Meningioma: Unlocking the Future of Brain Tumor Treatment

The most common primary brain tumor is undergoing a revolution in how it is diagnosed and treated.

Imagine being told you have a brain tumor, and then learning it's one of the most common types—a meningioma. For approximately 39,000 Americans who receive this diagnosis each year, the journey begins with understanding this complex condition 2 .

Meningiomas arise from the meninges, the protective layers surrounding the brain and spinal cord. While approximately 80% of these tumors are benign, their location can still cause serious health issues, including seizures, vision problems, and cognitive challenges 2 6 .

Recent breakthroughs in molecular profiling and targeted therapies are transforming how we classify and treat meningiomas, offering new hope to patients with recurrent or aggressive forms.

Understanding Meningiomas: More Than Just a "Benign" Tumor

Meningiomas represent about 41.7% of all central nervous system tumors, making them the most frequently diagnosed primary brain tumors in adults 6 . They affect about 10.15 out of every 100,000 people, with incidence rates rising with age and peaking in people in their 70s and 80s 6 .

These tumors originate from arachnoid cap cells in the meninges and can develop anywhere these protective coverings exist 8 . They're categorized into three grades based on their growth potential and likelihood of recurrence:

  • Grade 1 (Benign): Slow-growing tumors that account for 75-80% of all meningiomas 5 . With complete surgical removal, the prognosis is typically excellent 2 .
  • Grade 2 (Atypical): More aggressive tumors representing 20-25% of cases, with recurrence rates of 29-52% within five years 1 5 .
  • Grade 3 (Malignant): Rare, aggressive tumors comprising 1-6% of meningiomas, with 50-94% recurrence rates and a tendency to invade brain tissue 5 8 .

41.7%

of all CNS tumors are meningiomas

39,000

Americans diagnosed annually

Meningioma Grades and Recurrence Risks
WHO Grade Classification Prevalence Recurrence Rate Key Characteristics
Grade 1 Benign 75-80% 7-25% Slow-growing, excellent prognosis with complete resection
Grade 2 Atypical 20-25% 29-52% Intermediate growth, higher recurrence risk
Grade 3 Malignant 1-6% 50-94% Aggressive, invades brain tissue, may metastasize

The Molecular Revolution: Rethinking How We Classify Brain Tumors

The 2021 WHO Classification of Central Nervous System Tumors marked a pivotal shift by incorporating molecular criteria alongside traditional histology for the first time 1 6 . This recognizes that how a tumor looks under the microscope doesn't always predict its behavior.

Key Molecular Markers
  • TERT promoter mutations: These affect telomerase activity and are associated with particularly aggressive tumors. The 2021 classification designates meningiomas with TERT alterations as CNS WHO grade 3, regardless of their histological appearance 6 .
  • CDKN2A/B homozygous deletion: Loss of this tumor suppressor gene also now qualifies a meningioma for a grade 3 designation due to its association with inferior survival 6 .
  • NF2 gene mutations: The most common genetic alteration in meningiomas, occurring in 50-60% of cases, often linked to tumors along the brain's convexity 2 6 .
  • Non-NF2 mutations: Including TRAF7, AKT1, and SMO mutations, typically found in grade 1 meningiomas located in the skull base 6 8 .

The cIMPACT-NOW consortium has further refined these standards, proposing that meningiomas with chromosomal arm 1p deletion in combination with 22q deletion and/or NF2 mutations should be classified as CNS WHO grade 2, even if they appear grade 1 under microscopy 1 .

Common Molecular Alterations in Meningiomas
NF2 mutations (50-60%)
Non-NF2 mutations (20-30%)
TERT alterations (5-10%)
CDKN2A/B deletions (3-7%)

Inside a Groundbreaking Discovery: The TERT Biomarker Study

Methodology

A multi-institutional team led by researchers at Mayo Clinic examined over 1,200 meningioma samples from patients across Canada, Germany, and the United States 3 . Their goal was to determine whether TERT expression levels—even without full TERT mutations—could predict tumor behavior.

The researchers analyzed tumor specimens for:

  1. TERT promoter mutations (previously established marker of aggressiveness)
  2. TERT expression levels in mutation-negative tumors
  3. Correlation between TERT expression and clinical outcomes, including time to recurrence

Results and Analysis

The findings, published in Lancet Oncology, revealed that nearly one-third of meningiomas without TERT mutations showed high TERT expression 3 . These patients experienced significantly earlier tumor regrowth compared to those without TERT expression, though their outcomes were better than patients with full TERT mutations.

Most notably, researchers discovered that TERT-positive tumors behaved as if they were one grade worse than their official diagnosis. A grade 1 tumor with TERT expression acted more like a grade 2 tumor, and a grade 2 tumor with TERT expression behaved like a grade 3 tumor 3 .

"This makes TERT a promising new biomarker for identifying patients who may be at greater risk of developing aggressive disease," said Dr. Gelareh Zadeh, the study's senior author 3 .

Impact of TERT Expression on Meningioma Behavior
Tumor Grade TERT Status Observed Behavior Clinical Implications
Grade 1 High Expression Similar to Grade 2 May require closer monitoring, consider earlier intervention
Grade 2 High Expression Similar to Grade 3 Likely benefits from more aggressive treatment
Grade 3 High Expression Highly aggressive Maximum therapeutic intervention warranted

Emerging Therapies: Beyond the Scalpel

While surgery and radiation remain cornerstone treatments, several innovative approaches are showing promise for recurrent or aggressive meningiomas.

Peptide Receptor Radionuclide Therapy (PRRT)

Somatostatin receptor type 2 (SSTR2) is expressed in 80-95% of meningiomas, making it an ideal therapeutic target 5 6 .

The LUMEN-1 trial (EORTC-2334-BTG), activated in March 2025, is the first prospective randomized trial investigating [¹⁷⁷Lu]Lu-DOTATATE in recurrent meningioma 5 .

This approach uses a radioactive compound that binds specifically to SSTR2, delivering targeted radiation to tumor cells while sparing healthy tissue. Early studies have shown disease control rates of 57-63% in refractory meningiomas 5 6 .

Early disease control rate: ~60%
Targeted Molecular Therapies

Several targeted agents are under investigation for meningiomas with specific molecular profiles:

  • FAK inhibitors (GSK2256098): For NF2-mutated meningiomas 4 6
  • PI3K/AKT pathway inhibitors (capivasertib): For tumors with AKT mutations 4 6
  • Hedgehog pathway inhibitors (vismodegib): For SMO-mutated meningiomas 4 6
  • CDK inhibitors (abemaciclib): Targeting cell cycle progression 4 6
ANXA3 Protein Inhibition

Researchers at the University of Plymouth recently identified a protein called ANXA3 that drives growth in certain meningioma cells 7 . In laboratory experiments, blocking ANXA3 slowed or completely stopped tumor cell growth, particularly in meningiomas resulting from NF2 mutations 7 .

"This research brings hope — not just for treatment, but for better outcomes and quality of life," said Dr. Karen Noble of Brain Tumour Research 7 .

ANXA3

Inhibition shows promise in NF2-mutated meningiomas

The Scientist's Toolkit: Essential Research Reagents

Key Research Reagents in Meningioma Studies
Reagent Function Application in Meningioma Research
[¹⁷⁷Lu]Lu-DOTATATE SSTR2-targeting radiopharmaceutical Delivers targeted radiation to meningioma cells in PRRT 5
[⁶⁸Ga]Ga-DOTATATE SSTR2-targeting PET tracer Visualizes meningiomas and identifies candidates for PRRT 6
Anti-ANXA3 agents Inhibits ANXA3 protein function Blocks growth driver in NF2-mutated meningiomas 7
FAK Inhibitors Blocks focal adhesion kinase Targets NF2-deficient meningiomas 4 8
CDK Inhibitors Inhibits cell cycle progression Slows tumor growth in aggressive meningiomas 4

The Road Ahead: Challenges and Opportunities

Despite these promising developments, significant challenges remain. Validated biomarkers for treatment response are still lacking, and resistance mechanisms in aggressive meningiomas are not fully understood 8 . The blood-brain barrier also continues to pose obstacles for drug delivery, though techniques like convection-enhanced delivery are being explored to overcome this limitation 8 .

Future progress will require large-scale, biomarker-driven clinical trials to confirm the efficacy of emerging treatments and establish optimal combination regimens 8 . The integration of molecular profiling into standard diagnosis will continue to refine our ability to match patients with the most effective therapies.

Future Research Directions

Biomarker Validation

Establishing reliable biomarkers for treatment response and resistance mechanisms.

Clinical Trial Expansion

Large-scale trials to confirm efficacy of emerging targeted therapies.

Drug Delivery Innovation

Developing methods to overcome the blood-brain barrier for better drug penetration.

Combination Therapies

Exploring synergistic effects of multiple treatment approaches.

Conclusion: A New Era of Precision Medicine

The landscape of meningioma care is undergoing a remarkable transformation, moving from a one-size-fits-all approach to personalized, precision medicine. As research continues to unravel the molecular complexities of these common brain tumors, patients stand to benefit from more accurate prognoses and increasingly effective, targeted treatments.

"The work being done by our Centre of Excellence at Plymouth is world-leading," noted Dr. Karen Noble, "and now is the time to build on this momentum" 7 . With ongoing advances in molecular profiling and innovative therapies, the future for meningioma patients looks increasingly hopeful.

References