INDIGO: vorasidenib vs placebo gave median PFS 27.7 vs 11.1 months and delayed next intervention; survival benefit not yet shown.

Review: section 06

Q50GliomaLevel 2Systemic therapy

In RTOG 9802 (high-risk low-grade glioma), adding PCV to radiotherapy changed median overall survival from about:

  1. A13.3 to 7.8 years
  2. B15 to 16 months
  3. C2 to 3 years
  4. D7.8 to 13.3 years
  5. ENo change
Show answer

Answer: D. RT + PCV improved median survival from 7.8 to 13.3 years with long follow-up, establishing RT plus chemotherapy for low-grade gliomas needing treatment.

Review: section 06

Q51GliomaLevel 2Systemic therapy

In CATNON, which component improved survival in IDH-mutant grade 3 astrocytoma?

  1. AConcurrent daily temozolomide only
  2. BTwelve cycles of adjuvant temozolomide after RT
  3. CBevacizumab
  4. DWhole-brain RT
  5. ELomustine maintenance
Show answer

Answer: B. Adjuvant temozolomide improved survival (HR 0.54) in IDH-mutant tumours; concurrent temozolomide added little; IDH-wildtype tumours did not benefit.

Review: section 06

Q52MetastasesLevel 2Systemic therapy

Which approach is recommended for dexamethasone in a patient with a brain metastasis and no neurological symptoms?

  1. A16 mg daily until RT ends
  2. B4 mg daily lifelong
  3. CSteroids only during SRS, always
  4. DMethylprednisolone pulses
  5. ENo steroid
Show answer

Answer: E. Asymptomatic oedema does not need steroids; when needed, use the lowest effective dose (Vecht 1994: 4 mg as effective as 16 mg for many patients).

Review: section 06

Q53MetastasesLevel 2Local therapy

A fit 55-year-old with controlled breast cancer has a single 3.8 cm cerebellar metastasis with fourth-ventricle compression. Best initial local treatment?

  1. ASurgical resection followed by cavity SRS
  2. BSRS alone in a single fraction
  3. CWhole-brain RT alone
  4. DObservation
  5. ESteroids alone
Show answer

Answer: A. Large, symptomatic posterior fossa lesions with mass effect need resection; cavity SRS then reduces local recurrence (Mahajan) and preserves cognition versus WBRT (N107C).

Review: section 05

Q54MetastasesLevel 2Local therapy

After complete resection of a brain metastasis, observation without radiotherapy leads to local recurrence at 12 months in about:

  1. AAll patients
  2. B1% of patients
  3. CIt cannot recur
  4. DHalf of patients
  5. E10% of patients
Show answer

Answer: D. In the Mahajan trial local control at 12 months was 43% with observation vs 72% with cavity SRS.

Review: section 05

Q55MetastasesLevel 2Local therapy

A patient needs WBRT for 30 metastases. Which measures reduce cognitive decline?

  1. ASteroids for 1 year
  2. BProphylactic levetiracetam
  3. CAdding temozolomide
  4. DHigher dose per fraction
  5. EHippocampal-avoidance IMRT plus memantine
Show answer

Answer: E. NRG CC001 showed hippocampal avoidance plus memantine preserved cognition better than WBRT plus memantine.

Review: section 05

Q56MetastasesLevel 2Systemic therapy

A never-smoker with EGFR exon 19-deleted lung cancer has three asymptomatic 5–9 mm brain metastases. Which plan is reasonable?

  1. AProphylactic phenytoin and chemotherapy
  2. BOsimertinib with MRI in 6–8 weeks, SRS if lesions grow or cause symptoms
  3. CUpfront whole-brain RT then gefitinib
  4. DDexamethasone and observation only
  5. ECraniotomy for all three
Show answer

Answer: B. CNS-active TKIs control small brain metastases in most patients; keep SRS for symptomatic or progressing lesions.

Review: section 06

Q57MetastasesLevel 2Systemic therapy

A patient with a glioblastoma has a pulmonary embolism. CT head shows no bleeding. Which anticoagulant is suggested?

  1. AIVC filter only
  2. BAspirin
  3. CWarfarin as first choice
  4. DA direct oral anticoagulant (or LMWH if unsuitable)
  5. ENo anticoagulation
Show answer

Answer: D. DOACs were associated with less intracranial haemorrhage than LMWH in glioma cohorts (Carney 2019); anticoagulation is long-term for glioblastoma.

Review: section 06

Q58MetastasesLevel 2Systemic therapy

Which brain metastases carry a higher risk of spontaneous haemorrhage, so anticoagulation needs extra caution?

  1. AOvarian and bladder
  2. BMelanoma, renal cell, thyroid and choriocarcinoma
  3. CLymphoma and myeloma
  4. DSmall cell lung and colorectal
  5. EBreast and prostate
Show answer

Answer: B. These histologies bleed spontaneously more often; individualise anticoagulation decisions.

Review: section 06

Q59MetastasesLevel 2Systemic therapy

A patient with a glioma has been seizure-free for 2 years on levetiracetam and asks to stop. Approximately what proportion of glioma patients relapse after withdrawal?

  1. AAbout 90%
  2. BAbout 2%
  3. CAll
  4. DAbout a quarter
  5. ENone
Show answer

Answer: D. In observational data about 26% relapsed after withdrawal vs 8% who continued; tapering is a shared decision after long seizure freedom with stable disease.

Review: section 06

Q60MetastasesLevel 2Presentation, traps & genetics

A 40-year-old with HIV has a single ring-enhancing basal ganglia lesion. Which conditions top the differential?

  1. AColloid cyst and craniopharyngioma
  2. BOligodendroglioma and DNET
  3. CToxoplasmosis and primary CNS lymphoma
  4. DMeningioma and schwannoma
  5. EPilocytic astrocytoma and ependymoma
Show answer

Answer: C. In HIV, toxoplasmosis and EBV-related CNS lymphoma are leading causes; the CD4 count, toxoplasma serology and response to treatment guide the work-up.

Review: section 02

Q61GliomaLevel 2Presentation, traps & genetics

A 45-year-old on antituberculous treatment for 3 months for a "tuberculoma" has a growing periventricular, homogeneously enhancing, diffusion-restricting lesion. She is stable. What should be done?

  1. AExtend antituberculous treatment to 18 months
  2. BGross total resection
  3. CWithhold steroids if possible and arrange stereotactic biopsy for suspected lymphoma
  4. DDouble the steroid dose
  5. EWhole-brain RT empirically
Show answer

Answer: C. Growth on treatment needs tissue; the imaging suggests primary CNS lymphoma, which steroids can mask. Lymphoma is not resected.

Review: section 02

Q62GliomaLevel 2Presentation, traps & genetics

Which feature favours neurocysticercosis over a metastasis?

  1. ADural-based enhancement
  2. BA thick irregular ring with necrosis
  3. CA small cyst with an eccentric dot (scolex) and calcified lesions elsewhere
  4. DMultiple large lesions with extensive oedema in a smoker
  5. ELesions at the grey–white junction that grow over weeks
Show answer

Answer: C. The scolex and coexisting calcified cysts are typical of NCC, a common cause of seizures in India; serology and follow-up imaging help.

Review: section 02

Q63GliomaLevel 2Screening, workup & staging

Which MRI feature best distinguishes a pyogenic abscess from a necrotic tumour?

  1. AMass effect
  2. BSurrounding oedema
  3. CRestricted diffusion in the cavity centre
  4. DEnhancement
  5. ET2 hyperintensity
Show answer

Answer: C. Pus restricts diffusion; necrotic tumour centres usually do not. Spectroscopy can also help.

Review: section 03

Q64GliomaLevel 2Systemic therapy

Which is the best option at first recurrence of glioblastoma in a fit patient with a small, focal recurrence 14 months after diagnosis?

  1. AWhole-brain RT
  2. BBevacizumab plus lomustine because it prolongs survival
  3. CHigh-dose dexamethasone only
  4. DConsider re-resection and/or re-irradiation, or a single agent such as lomustine, after MDT review; offer a trial
  5. ENivolumab because it beat bevacizumab
Show answer

Answer: D. No agent clearly prolongs survival at recurrence; lomustine ± bevacizumab improved PFS only (EORTC 26101), and nivolumab did not beat bevacizumab (CheckMate 143). Local therapy helps selected focal relapses.

Review: section 06

Q65PaediatricLevel 2Systemic therapy

A 7-year-old has a progressive unresectable hypothalamic low-grade glioma with BRAF V600E. Compared with carboplatin–vincristine, dabrafenib plus trametinib gave:

  1. AShorter PFS
  2. BIdentical outcomes
  3. CMore grade 3–4 toxicity
  4. DNo responses
  5. EHigher response (47 vs 11%) and longer PFS (20.1 vs 7.4 months)
Show answer

Answer: E. Bouffet 2023 established BRAF/MEK inhibition as first-line therapy for BRAF V600E paediatric LGG, with fewer severe side effects.

Review: section 06

Q66PaediatricLevel 2Systemic therapy

For a child with progressive low-grade glioma and a KIAA1549-BRAF fusion, which targeted drug has single-arm phase 2 evidence (FIREFLY-1)?

  1. ATovorafenib
  2. BVorasidenib
  3. COsimertinib
  4. DImatinib
  5. ELarotrectinib
Show answer

Answer: A. Tovorafenib, a type II RAF inhibitor, gave a response rate of about 67% in relapsed BRAF-altered paediatric LGG.

Review: section 06

Q67PaediatricLevel 2Systemic therapy

Long-term overall survival in paediatric low-grade glioma is about:

  1. A50% at 1 year
  2. B30% at 5 years
  3. C100% with no progression
  4. D10% at 5 years
  5. E90% at 20 years, though about half progress at some point
Show answer

Answer: E. Survival is excellent but many children need several lines of therapy; preserving vision, endocrine function and cognition is central.

Review: section 06

Q68PaediatricLevel 2Screening, workup & staging

Which staging is needed after surgery for medulloblastoma?

  1. ABone marrow biopsy only
  2. BMRI of the whole spine and lumbar CSF cytology
  3. CNo staging
  4. DChest X-ray only
  5. EPET-CT only
Show answer

Answer: B. Leptomeningeal spread changes risk group and craniospinal dose; CSF is sampled about 2 weeks after surgery.

Review: section 03

Q69PaediatricLevel 2Local therapy

A 2-year-old has a completely resected malignant embryonal tumour. Why is radiotherapy usually delayed or avoided?

  1. AChildren do not tolerate MRI
  2. BEmbryonal tumours do not recur
  3. CCranial RT in very young children causes severe neurocognitive and endocrine harm
  4. DRT does not work in children
  5. EChemotherapy is never used in infants
Show answer

Answer: C. Chemotherapy-based strategies in young children aim to avoid or delay RT because of its effect on the developing brain.

Review: section 05

Q70PaediatricLevel 2Local therapy

Hypofractionated radiotherapy for DIPG (39–45 Gy over about 3 weeks):

  1. AWas non-inferior to conventional RT in a randomised trial of 253 children
  2. BDoubled survival
  3. CWas inferior
  4. DReplaces the need for steroids
  5. EIs never used
Show answer

Answer: A. Zaghloul 2022 showed non-inferiority; shorter courses reduce anaesthesia sessions, travel and cost for families.

Review: section 05

Q71PaediatricLevel 2Systemic therapy

After gross total resection of a posterior fossa ependymoma in a 6-year-old, what is suggested?

  1. ACraniospinal RT plus maintenance chemotherapy
  2. BObservation alone
  3. CBevacizumab
  4. DFocal conformal radiotherapy
  5. ETemozolomide alone
Show answer

Answer: D. Focal RT after complete resection is standard; post-RT maintenance chemotherapy did not improve outcomes (ACNS0831).

Review: section 06

Q72PaediatricLevel 2Biomarkers

Loss of H3K27 trimethylation on immunohistochemistry in a posterior fossa ependymoma indicates:

  1. AMedulloblastoma
  2. BSupratentorial ZFTA fusion ependymoma
  3. CPosterior fossa group A (PFA), the higher-risk group
  4. DSubependymoma
  5. EMyxopapillary ependymoma
Show answer

Answer: C. PFA tumours (infants and young children) lose H3K27me3 and carry a worse prognosis, especially with 1q gain or 6q loss.

Review: section 04

Q73PaediatricLevel 2Biomarkers

In SHH-activated medulloblastoma in a 10-year-old, which germline test is particularly important?

  1. AHER2
  2. BIDH1
  3. CTP53 (Li-Fraumeni)
  4. DAPC
  5. EBRCA1
Show answer

Answer: C. Germline TP53 variants occur in a substantial minority of SHH medulloblastomas in older children and change RT planning and family screening.

Review: section 04

Q74MetastasesLevel 2Systemic therapy

A patient with glioblastoma on dexamethasone needs gastric protection. Which choice is suggested by recent pooled data?

  1. AHigh-dose omeprazole
  2. BAn H2 blocker rather than a proton pump inhibitor
  3. CSucralfate with PPI
  4. DPantoprazole for life
  5. ENo protection ever
Show answer

Answer: B. A pooled analysis of five trials linked PPI use with shorter survival in glioblastoma (association, not proof); avoiding routine PPIs is a cautious approach.

Review: section 06

Q75GliomaLevel 2Survivorship

Which follow-up schedule is appropriate after chemoradiation for glioblastoma?

  1. ACT every 2 years
  2. BPET-CT monthly
  3. CMRI about 4 weeks after RT, then every 2–3 months for 2–3 years
  4. DMRI only at symptoms
  5. ENo imaging after 6 months
Show answer

Answer: C. NCCN suggests early post-RT MRI and frequent MRI during adjuvant therapy and the first 2–3 years.

Review: section 08

Q76GliomaLevel 2At a glance

India records about how many new malignant brain and CNS tumours a year (GLOBOCAN 2022)?

  1. AAbout 32,000
  2. BAbout 3,200
  3. CAbout 1.5 million
  4. DAbout 320,000
  5. EAbout 1,000
Show answer

Answer: A. About 32,000 new cases and 28,000 deaths in 2022; benign tumours are not counted in these estimates.

Review: section 01

Level 3 · Challenging

DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.

Q77GliomaLevel 3Systemic therapy

A 45-year-old with MGMT-methylated glioblastoma, KPS 90, asks whether lomustine plus temozolomide is better than standard temozolomide. Which statement is most accurate?

  1. AIt is the standard for unmethylated tumours
  2. BCeTeG/NOA-09 suggested longer survival, but the trial was small and toxicity higher; it is an option, not the standard
  3. CIt removes the need for radiotherapy
  4. DIt doubled PFS in a large phase 3 trial
  5. EIt is inferior and should not be used
Show answer

Answer: B. CeTeG/NOA-09 enrolled 141 patients; median survival 48 vs 31 months in the prespecified analysis, with more haematological toxicity and nausea.

Review: section 06

Q78GliomaLevel 3Systemic therapy

Which first-line strategy WORSENED survival compared with temozolomide in MGMT-unmethylated glioblastoma?

  1. AShort-course RT in the elderly
  2. BLomustine–temozolomide
  3. CRadiotherapy plus temozolomide
  4. DRadiotherapy plus nivolumab (CheckMate 498)
  5. ETumour-treating fields
Show answer

Answer: D. CheckMate 498: median OS 13.4 vs 14.9 months (HR 1.31) with nivolumab; checkpoint inhibitors have not worked in unselected glioblastoma.

Review: section 06

Q79GliomaLevel 3Systemic therapy

A patient with glioblastoma is stable after 6 adjuvant temozolomide cycles and asks to continue to 12. The best evidence shows:

  1. ABetter survival only if unmethylated
  2. BA 6-month survival gain
  3. CNo survival benefit from extending beyond 6 cycles, with more toxicity
  4. DThat 24 cycles are standard
  5. EThat stopping causes immediate relapse
Show answer

Answer: C. GEINO 14-01 and a pooled EORTC/RTOG analysis found no OS benefit from extended temozolomide.

Review: section 06

Q80GliomaLevel 3Systemic therapy

In EF-14, which limitation is most important when interpreting the survival gain with tumour-treating fields?

  1. ASurvival was worse
  2. BIt tested RT dose escalation
  3. CIt enrolled only unmethylated patients
  4. DNo sham device; open-label design
  5. EToo few patients
Show answer

Answer: D. The 695-patient trial was unblinded without sham control; the 5-month OS difference is unlikely to be explained by placebo alone, but the design matters.

Review: section 06

Q81GliomaLevel 3Systemic therapy

A 29-year-old with a grade 3 IDH-mutant astrocytoma (CDKN2A/B intact) after resection. Best evidence-based adjuvant plan?

  1. ATemozolomide alone without RT
  2. BVorasidenib alone
  3. CObservation
  4. DRT (about 59.4 Gy) followed by 12 cycles of temozolomide
  5. ERT alone
Show answer

Answer: D. CATNON supports adjuvant temozolomide after RT for IDH-mutant grade 3 astrocytoma (median about 12.5 years). Vorasidenib has no data in grade 3 disease.

Review: section 06

Q82GliomaLevel 3Systemic therapy

For a newly diagnosed codeleted grade 3 oligodendroglioma, the evidence for RT plus PCV is strongest for which outcome?

  1. ASeizure control only
  2. BProgression-free survival only, no OS data
  3. CQuality of life only
  4. DResponse rate only
  5. EOverall survival nearly doubled with long-term follow-up
Show answer

Answer: E. RTOG 9402 (13.2 vs 7.3 years) and EORTC 26951 (14.2 vs 9.3 years) in codeleted tumours; about a third alive at 20 years with RT + PCV.

Review: section 06

Q83GliomaLevel 3Systemic therapy

A 50-year-old with a bihemispheric, multilobar codeleted oligodendroglioma would need near whole-brain RT. A reasonable initial approach is:

  1. AResection of both hemispheres
  2. BNo treatment ever
  3. CChemotherapy first (PCV or temozolomide), deferring RT
  4. DBevacizumab
  5. EWhole-brain RT immediately
Show answer

Answer: C. When the RT field would be very large, chemotherapy alone is a reasonable start because of neurocognitive risk, accepting that it is inferior to combined therapy in trials.

Review: section 06

Q84GliomaLevel 3Systemic therapy

INDIGO enrolled patients with residual grade 2 IDH-mutant glioma. Which patient was outside its eligibility?

  1. AA patient with an enhancing tumour on steroids with uncontrolled symptoms
  2. BA patient with an oligodendroglioma after surgery only
  3. CA 40-year-old with measurable non-enhancing residual tumour
  4. DA 16-year-old with an astrocytoma
  5. EA patient with KPS 90
Show answer

Answer: A. INDIGO required measurable non-enhancing disease, no prior treatment except surgery, KPS ≥80 and no steroids; patients with uncontrolled symptoms need RT plus chemotherapy.

Review: section 06

Q85GliomaLevel 3Biomarkers

A 22-year-old has a thalamic diffuse glioma with H3 K27M. Which statement is correct?

  1. ASurgery is usually curative
  2. BIDH testing defines it
  3. CIt is a diffuse midline glioma, CNS WHO grade 4, regardless of histology
  4. DIt is grade 2 if there is no necrosis
  5. EIt responds to vorasidenib
Show answer

Answer: C. H3 K27-altered diffuse midline gliomas are grade 4; dordaviprone has activity at recurrence (pooled response about 20%).

Review: section 04

Q86GliomaLevel 3Systemic therapy

An adult with a recurrent BRAF V600E-mutant glioma. Which treatment showed responses in a basket trial?

  1. ACetuximab
  2. BOsimertinib
  3. CImatinib
  4. DDabrafenib plus trametinib (ROAR)
  5. EVorasidenib
Show answer

Answer: D. ROAR showed durable responses in BRAF V600E high-grade and low-grade gliomas; tumour-agnostic approval followed.

Review: section 06

Q87GliomaLevel 3Local therapy

Dose escalation of radiotherapy above 60 Gy for glioblastoma:

  1. AHalves toxicity
  2. BHas not improved survival with photons
  3. CIs standard with brachytherapy
  4. DIs required for MGMT-unmethylated tumours
  5. EDoubles survival
Show answer

Answer: B. Stereotactic boosts, brachytherapy and photon IMRT escalation (NRG BN001) did not improve survival; proton escalation is in trials.

Review: section 05

Q88GliomaLevel 3Local therapy

Why is a margin of about 2 cm used around the gross tumour in glioblastoma radiotherapy?

  1. ATo treat the spinal cord
  2. BTo cover the other hemisphere
  3. C80–90% of recurrences arise within 2 cm of the original tumour
  4. DBecause glioblastoma metastasises to bone
  5. EBecause steroids shrink the tumour
Show answer

Answer: C. Infiltration beyond visible enhancement explains in-field and marginal relapses; trials are testing smaller margins with adaptive MRI.

Review: section 05

Q89GliomaLevel 3Systemic therapy

A woman on concurrent temozolomide has platelets of 60 × 10⁹/L in week 3. What is appropriate?

  1. ASwitch to lomustine immediately
  2. BStop RT and temozolomide permanently
  3. CHold temozolomide, continue RT, monitor counts
  4. DContinue temozolomide unchanged
  5. EGive G-CSF
Show answer

Answer: C. Hold temozolomide when platelets fall below 100 × 10⁹/L in the concurrent phase; RT can continue through mild-moderate thrombocytopenia. Women have 2–3 times more haematological toxicity.

Review: section 06

Q90MetastasesLevel 3Local therapy

In the randomised trial of SRS vs hippocampal-avoidance WBRT for 5–20 brain metastases (Aizer 2026), which was found?

  1. ABetter symptom scores with SRS and similar survival; more new lesions but less progression of treated lesions
  2. BBetter survival with WBRT
  3. CSRS was not feasible beyond 10 lesions
  4. DMore fatigue with SRS
  5. EIdentical rates of new lesions
Show answer

Answer: A. SRS improved symptom control and fatigue, with similar overall intracranial progression and survival (8.3 vs 8.5 months).

Review: section 05

Q91MetastasesLevel 3Local therapy

In QUARTZ, adding WBRT to dexamethasone and supportive care in NSCLC patients unsuitable for surgery or SRS:

  1. AIncreased survival by 6 months
  2. BWas only tested in breast cancer
  3. CImproved quality of life markedly
  4. DDoubled survival
  5. EDid not improve survival or quality-adjusted life
Show answer

Answer: E. Median survival was about 2 months in both arms; for poor-prognosis patients, supportive care alone is reasonable.

Review: section 05

Q92MetastasesLevel 3Screening, workup & staging

Which variables feed the lung adenocarcinoma Graded Prognostic Assessment?

  1. AHistological grade only
  2. BTumour size only
  3. CCEA and LDH
  4. DSex and smoking only
  5. EKPS, age, extracranial metastases, number of brain metastases and EGFR/ALK status
Show answer

Answer: E. The disease-specific GPA uses performance status, age, extracranial disease, number of lesions and genotype; prognosis now varies widely by cancer type.

Review: section 03

Q93MetastasesLevel 3Local therapy

After radiosurgery for melanoma brain metastases on immunotherapy, new enhancement appears at 6 months with low perfusion. The patient is well. Likely diagnosis?

  1. AAbscess
  2. BNew primary glioma
  3. CDefinite progression requiring WBRT
  4. DRadiation necrosis
  5. EHaemorrhage
Show answer

Answer: D. Radiation necrosis occurs in 10–25% after SRS, more with immunotherapy or targeted therapy; perfusion imaging, MRS or tissue helps. Symptomatic necrosis can be treated with steroids or bevacizumab.

Review: section 05

Q94MetastasesLevel 3Systemic therapy

A meta-analysis comparing DOACs and LMWH in primary brain tumours found intracranial haemorrhage rates of about:

  1. A15% with DOACs vs 1% with LMWH
  2. BHigher with DOACs
  3. CEqual at 50%
  4. D3% with DOACs vs 26% with LMWH
  5. E0% with both
Show answer

Answer: D. In primary brain tumours bleeding was markedly lower with DOACs (RR about 0.2); in brain metastases the difference was not significant.

Review: section 06

Q95MetastasesLevel 3Systemic therapy

For which patient is pharmacological VTE prophylaxis recommended?

  1. AEvery outpatient with glioblastoma
  2. BA patient in the immediate postoperative period after craniotomy
  3. CNobody, ever
  4. DAll patients receiving temozolomide
  5. EAll patients with brain metastases on SRS
Show answer

Answer: B. Outpatient prophylaxis (PRODIGE) did not show clear benefit and trended to more bleeding; postoperative prophylaxis is standard.

Review: section 06

Q96MetastasesLevel 3Systemic therapy

A patient on a CYP3A-metabolised TKI has a seizure from a brain metastasis. Which drug would you avoid?

  1. ALamotrigine
  2. BLacosamide
  3. CBrivaracetam
  4. DCarbamazepine
  5. ELevetiracetam
Show answer

Answer: D. Carbamazepine, phenytoin and phenobarbital induce CYP3A and lower levels of many TKIs, chemotherapy drugs and dexamethasone.

Review: section 06

Q97MetastasesLevel 3Local therapy

Which statement about postoperative SRS versus WBRT after metastasis resection (N107C) is correct?

  1. ANeither was better on any measure
  2. BSRS reduced cognitive deterioration but had lower surgical-bed control
  3. CWBRT caused less cognitive decline
  4. DSRS improved survival
  5. EBoth had identical local control
Show answer

Answer: B. Cognitive deterioration at 6 months 52 vs 85%; surgical-bed control was lower with single-fraction SRS, partly because large cavities got low doses (hence fractionated SRS today).

Review: section 05

Q98PaediatricLevel 3Systemic therapy

A 14-year-old with a hemispheric high-grade glioma has café-au-lait spots, consanguineous parents and a sibling with lymphoma. The tumour is hypermutated. Which approach is suggested after RT?

  1. ADabrafenib plus trametinib
  2. BVorasidenib
  3. CObservation
  4. DAnti-PD-1 therapy, with germline testing for constitutional MMR deficiency
  5. EHigh-dose methotrexate
Show answer

Answer: D. Biallelic (constitutional) MMR deficiency causes hypermutant gliomas that can respond to checkpoint inhibitors; family counselling and cancer surveillance follow.

Review: section 06

Q99PaediatricLevel 3Systemic therapy

For a 5-year-old with a hemispheric H3-wildtype/IDH-wildtype high-grade glioma after maximal resection, which post-operative approach is most used outside a trial?

  1. AObservation
  2. BCraniospinal irradiation alone
  3. CBevacizumab added to RT and temozolomide
  4. DVincristine and carboplatin only
  5. EFocal RT with temozolomide, then adjuvant temozolomide and lomustine
Show answer

Answer: E. ACNS0423 supports temozolomide with RT followed by temozolomide plus lomustine; HERBY showed no benefit from bevacizumab.

Review: section 06

Q100PaediatricLevel 3Systemic therapy

A child with DIPG asks about chemotherapy with RT. What does the evidence show?

  1. ATemozolomide doubles survival
  2. BHigh-dose chemotherapy with stem cell rescue cures most
  3. CBevacizumab is standard
  4. DNo systemic therapy has improved survival; trials are encouraged
  5. EChemotherapy replaces RT
Show answer

Answer: D. Decades of trials have not improved survival beyond RT; median survival remains under a year. Dordaviprone is being studied in H3 K27M gliomas.

Review: section 06

Q101PaediatricLevel 3Local therapy

Which radiation-related late effect is most strongly associated with young age at treatment and larger fields?

  1. AHair greying only
  2. BCataract only
  3. CSkin cancer only
  4. DNeurocognitive decline (falling IQ)
  5. ECardiomyopathy
Show answer

Answer: D. IQ decline, endocrine deficits (growth hormone first), hearing loss (with cisplatin), vasculopathy and second tumours are the major late effects of cranial RT in children.

Review: section 05

Q102PaediatricLevel 3Systemic therapy

In COG A9952 (young children with progressive LGG), carboplatin–vincristine versus thioguanine-procarbazine-lomustine-vincristine (TPCV) showed:

  1. ATPCV doubled overall survival
  2. BSimilar overall survival (86–87% at 5 years), with CV better tolerated
  3. CBoth arms had 20% survival
  4. DNeither drug regimen was tolerated
  5. ECV was clearly inferior
Show answer

Answer: B. Five-year EFS 39 vs 52% (not significant) and OS 86 vs 87%; CV became the common first-line chemotherapy.

Review: section 06

Q103PaediatricLevel 3Systemic therapy

An NF1-associated optic pathway glioma is enlarging slightly on MRI but vision is stable. The best approach is:

  1. AStart carboplatin for size increase alone
  2. BContinue surveillance with regular ophthalmology; treat for visual decline
  3. CImmediate radiotherapy
  4. DBiopsy now
  5. EResection of the optic nerve
Show answer

Answer: B. NF1 optic pathway gliomas are often indolent; treatment is guided by vision. RT is avoided in NF1 because of second tumours and vasculopathy.

Review: section 06

Q104PaediatricLevel 3Systemic therapy

Which statement about BRAF V600E paediatric low-grade glioma is correct?

  1. AIt is best treated with vorasidenib
  2. BIt responds poorly to chemotherapy and better to BRAF/MEK inhibitors
  3. CIt never transforms
  4. DIt predicts cure with surgery alone in all cases
  5. EIt is the commonest alteration in cerebellar pilocytic astrocytoma
Show answer

Answer: B. BRAF V600E LGG (especially with CDKN2A deletion) has worse outcomes with chemotherapy; KIAA1549-BRAF fusion is the usual cerebellar alteration.

Review: section 06

Q105GliomaLevel 3Presentation, traps & genetics

A 26-year-old with a glioma has multiple café-au-lait macules and a sister with colon cancer at 30. The glioma is IDH-wildtype and hypermutated after no prior therapy. Which germline condition should be considered?

  1. AMEN1
  2. BFamilial hypercholesterolaemia
  3. CLynch syndrome or constitutional mismatch-repair deficiency
  4. DHereditary spherocytosis
  5. EBRCA2
Show answer

Answer: C. MMR deficiency is enriched in early-onset gliomas (about 12% at 18–39 in one series); check MMR proteins and refer for germline testing.

Review: section 02

Q106GliomaLevel 3Systemic therapy

Dordaviprone was approved for recurrent H3 K27M-mutant diffuse midline glioma on the basis of:

  1. AIDH inhibition
  2. BEfficacy in DIPG only
  3. CA randomised phase 3 survival benefit
  4. DResponses in all patients
  5. EA pooled analysis of selected patients with response rate about 20%; confirmatory randomised trial ongoing
Show answer

Answer: E. Approval was conditional on the ongoing ACTION trial; the pooled analysis selected 50 of over 400 patients, so comparison with historical controls is difficult.

Review: section 06

Q107GliomaLevel 3Systemic therapy

In RTOG 1205, adding re-irradiation to bevacizumab for recurrent glioblastoma:

  1. AWas tested only in children
  2. BImproved PFS but not overall survival
  3. CImproved overall survival by a year
  4. DHad no effect on PFS
  5. EWorsened survival
Show answer

Answer: B. PFS improved (HR 0.73) without OS benefit (10.1 vs 9.7 months); re-irradiation is individualised.

Review: section 06

Q108MetastasesLevel 3Local therapy

Which feature best predicts benefit from surgical resection of a single brain metastasis in Patchell-era trials?

  1. AActive widespread metastases
  2. BControlled extracranial disease and good performance status
  3. CAge over 70
  4. DMultiple brain lesions
  5. ELow Karnofsky score
Show answer

Answer: B. In the Dutch trial, benefit was confined to patients with stable extracranial disease (median 12 months); active systemic disease abolished the gain.

Review: section 05

Q109MetastasesLevel 3Local therapy

Within what distance of the hippocampi do metastases make hippocampal-avoidance WBRT inappropriate?

  1. A2 cm
  2. B10 cm
  3. C5 mm
  4. D5 cm
  5. EAny distance
Show answer

Answer: C. Lesions within 5 mm of the hippocampi need conventional WBRT so that the avoidance region does not underdose tumour.

Review: section 05

Level 1 · Basics

Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.

Q110GliomaLevel 1Biomarkers

Mutant IDH1/2 enzymes produce which oncometabolite?

  1. ASuccinate
  2. BAlpha-ketoglutarate
  3. CCitrate
  4. DLactate
  5. E2-hydroxyglutarate
Show answer

Answer: E. Mutant IDH converts alpha-ketoglutarate to 2-hydroxyglutarate, which inhibits TET DNA demethylases and histone demethylases, producing the CpG-island hypermethylated phenotype. 2-HG can be detected by MR spectroscopy.

Review: section 04

Q111GliomaLevel 1Biomarkers

Loss of nuclear ATRX staining in an IDH-mutant diffuse glioma indicates:

  1. APilocytic astrocytoma
  2. BGlioblastoma, IDH-wildtype
  3. COligodendroglioma
  4. DA failed stain only
  5. EAstrocytic lineage (IDH-mutant astrocytoma)
Show answer

Answer: E. ATRX loss and strong p53 staining mark IDH-mutant astrocytoma and are mutually exclusive with 1p/19q codeletion; vessels retain ATRX and serve as the internal control.

Review: section 04

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, predicted lung function, NNT), CT and fluid findings, reading trial results, sequencing traps.

Q112GliomaLevel 2Biomarkers

Which marker is diagnostic, prognostic AND predictive in oligodendroglioma?

  1. AChromosome 7 gain
  2. BEGFR amplification
  3. CATRX loss
  4. DKi-67 index
  5. E1p/19q codeletion
Show answer

Answer: E. 1p/19q codeletion defines oligodendroglioma, predicts long survival and predicts marked benefit from PCV with radiotherapy (EORTC 26951/RTOG 9402).

Review: section 04

Q113GliomaLevel 2Biomarkers

FISH shows 1p/19q "codeletion" but IDH sequencing is wild-type in a 64-year-old with an enhancing tumour. What is the most likely explanation?

  1. AMetastasis
  2. BOligodendroglioma, IDH-wildtype
  3. CPilocytic astrocytoma
  4. DPartial 1p/19q losses in an IDH-wildtype glioma such as glioblastoma
  5. EA false-negative IDH test, so treat as oligodendroglioma
Show answer

Answer: D. True whole-arm 1p/19q codeletion is essentially always accompanied by IDH mutation. FISH probes cannot distinguish partial losses; look for EGFR, TERT and +7/−10.

Review: section 04

Q114GliomaLevel 2Biomarkers

A 17-year-old has a hemispheric high-grade glioma with ATRX loss and strong p53, but IDH1 R132H is negative and IDH sequencing is wild-type. Which test is most important next?

  1. ABRAF fusion
  2. BMGMT methylation
  3. CEGFR amplification
  4. DH3 G34 mutation
  5. E1p/19q codeletion
Show answer

Answer: D. Diffuse hemispheric glioma, H3 G34-mutant, mimics IDH-mutant astrocytoma (ATRX loss, p53) but is IDH-wildtype and grade 4.

Review: section 04

Q115GliomaLevel 2Biomarkers

A pathology report reads "Diffuse astrocytoma, NOS". What does NOS mean?

  1. ABenign tumour
  2. BMolecular testing was not done or failed, so the integrated diagnosis cannot be made
  3. CNo residual tumour
  4. DNot of glial origin
  5. ETesting was done and the tumour fits no defined type
Show answer

Answer: B. NOS = information missing (ask for the tests); NEC = tests done but the tumour does not fit a WHO type (consider methylation profiling).

Review: section 04

Level 3 · Challenging

DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.

Q116GliomaLevel 3Biomarkers

A recurrent glioblastoma treated with temozolomide is now hypermutated with MSH6 loss. Which statement is correct?

  1. ATreatment-induced hypermutation does not reliably predict benefit from checkpoint inhibitors, and MSH6 loss confers temozolomide resistance
  2. BPembrolizumab is the standard of care
  3. CIt indicates a new IDH mutation
  4. DIt proves Lynch syndrome
  5. EIt predicts response to more temozolomide
Show answer

Answer: A. Touat 2020 found that temozolomide-induced hypermutation did not translate into checkpoint-inhibitor responses, unlike germline constitutional MMR deficiency.

Review: section 04

Q117GliomaLevel 3Biomarkers

An IDH1 R132C (not R132H) mutation is found in a 30-year-old with an astrocytoma whose mother had breast cancer at 32. What should be offered?

  1. ABRCA testing only
  2. BVorasidenib is contraindicated
  3. CGermline TP53 testing for Li-Fraumeni syndrome
  4. DRepeat IDH IHC
  5. ENo further action
Show answer

Answer: C. Non-canonical IDH1 R132C is enriched in Li-Fraumeni-associated gliomas; the family history strengthens the case for germline TP53 testing.

Review: section 04

Q118GliomaLevel 3Biomarkers

Which statement about MGMT testing is correct?

  1. AIt is not useful in older adults
  2. BAssays vary and there is no universal cut-off; if the result is unavailable, fit patients still receive temozolomide
  3. CIt defines oligodendroglioma
  4. DIt is tested by IHC for IDH
  5. EUnmethylated tumours should never receive temozolomide
Show answer

Answer: B. MGMT is prognostic and predictive in glioblastoma and guides therapy in older or frail patients, but methods (MSP, pyrosequencing, arrays) and thresholds differ.

Review: section 04

Q119PaediatricLevel 3Biomarkers

Why should first-generation BRAF inhibitors be avoided in KIAA1549-BRAF fusion-positive pilocytic astrocytoma?

  1. AThey can paradoxically activate MAPK signalling in fusion-positive tumours
  2. BFusions are always benign
  3. CThey cause DIPG
  4. DThey do not cross the blood-brain barrier at all
  5. EThey are only licensed in adults
Show answer

Answer: A. Type I BRAF inhibitors act on V600E monomers and may enhance signalling through BRAF fusions; type II RAF inhibitors (tovorafenib) or MEK inhibitors are used instead.

Review: section 04

Level 1 · Basics

Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.

Q120GliomaLevel 1Biomarkers

Which is the earliest (founding) genetic event in IDH-mutant astrocytoma and oligodendroglioma?

  1. APTEN loss
  2. BMGMT methylation
  3. CCDKN2A/B deletion
  4. DIDH1 or IDH2 mutation
  5. EEGFR amplification
Show answer

Answer: D. IDH mutation is truncal: present in every tumour cell and retained at recurrence. 1p/19q codeletion, TP53/ATRX changes and CDKN2A/B loss come later.

Review: section 04

Q121GliomaLevel 1Biomarkers

Which three core pathways are altered in nearly all glioblastomas (TCGA 2008)?

  1. AMismatch repair, base excision and nucleotide excision repair
  2. BWNT, Hedgehog and Notch
  3. CRTK/RAS/PI3K, p53 and RB
  4. DBRCA, ATM and PALB2
  5. EJAK-STAT, NF-kB and TGF-beta
Show answer

Answer: C. Growth signalling (EGFR, PDGFRA, PTEN, NF1), the p53 pathway (TP53, MDM2/4, p14ARF) and the RB cell-cycle pathway (CDKN2A/B, CDK4, RB1).

Review: section 04

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, predicted lung function, NNT), CT and fluid findings, reading trial results, sequencing traps.

Q122GliomaLevel 2Biomarkers

How does mutant IDH lead to widespread DNA hypermethylation?

  1. AIt deletes the MGMT gene
  2. BIt causes 1p/19q loss
  3. C2-hydroxyglutarate inhibits alpha-ketoglutarate-dependent TET demethylases
  4. DIt directly methylates CpG islands
  5. EIt activates DNMT3A transcription
Show answer

Answer: C. Mutant IDH gains a new function, producing 2-HG, which competitively blocks TET DNA demethylases and histone demethylases, creating the glioma CpG-island methylator phenotype.

Review: section 04

Q123GliomaLevel 2Biomarkers

How is the whole-arm 1p/19q codeletion of oligodendroglioma generated?

  1. AGradual point deletions over many years
  2. BChromothripsis of chromosome 7
  3. CViral integration
  4. DLoss of the whole of chromosomes 1 and 19
  5. EAn unbalanced t(1;19) translocation followed by loss of the derivative chromosome
Show answer

Answer: E. A single translocation event between 1q and 19p, with loss of the der(1;19) chromosome, removes 1p and 19q together.

Review: section 04

Q124GliomaLevel 2Biomarkers

Why do IDH-wildtype glioblastomas often lie next to the lateral ventricles?

  1. AThey appear to arise from subventricular-zone neural stem cells carrying low-level driver mutations
  2. BRadiotherapy targets the ventricles
  3. CThey are metastases
  4. DEpendymal cells always transform
  5. ECSF carries tumour cells from elsewhere
Show answer

Answer: A. Lee 2018 found driver mutations in astrocyte-like stem cells of the subventricular zone that migrated to form the tumour.

Review: section 04

Q125GliomaLevel 2Biomarkers

Why does bevacizumab shrink enhancement and oedema quickly in glioblastoma without prolonging survival?

  1. AIt kills all tumour cells within days
  2. BIt normalises leaky VEGF-driven vessels without eliminating the infiltrating tumour cells
  3. CIt reverses MGMT methylation
  4. DIt repairs TP53
  5. EIt blocks IDH
Show answer

Answer: B. Hypoxia → HIF → VEGF drives leaky microvascular proliferation; blocking VEGF tightens vessels (less enhancement and oedema) but infiltrative, non-enhancing tumour continues.

Review: section 04

Level 3 · Challenging

DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.

Q126GliomaLevel 3Biomarkers

Single-cell RNA sequencing of glioblastoma (Patel 2014) showed:

  1. AMesenchymal cells are absent
  2. BGlioblastoma cells are genetically identical
  3. CSeveral expression subtypes coexist within one tumour
  4. DEach tumour has a single uniform subtype
  5. EAll cells carry EGFRvIII
Show answer

Answer: C. Intratumoural heterogeneity helps explain why single-pathway targeted drugs have failed in glioblastoma.

Review: section 04

Q127PaediatricLevel 3Biomarkers

How does the histone H3 K27M mutation drive diffuse midline glioma?

  1. AIt produces 2-hydroxyglutarate
  2. BIt inhibits PRC2, causing global loss of H3K27 trimethylation
  3. CIt amplifies EGFR
  4. DIt activates BRAF
  5. EIt silences MGMT
Show answer

Answer: B. K27M acts as an oncohistone that blocks the EZH2-containing PRC2 complex; loss of H3K27me3 on immunohistochemistry is a diagnostic surrogate. It is mutually exclusive with IDH mutation.

Review: section 04

Prepared and reviewed by Dr. Haritha Chiramana for teaching. Facts compiled from current guidelines, primary trials and evidence summaries, written in our own words; drawings are original schematics, not patient images; no doses are included.