Brain Tumour Treatment in Aurangabad — Coordinated Oncology Care at Karnawat Cancer Hospital
- DM Medical Oncology — Gold Medalist, ESMO Certified
- Coordinated Multidisciplinary Brain Tumour Care
- Molecular Tumour Profiling & Targeted Treatment Planning
- Supportive & Palliative Care for Brain Tumour Patients
- Second Opinion for Brain Tumour Diagnosis
Brain Tumour — Key Facts
| STATISTIC | FIGURE | CONTEXT |
|---|---|---|
| New brain tumour cases per year (India) | ~28,000+ | Primary brain tumours; excludes metastatic brain tumours |
| Most common malignant brain tumour in adults | Glioblastoma (GBM) | WHO Grade 4; most aggressive primary brain tumour |
| Brain metastases vs primary tumours | 10:1 ratio | Brain metastases from other cancers are far more common than primary brain tumours |
| Most common cancers causing brain metastases | Lung, Breast, Melanoma, Kidney, Colorectal | Lung cancer is the most frequent cause of brain metastases |
| Median survival — Glioblastoma (GBM) | ~15–18 months with treatment | With surgery + chemoradiation; varies by MGMT status |
| 5-year survival — Grade 2 Glioma (IDH mutant) | ~70–80% | Significantly better prognosis than high-grade gliomas |
| Most common benign brain tumour | Meningioma | ~37% of all primary brain tumours; often curable with surgery |
What Is a Brain Tumour? Understanding the Diagnosis
Primary Brain Tumours
Primary brain tumours originate within the brain itself — from brain cells (neurons or glial cells), the meninges (brain covering), or other structures within the skull. They are classified by the type of cell from which they arise and by a grading system that reflects how aggressively they grow. Primary brain tumours do not commonly spread outside the brain to other organs. However, high-grade primary brain tumours are locally destructive — meaning they invade and destroy surrounding brain tissue.
Secondary (Metastatic) Brain Tumours
Metastatic brain tumours arise when cancer from another organ — most commonly the lungs, breasts, skin (melanoma), kidneys, or colon — spreads to the brain through the bloodstream. Brain metastases are 10 times more common than primary brain tumours and represent advanced disease in the original cancer. Treatment approach differs significantly between primary and metastatic brain tumours — making accurate diagnosis and pathology essential before any treatment decision.
The Brain's Functional Anatomy — Why Location Matters
The brain is divided into regions, each controlling specific functions. The location of a tumour determines what symptoms it causes and how surgically accessible it is:
- Frontal lobe — personality, decision-making, voluntary movement
- Parietal lobe — sensory processing, spatial awareness, language comprehension
- Temporal lobe — memory, hearing, language (dominant hemisphere)
- Occipital lobe — vision and visual processing
- Cerebellum — balance and coordination
- Brain stem — controls breathing, heart rate, consciousness; tumours here carry very high surgical risk
Types of Brain Tumours — WHO Classification and Grading
Gliomas — Tumours of Brain Glial Cells
Gliomas are the most common malignant primary brain tumours, arising from the supportive glial cells of the brain. They are now classified primarily by molecular markers rather than just appearance under the microscope.
- Glioblastoma (GBM) — WHO Grade 4 astrocytoma. The most aggressive and most common malignant primary brain tumour in adults. Grows rapidly and diffusely infiltrates surrounding brain tissue. Most GBMs are IDH wild-type. Median survival 15–18 months with optimal treatment.
- Astrocytoma IDH-mutant — WHO Grade 2 or 3. Slower growing. IDH mutation is a favourable prognostic marker. Can progress to higher grade over time.
- Oligodendroglioma — WHO Grade 2 or 3. IDH-mutant and 1p/19q co-deleted. Best prognosis among malignant gliomas; responds well to chemotherapy and radiation.
- Diffuse Midline Glioma (H3 K27M-mutant) — WHO Grade 4. Occurs in children and young adults; affects thalamus, pons, spinal cord. Poor prognosis.
Meningioma
Meningiomas arise from the meninges — the three-layered membrane covering the brain and spinal cord. They are the most common primary brain tumour overall (~37%). Most are WHO Grade 1 (benign) and grow slowly.
- Grade 1 meningioma — Benign; often curable with surgery alone
- Grade 2 meningioma (atypical) — Higher recurrence risk; may require post-operative radiation
- Grade 3 meningioma (anaplastic) — Rare; aggressive; treatment similar to malignant tumours
Brain Metastases
Cancer that has spread to the brain from another primary site. The most common sources are lung cancer, breast cancer, melanoma, renal cell carcinoma, and colorectal cancer. Multiple brain metastases are common. Treatment depends on the number, size, and location of metastases, and the status of the primary cancer.
Medulloblastoma
The most common malignant brain tumour in children — arises in the cerebellum. Now classified into molecular subgroups (WNT, SHH, Group 3, Group 4) with different prognoses. Treatment: surgery + radiation (craniospinal) + chemotherapy.
Ependymoma
Arises from ependymal cells lining the ventricles and spinal canal. Can occur at any age; more common in children. RELA fusion and ZFTA fusion are molecular subtypes. Surgery is the primary treatment; radiation for incompletely resected or high-grade tumours.
Primary CNS Lymphoma
A diffuse large B-cell lymphoma (DLBCL) confined to the brain, eyes, spinal cord, or leptomeninges — without systemic disease. Occurs most commonly in older adults and in immunocompromised patients (HIV, post-transplant). Does not require surgery for diagnosis — stereotactic biopsy is sufficient. Treated with systemic chemotherapy; not radiated upfront in most patients.
Pituitary Tumours (Pituitary Adenoma)
Tumours of the pituitary gland, located at the base of the brain. Most are benign. May be functioning (secreting hormones — prolactin, growth hormone, ACTH) or non-functioning. Can compress the optic chiasm causing vision loss. Usually treated surgically via trans-sphenoidal approach.
Acoustic Neuroma (Vestibular Schwannoma)
Benign tumour of the nerve sheath of the vestibulocochlear nerve. Causes progressive unilateral hearing loss, tinnitus, and balance problems. Treatment: surveillance, stereotactic radiosurgery (Gamma Knife / CyberKnife), or surgery depending on size and growth.
Molecular Markers in Brain Tumours — Why They Matter
| MARKER | WHAT IT MEANS | CLINICAL SIGNIFICANCE |
|---|---|---|
| IDH Mutation (IDH1 / IDH2) | Mutation in isocitrate dehydrogenase enzyme | IDH-mutant gliomas have significantly better prognosis than IDH wild-type. A positive IDH mutation in an adult glioma means slower growth and better response to treatment. |
| MGMT Promoter Methylation | Silencing of MGMT DNA repair gene by methylation | MGMT-methylated GBMs respond better to chemotherapy (DNA-damaging agents). A key predictor of treatment benefit in glioblastoma. |
| 1p/19q Co-deletion | Deletion of chromosome arms 1p and 19q | Defines oligodendroglioma. Associated with excellent chemosensitivity and better long-term prognosis. |
| EGFR Amplification / EGFRvIII | EGFR gene amplification or mutant splice form | Common in IDH wild-type GBM. Indicates highly proliferative tumour biology. |
| TERT Promoter Mutation | TERT gene promoter mutation | Associated with IDH wild-type GBM; also seen in IDH-mutant oligodendroglioma. |
| H3 K27M Mutation | Histone H3 mutation | Defines diffuse midline glioma — a distinct, aggressive entity in children/young adults. |
| ATRX Loss | ATRX gene inactivation | Seen in IDH-mutant astrocytomas; helps distinguish from oligodendroglioma. |
Risk Factors for Brain Tumours
Ionising Radiation
The only well-established environmental risk factor for primary brain tumours. Previous radiation to the head — whether therapeutic (childhood brain radiation) or from environmental exposure — increases brain tumour risk. Note: diagnostic CT scans and mobile phones have NOT been proven to cause brain tumours.
Immune Suppression
Primary CNS lymphoma is strongly associated with immunosuppression — HIV infection, post-organ transplant immunosuppression. Risk is dramatically reduced with immune reconstitution in HIV patients.
Age and Sex
Many primary brain tumours increase in incidence with age. Glioblastoma peaks at 55–75 years. Meningiomas are twice as common in women (possibly due to hormonal influence). Medulloblastoma is predominantly a childhood tumour.
Factors NOT Proven to Cause Brain Tumours
Despite widespread public concern, the following have NOT been established as brain tumour risk factors by current evidence: mobile phone/electromagnetic radiation, Wi-Fi, power lines, hair dyes, or head injury.
Hereditary Cancer Syndromes
- Neurofibromatosis type 1 (NF1) — increased risk of optic pathway gliomas and other CNS tumours
- Neurofibromatosis type 2 (NF2) — bilateral acoustic neuromas (vestibular schwannomas), meningiomas, ependymomas
- Li-Fraumeni Syndrome (TP53 mutation) — increased risk of gliomas
- Von Hippel-Lindau disease — cerebellar hemangioblastomas
- Turcot Syndrome — brain tumours associated with colorectal polyposis
Brain Tumour Symptoms — When to Seek Urgent Evaluation
Raised Intracranial Pressure — General Symptoms
- Persistent or progressively worsening headache — classically worst in the morning and on waking; aggravated by bending forward, coughing, or straining
- Nausea and vomiting — especially projectile vomiting without nausea in the morning
- Papilloedema — swelling of the optic disc (visible on eye examination); causes blurred or double vision
- Altered consciousness or confusion
- Seizures (fits) — a new-onset seizure in an adult always warrants brain imaging
Focal Neurological Deficits — Location-Dependent Symptoms
- Weakness or paralysis on one side of the body (hemiparesis) — frontal lobe tumours
- Speech difficulty (aphasia — unable to speak or understand) — dominant temporal/frontal lobe tumours
- Memory loss or personality/behaviour change — frontal lobe tumours (often noticed by family first)
- Vision problems — loss of part of the visual field; double vision
- Balance and coordination problems, unsteady gait — cerebellar tumours
- Sensory disturbances — numbness, tingling on one side — parietal lobe tumours
- Hearing loss, tinnitus, facial numbness — acoustic neuromas or posterior fossa tumours
Symptom Onset — Clue to Tumour Grade
EMERGENCY: Sudden severe headache (“thunderclap” — worst headache of life), rapid deterioration in consciousness, or new focal weakness is a neurological emergency. Go to the nearest emergency department immediately.
How Is a Brain Tumour Diagnosed?
Step 1: MRI Brain (With and Without Contrast)
MRI is the gold standard imaging for brain tumours. It provides detailed images of tumour location, size, extent of surrounding oedema, involvement of eloquent cortex, and relationship to critical structures. Essential sequences:
- T1 post-contrast — tumour enhancement pattern (ring enhancement is characteristic of GBM)
- T2/FLAIR — infiltration extent; low-grade gliomas are often non-enhancing but show T2/FLAIR signal abnormality
- DWI (Diffusion-weighted imaging) — helps distinguish tumour from abscess; useful in lymphoma
- MR Perfusion — assesses tumour vascularity; helps distinguish high-grade from low-grade; identifies pseudoprogression
- MR Spectroscopy — metabolic fingerprint of the tumour (choline:NAA ratio); helps characterise tumour vs radiation necrosis
- fMRI (Functional MRI) — maps eloquent cortex (speech, motor areas) for surgical planning
- MR Tractography (DTI) — maps white matter tracts for surgical planning
Step 2: CT Scan
CT scan of the brain is the first imaging in acute presentations (emergency). Useful for detecting haemorrhage, calcification, and bony involvement. CT chest/abdomen/pelvis is performed when metastatic brain tumour is suspected, to identify the primary cancer.
Step 3: Tissue Biopsy — Definitive Diagnosis
Histological and molecular examination of tumour tissue is required for definitive diagnosis. Options:
- Craniotomy with maximal safe resection — Surgery to remove as much tumour as possible. The resected tissue is sent for histology and molecular analysis. Preferred approach when the tumour is in a surgically accessible location.
- Stereotactic biopsy — CT- or MRI-guided needle biopsy under local or general anaesthesia. Used for deep-seated, inaccessible tumours, or when surgery carries unacceptable risk. Provides a small tissue sample for diagnosis — not therapeutic.
- Liquid biopsy — Circulating tumour DNA (ctDNA) from blood or cerebrospinal fluid. Emerging technique; not yet standard for brain tumours.
Step 4: Molecular/Genetic Testing on Tumour Tissue
All WHO-recommended molecular markers should be tested: IDH1/IDH2 mutation, MGMT promoter methylation, 1p/19q co-deletion, ATRX expression, TERT promoter mutation, H3 K27M mutation, EGFR amplification. These results — not just the microscopy — determine the final WHO tumour classification and drive treatment decisions.
Step 5: Additional Tests
- Ophthalmology evaluation — Fundoscopy to check for papilloedema; visual field assessment for tumours near optic pathways
- Neuropsychological assessment — Baseline cognitive function (memory, language, attention) before surgery or radiation
- Electroencephalogram (EEG) — If seizures are present or suspected
- Lumbar puncture (CSF analysis) — For leptomeningeal spread assessment; in medulloblastoma and lymphoma