# Radioligand Therapy for Meningiomas: What Today's Evidence Shows and What the Future May Hold This review summarizes the current evidence on peptide receptor radionuclide therapy (PRRT) for meningiomas, the most common primary brain tumors. While most meningiomas are benign and treatable with surgery or radiotherapy, about one in five are higher-grade tumors that resist standard treatment and recur. PRRT delivers radioactive isotopes directly to tumor cells by targeting somatostatin receptors, which are present on the majority of meningiomas regardless of grade. The authors review preclinical findings, clinical evidence, safety data, and emerging strategies. These strategies include dosimetry-guided treatment and combination approaches. The authors conclude that PRRT shows therapeutic potential for aggressive or refractory meningiomas. PRRT requires further prospective trials. # Radioligand Therapy for Meningiomas: What Today's Evidence Shows and What the Future May Hold ## Table of Contents - Key Points - Background: Why This Research Matters - How Meningiomas Are Diagnosed and Imaged - Current Standard Treatments for Meningiomas - Peptide Receptor Radionuclide Therapy (PRRT) - Preclinical Studies: The Foundation of PRRT Research - Clinical Implications: What This Means for Patients - Limitations: What the Study Could Not Prove - Recommendations and Future Directions - Frequently Asked Questions - Source Information ## Key Points - PRRT is an investigational treatment for aggressive or recurrent meningioma that has progressed despite surgery and radiotherapy. - It targets somatostatin receptors, which are present on most meningiomas regardless of grade and often preserved after previous treatments. - PRRT is not approved by the FDA or EMA for meningioma and should only be considered at specialized centers with multidisciplinary care. - In large neuroendocrine tumor series, serious blood-related side effects occurred in about 1–9% of patients; most side effects are mild and reversible. - No randomized controlled trials have proven PRRT's effectiveness in meningioma; further prospective trials are needed to define optimal use. ## Background: Why This Research Matters Meningioma is the most common primary tumor that starts inside the skull. It occurs in approximately 8.8 out of every 100,000 people. These tumors grow from the meningeal membranes, which are the protective layers covering the brain and spinal cord. Most meningiomas grow slowly and do not invade surrounding tissue. Many meningiomas are found by chance during brain imaging that was done for unrelated reasons. Others cause symptoms depending on where they are located. Common symptoms include: - Headaches caused by increased pressure inside the skull - Focal neurological deficits (weakness or loss of function in specific body areas) - Cranial nerve dysfunction (problems with nerves that control vision, facial movement, or hearing) - Epileptic seizures caused by irritation of the brain surface According to the World Health Organization (WHO) classification system for brain tumors, about 80% of meningiomas are classified as WHO grade I. These are generally considered benign. The remaining cases are classified as WHO grade II (atypical) or grade III (anaplastic). Higher-grade tumors show more cell division, invade the brain, behave more aggressively, and have much higher recurrence rates. The table below summarizes the biological behavior, recurrence risk, and somatostatin receptor expression patterns across the three WHO grades: - **WHO Grade I:** Benign, slow-growing; approximately 7–23% five-year recurrence rate after complete surgical removal; high somatostatin receptor expression, mainly subtype 2 (SSTR2) - **WHO Grade II:** Atypical, invasive; approximately 50–55% five-year recurrence rate; high to moderate receptor expression, mainly SSTR2 - **WHO Grade III:** Anaplastic, aggressive; approximately 72–78% five-year recurrence rate; variable but frequently preserved SSTR2 expression These recurrence rates apply after gross total resection, which means complete removal of the visible tumor during surgery. Beyond the WHO grade, meningiomas show significant differences between patients and even within a single tumor at the genetic, epigenetic, and cellular levels. Recurrent molecular alterations include NF2 loss, TRAF7 mutations, KLF4 mutations, AKT1 mutations, SMO mutations, and dysregulation of the PI3K/AKT/mTOR signaling pathway. These alterations define biologically distinct subgroups of meningioma with different growth patterns, recurrence risks, and treatment vulnerabilities. Recent advances in molecular profiling and single-cell analysis have revealed the complexity of the meningioma tumor microenvironment. This includes dynamic interactions between tumor cells, immune cells, and blood vessels that may influence how sensitive the tumor is to radiation and how it resists treatment. This molecular heterogeneity has important treatment implications. Several signaling pathways and genetic drivers have been proposed as potential treatment targets in meningioma, including: - Angiogenic signaling through VEGF (vascular endothelial growth factor) - Immune checkpoint pathways (PD-L1, PD-L2, CTLA-4) - Hedgehog signaling (SMO mutations) - PI3K/AKT/mTOR pathway activation However, clinical translation of these targets has so far produced limited and inconsistent results. No systemic therapy has emerged as a broadly effective standard treatment for recurrent or refractory meningioma. In contrast to many pathway-specific alterations that characterize only certain molecular subsets of meningioma, somatostatin receptor (SSTR) expression is a unifying biological feature. It is observed across the majority of tumors, largely independent of WHO grade or driver mutation status. High-level expression of somatostatin receptors — particularly somatostatin receptor subtype 2 (SSTR2) — has been consistently demonstrated in meningiomas. This makes SSTR2 one of their most distinctive molecular characteristics. Importantly, SSTR expression is often preserved in recurrent or treatment-refractory disease. This makes it an attractive target even in advanced clinical settings. This biological feature provides the foundation for both receptor-based molecular imaging and targeted radionuclide therapy, forming the basis of the theranostic concept in meningioma management. Peptide receptor radionuclide therapy (PRRT) exploits this molecular vulnerability. It works by coupling somatostatin analogues to therapeutic radionuclides, which enables selective delivery of ionizing radiation to SSTR-expressing tumor cells. Unlike conventional external-beam radiotherapy, PRRT delivers continuous low-dose-rate irradiation at the cellular level. This property may be particularly relevant for slowly proliferating but radiation-resistant tumor populations. The success of PRRT in neuroendocrine tumors has provided a strong biological and clinical rationale for its investigation in meningioma. This is particularly true for patients with recurrent, inoperable, or radiation-refractory disease. While surgery and radiotherapy remain the established cornerstones of meningioma management, a subset of patients eventually exhausts standard local treatment options. In this context, SSTR-targeted radionuclide therapy has emerged as a biologically rational investigational approach. The aim of this review is to synthesize current evidence on PRRT in meningioma from a translational perspective. The authors focus on the biological rationale underlying SSTR targeting. The authors summarize relevant preclinical findings. The authors critically evaluate the heterogeneous clinical literature. The authors discuss emerging strategies that may shape the future integration of PRRT into personalized meningioma therapy. ## How Meningiomas Are Diagnosed and Imaged Magnetic resonance imaging (MRI) remains the gold standard for the diagnosis and follow-up of meningiomas. When MRI is unavailable, computed tomography (CT) may be considered as an alternative. Conventional radiological imaging is essential for accurately assessing tumor extent. Conventional radiological imaging is essential for identifying distant tumor sites within the skull. Conventional radiological imaging is essential for evaluating peritumoral edema (swelling around the tumor), bone involvement, and adjacent neurovascular structures. On MRI, meningiomas typically appear isointense on T1-weighted images. This means they have similar brightness to normal brain tissue on those images. They appear hyperintense (brighter) on T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences. They also show strong and usually homogeneous contrast enhancement. To ensure precise evaluation and comparability across clinical trials, the use of standardized response assessment criteria is recommended. Such criteria include those defined by the Response Assessment in Neuro-Oncology (RANO) working group. As mentioned earlier, meningiomas frequently express somatostatin receptors on their cell surface, predominantly SSTR2. These receptors can be visualized using SSTR-targeted radiopharmaceuticals. For positron emission tomography (PET), commonly used tracers include: - [68Ga]Ga-DOTATATE - [68Ga]Ga-DOTATOC - [68Ga]Ga-DOTANOC - [18F]F-SiTATE — a SiFAlin-tagged [Tyr3]-octreotate - [64Cu]Cu-DOTATATE Single photon emission computed tomography (SPECT) imaging can be performed using [99mTc]Tc-EDDA-Hynic-TOC or [111In]In-Pentetreotide. These techniques provide valuable functional information about receptor density, tumor extent, and spatial relationships to surrounding healthy tissue. They may be particularly useful for confirming recurrence in postoperative settings where conventional MRI can be challenging to interpret. Because normal brain tissue takes up very little of these tracers, SSTR-targeted imaging offers superior contrast between the lesion and background tissue. High tracer accumulation in meningiomas has been shown to improve detection sensitivity compared with contrast-enhanced MRI alone. In addition to its diagnostic value, SSTR imaging plays a pivotal role in identifying candidates for peptide receptor radionuclide therapy. Sufficient receptor expression is a prerequisite for treatment eligibility. However, several important limitations of SSTR-based imaging must be considered: - Meningiomas show substantial heterogeneity in SSTR expression both within a single tumor and across multiple lesions. This may result in uneven tracer uptake. - SSTR expression may change over time, particularly after surgery or radiotherapy. This highlights the importance of performing molecular imaging close to the time when PRRT is being considered. - False-positive uptake may occur due to physiological SSTR expression in structures such as the pituitary gland, venous sinuses, or inflammatory tissue. This is particularly relevant in anatomically complex skull base regions. Importantly, tracer uptake intensity does not necessarily reflect how sensitive the tumor is to radiation. High standardized uptake values (SUVs) alone do not guarantee therapeutic efficacy. These considerations underscore that SSTR imaging should be interpreted together with anatomical imaging, clinical presentation, and prior treatment history. It should not serve as a stand-alone decision-making tool. Beyond lesion detection, molecular imaging also contributes to radiotherapy planning. Filippi and colleagues demonstrated that integrating SSTR-targeted PET with MRI significantly improves lesion delineation. This is particularly true for meningiomas located at the skull base or near the falx cerebri (the fold of tissue that separates the two halves of the brain). Better delineation enables more precise target volume definition and potentially reduces irradiation of adjacent critical structures. Collectively, conventional MRI and SSTR-targeted molecular imaging provide complementary anatomical and biological information. Both are essential for accurate diagnosis, treatment planning, and patient selection. Ongoing developments in quantitative imaging may further refine the diagnostic and predictive value of SSTR imaging in the future. These developments include volumetric assessment and advanced PET analysis. This refinement is particularly relevant in the context of personalized radionuclide therapy. ## Current Standard Treatments for Meningiomas The management of meningiomas must be individualized. The decision to treat depends on tumor size, anatomical location, growth dynamics, and the presence or progression of neurological symptoms. Many incidentally detected or slowly growing meningiomas can be managed conservatively with active surveillance. Intervention becomes necessary when there is documented tumor progression or the development of new or worsening neurological deficits. These deficits are often related to critical tumor size or involvement of eloquent structures (areas of the brain responsible for important functions such as speech or movement). Surgical resection and radiotherapy remain the established, evidence-based cornerstones of meningioma treatment. Whenever feasible, maximal safe surgical resection is the preferred first-line approach. Long-term disease control is strongly influenced by both the extent of resection and the underlying biological aggressiveness of the tumor. Despite advances in neurosurgical techniques and radiation delivery, meningiomas — particularly higher-grade lesions — remain prone to recurrence and progression, even after apparently optimal local treatment. Radiotherapy plays a central role as an adjuvant (additional) or definitive treatment modality. It is especially important for incompletely resected tumors, higher-grade meningiomas, or surgically inaccessible lesions. Modern radiotherapy techniques, including fractionated external-beam radiotherapy and stereotactic approaches, have improved local control while limiting toxicity to surrounding critical structures. Nevertheless, a clinically relevant subset of patients ultimately develops recurrent or progressive disease despite prior surgery and radiotherapy. Importantly, even WHO grade I meningiomas can pose significant therapeutic challenges when located in anatomically complex regions such as the skull base or cavernous sinus. In these locations, surgical morbidity is high and complete resection is often not achievable. In patients who are no longer candidates for further surgical or radiotherapeutic intervention, treatment options become limited. Management decisions increasingly focus on disease stabilization and symptom control rather than curative intent. In this setting, systemic therapies and other non-standard approaches have been explored. However, robust evidence supporting their efficacy remains lacking. To date, no systemic treatment has demonstrated consistent, practice-changing benefit in meningioma. No randomized controlled trials have established an effective standard systemic therapy. Various targeted agents and multikinase inhibitors have been investigated, with reports of disease stabilization or occasional partial responses in small, non-randomized cohorts. In particular, inhibitors of vascular endothelial growth factor (VEGF) signaling have shown some potential to slow tumor progression in heavily pretreated patients. However, responses are typically modest and transient. Overall, these approaches remain investigational and are generally considered palliative. Taken together, current standard-of-care strategies for meningioma rely predominantly on local treatment modalities. Effective systemic options remain an unmet clinical need. This therapeutic gap has prompted increasing interest in biologically targeted approaches that exploit molecular features shared across meningioma subtypes. Among these, somatostatin receptor-directed strategies have gained particular attention. ## Peptide Receptor Radionuclide Therapy (PRRT) Among the major innovations in nuclear medicine, theranostic concepts represent a paradigm shift. Theranostics enables individualized, target-specific therapeutic approaches that extend beyond conventional oncologic management. This strategy is based on using a diagnostic imaging tracer to visualize a tumor-specific molecular target in the body. This is followed by administration of the same or an analogous molecule labeled with an alpha- or beta-emitting radionuclide for therapeutic purposes. Somatostatin receptor-targeted theranostics have been successfully established in patients with neuroendocrine tumors and have subsequently been explored as a potential treatment option in meningioma. At present, randomized clinical trials involving large patient groups are not available to evaluate the efficacy of PRRT in meningioma. Consequently, PRRT has not been approved by regulatory authorities such as the FDA (U.S. Food and Drug Administration) or EMA (European Medicines Agency) for this indication. It is currently considered an investigational treatment option. In the absence of meningioma-specific protocols, treatment regimens have largely been extrapolated from established neuroendocrine tumor protocols. This practice introduces uncertainty regarding optimal dosing, cycle number, and patient selection. Recommendations for the application of PRRT in meningioma are informed by joint guidance. This joint guidance comes from the IAEA (International Atomic Energy Agency) and EANM (European Association of Nuclear Medicine). This joint guidance also comes from RANO (Response Assessment in Neuro-Oncology) and SNMMI (Society of Nuclear Medicine and Molecular Imaging). Patient selection criteria and radiopharmaceutical use are commonly based on the NANETS/SNMMI consensus statement. It should be noted, however, that these recommendations are primarily derived from experience in neuroendocrine tumors and have not been prospectively validated in meningioma populations. The most widely used radiopharmaceuticals for SSTR-directed radionuclide therapy are: - [177Lu]Lu-DOTATATE or [177Lu]Lu-DOTATOC (lutetium-177 labeled) - [90Y]Y-DOTATATE or [90Y]Y-DOTATOC (yttrium-90 labeled) In patients with impaired kidney function, [177Lu]Lu-DOTATATE is generally preferred because it has a lower incidence of kidney toxicity. The commonly applied administered activities are 7.4 GBq (gigabecquerels) for 177Lu-labeled compounds and 3.7 GBq for 90Y-labeled compounds. These reflect standard practice rather than meningioma-specific optimization. The number of PRRT cycles typically ranges from two to five. Four cycles represent the most frequently applied regimen. Intervals between treatment cycles usually range from 6 to 12 weeks. If a cycle cannot be administered within the recommended timeframe, treatment may be postponed for up to 16 weeks without requiring modification of the overall treatment plan. It should be emphasized that these dosing schemes and cycle numbers originate from neuroendocrine tumor practice and remain empirical in the context of meningioma. In patients with relapsed or refractory meningiomas, PRRT should be considered only after confirmation of elevated somatostatin receptor expression by recent hybrid imaging (SPECT/CT or PET/CT). This imaging should preferably be performed within two months prior to treatment initiation. A recent brain MRI, ideally obtained within two weeks, should also be available. Additional eligibility requirements generally include: - A Karnofsky performance status of at least 60% (a measure of how well a patient can carry out daily activities) - An ECOG score not exceeding 2 (another measure of functional status, where lower numbers indicate better function) - Baseline assessment of kidney, liver, and bone marrow function, following laboratory criteria outlined in the corresponding guidelines Discontinuation of long-acting somatostatin analogues and corticosteroids prior to PRRT is advised. These agents may interfere with receptor targeting or downregulate SSTR expression. Radiopharmaceuticals are typically administered via intravenous infusion. Two intravenous accesses are recommended — one for the radiopharmaceutical and one for the amino acid solution. Alternative approaches such as dual-chamber ports, alternating infusion through a single catheter, or intra-arterial administration may be considered in selected cases. Positively charged amino acids, such as L-lysine and/or L-arginine, are co-administered to reduce kidney toxicity. These amino acids work by competitively inhibiting the reabsorption of the radioligand in the proximal tubules of the kidney. Antiemetic prophylaxis (medication to prevent nausea and vomiting), commonly with metoclopramide or ondansetron, is recommended prior to amino acid infusion and may be repeated if necessary. The radiopharmaceutical is typically administered with physiological saline over 10 to 30 minutes using gravity infusion, infusion pumps, or automated syringe systems. All procedures must be conducted in compliance with local radiation safety regulations. Adequate hydration, reinforced personal hygiene measures, and continuous monitoring by qualified personnel are essential components of safe PRRT delivery. Available evidence suggests that PRRT is generally well tolerated, with predominantly manageable and reversible adverse effects. While most toxicity data originate from large neuroendocrine tumor cohorts, smaller retrospective studies in meningioma patients report comparable safety profiles. According to the Common Terminology Criteria for Adverse Events (CTCAE), grade 3 and 4 toxicities are mainly transient hematologic events (blood-related side effects). These include: - Neutropenia (low white blood cell count) — reported in approximately 1% of patients in large neuroendocrine tumor series - Thrombocytopenia (low platelet count) — reported in approximately 2% of patients - Lymphopenia (low lymphocyte count) — reported in approximately 9% of patients The most frequently observed adverse events are grade 1–2 nausea and vomiting. These are largely attributed to the amino acid co-infusion and typically resolve after completion of treatment. In an ongoing prospective study evaluating [177Lu]Lu-DOTATATE in meningioma, adverse events were reported in approximately 10% of patients receiving four or more treatment cycles. No grade 4 toxicities were confirmed by laboratory analysis. Although encouraging safety profiles and signs of clinical activity have been reported in available PRRT studies involving refractory meningioma patients, comprehensive and methodologically homogeneous evidence remains limited. This narrative review is therefore based on a structured literature search of PubMed. The search included preclinical studies, retrospective clinical series, prospective trials, and relevant consensus guidelines published up to 2025. Case reports and conference abstracts without full-text availability were excluded. Given the heterogeneity of the available data, the aim was not to provide an exhaustive systematic review. Instead, the goal was a critical synthesis of biologically and clinically relevant evidence. ## Preclinical Studies: The Foundation of PRRT Research Preclinical investigations serve as the foundational basis for the development of medical therapies, and PRRT is no exception. This section focuses first on available tumor models, which play a pivotal role in determining the translational relevance of radiobiological experiments. Following the description of tumor models, the authors address various approaches to radiopharmaceutical modulation. These include optimization strategies related to the choice of radionuclide, for example, beta-emitters versus alpha-emitters. These include optimization strategies related to the targeting vector or pharmacophore. These include optimization strategies related to improvements in the overall potency and stability of the compound. Preclinical studies have also explored the possibility of modifying the tumor microenvironment to enhance radionuclide uptake or therapeutic response. Finally, emerging combination strategies have been reported at the preclinical stage to improve PRRT efficacy. These include the use of radiosensitizing agents, DNA repair inhibitors, immunotherapies, or integration with external beam radiation. **Meningioma Models** Meningiomas exhibit pronounced intra-tumoral and inter-patient heterogeneity at the cellular, transcriptional, and microenvironmental levels. This poses a fundamental challenge for preclinical modeling. Recent human longitudinal single-cell and spatial transcriptomic analyses have demonstrated that individual meningiomas comprise multiple coexisting tumor cell states. These cell states can dynamically evolve over time, particularly during progression from primary to recurrent disease. These studies further reveal substantial variability in proliferative activity, metabolic programs, and DNA damage-response signatures both within and between tumors. In parallel, the tumor microenvironment — the surrounding cells, blood vessels, and immune cells — contributes to treatment resistance and may influence how well radionuclide therapy works. Preclinical models that account for this complexity are essential for testing new PRRT approaches and predicting which patients are most likely to benefit. ## Clinical Implications: What This Means for Patients For patients with aggressive or recurrent meningiomas, PRRT represents a promising investigational option when surgery and radiotherapy have been exhausted. The key clinical implications from this review are: - **A targeted approach:** PRRT delivers radiation directly to tumor cells by targeting somatostatin receptors, which are present on the majority of meningiomas regardless of grade. This means that even some higher-grade tumors may be eligible for this treatment. - **Theranostic pairing:** The same molecular target used for imaging can be used for treatment. This allows doctors to first confirm that a patient's tumor expresses sufficient somatostatin receptors before proceeding with therapy. - **Preserved target in recurrent disease:** SSTR expression is often maintained even in tumors that have returned after previous treatments. This makes PRRT a viable option even in advanced settings. - **Manageable safety profile:** Available evidence suggests that PRRT is generally well tolerated. Most side effects are mild to moderate and reversible, with grade 3–4 blood-related toxicities occurring in approximately 1–9% of patients in large neuroendocrine tumor series. - **Not yet approved for meningioma:** PRRT has not been approved by the FDA or EMA for meningioma. It is considered an investigational treatment option and should be discussed carefully with a multidisciplinary care team. Patients who may be candidates for PRRT typically have recurrent or refractory meningioma that has progressed despite surgery and radiotherapy. They must have confirmed elevated somatostatin receptor expression on recent imaging, adequate organ function, and a performance status that allows them to undergo treatment. ## Limitations: What the Study Could Not Prove The authors acknowledge several important limitations of the current evidence: - **No randomized controlled trials:** At present, no randomized clinical trials involving large patient cohorts are available to evaluate the efficacy of PRRT in meningioma. This means that the true benefit of PRRT compared with other treatments remains uncertain. - **Extrapolated protocols:** Treatment regimens have largely been extrapolated from neuroendocrine tumor protocols. This introduces uncertainty regarding optimal dosing, cycle number, and patient selection for meningioma specifically. - **Heterogeneous data:** The available clinical literature is heterogeneous, making it difficult to draw firm conclusions. Most studies are retrospective and involve small numbers of patients. - **Imaging limitations:** SSTR expression can vary within a single tumor and across multiple lesions. It can also change over time, particularly after surgery or radiotherapy. Tracer uptake intensity does not necessarily predict how well a tumor will respond to treatment. - **No standard systemic therapy exists:** To date, no systemic treatment has demonstrated consistent, practice-changing benefit in meningioma. No randomized controlled trials have established an effective standard systemic therapy. - **Preclinical modeling challenges:** Meningioma heterogeneity poses a fundamental challenge for preclinical modeling. Tumor models may not fully capture the complexity of human meningioma. ## Recommendations and Future Directions Based on the current evidence, the authors make the following observations and recommendations: 1. **PRRT should be considered only in specialized centers** with experience in radionuclide therapy and multidisciplinary care of meningioma patients. 1. **Patient selection is critical.** Candidates should have confirmed elevated somatostatin receptor expression on recent hybrid imaging (SPECT/CT or PET/CT), preferably within two months prior to treatment initiation. 1. **Baseline organ function must be assessed** before treatment, including kidney, liver, and bone marrow function. 1. **Long-acting somatostatin analogues and corticosteroids should be discontinued** prior to PRRT, as these agents may interfere with receptor targeting. 1. **Further prospective trials are needed** to define the optimal clinical application of PRRT in meningioma. These trials should establish standardized protocols for dosing, cycle number, and patient selection. 1. **Advances in dosimetry, quantitative imaging, and radiomics** are beginning to refine patient selection and improve response prediction. These tools may help identify which patients are most likely to benefit from PRRT. 1. **Combination strategies** — including radiosensitizing agents, DNA repair inhibitors, immunotherapies, or integration with external beam radiation — are being explored at the preclinical stage and may improve PRRT efficacy in the future. In conclusion, current evidence highlights the therapeutic potential of radionuclide therapy in aggressive or refractory meningiomas. The authors underscore the need for further prospective trials to define its optimal clinical application. For patients who have exhausted standard treatment options, PRRT represents a biologically rational investigational approach that warrants discussion with a specialized care team. ## Frequently Asked Questions ### What is PRRT and how does it work for meningioma? PRRT is an investigational treatment that attaches radioactive isotopes to a molecule that binds somatostatin receptors, which are present on most meningiomas regardless of grade. It delivers continuous low-dose radiation directly to tumor cells. It is not approved by the FDA or EMA for meningioma and is only available in specialized centers with experience in radionuclide therapy. ### Who might be eligible for PRRT? Candidates typically have recurrent or refractory meningioma that has progressed despite surgery and radiotherapy. They must have confirmed elevated somatostatin receptor expression on recent hybrid imaging, preferably within two months before treatment. Other requirements include adequate kidney, liver, and bone marrow function, a Karnofsky performance status of at least 60%, and an ECOG score no higher than 2. ### What happens during a PRRT infusion? The radiopharmaceutical is given through an intravenous line, usually over 10 to 30 minutes. You also receive an amino acid solution through a second IV line to protect your kidneys. Anti-nausea medication is given beforehand. The procedure follows local radiation safety rules, and you will be monitored by qualified staff. Hydration and personal hygiene measures are important. ### What are the common side effects of PRRT? The most frequent side effects are mild to moderate nausea and vomiting, largely from the amino acid infusion, which usually resolve after treatment. Serious blood-related side effects are uncommon: in large neuroendocrine tumor series, low white blood cell count occurred in about 1%, low platelets in about 2%, and low lymphocytes in about 9% of patients. Most side effects are manageable and reversible. ### How many PRRT cycles will I need and how often? The number of cycles typically ranges from two to five, with four cycles being the most common regimen. Intervals between cycles usually range from 6 to 12 weeks. If a cycle cannot be given within that timeframe, treatment may be postponed for up to 16 weeks without changing the overall plan. These schedules are based on neuroendocrine tumor practice, not meningioma-specific studies. ### Why do I need a somatostatin receptor imaging scan before PRRT? The scan confirms that your tumor expresses enough somatostatin receptors for PRRT to work. It is usually done with PET/CT or SPECT/CT within two months before treatment. However, high tracer uptake does not guarantee that the tumor will respond to radiation. The scan results are interpreted together with MRI, your symptoms, and treatment history, not as a stand-alone decision tool. ### When should a patient with recurrent or refractory meningioma seek a second opinion about PRRT? A second opinion is worth seeking when surgery and radiotherapy have been exhausted and PRRT is being considered. PRRT is not approved by the FDA or EMA for meningioma and remains investigational, with regimens extrapolated from neuroendocrine tumor protocols, so dosing, cycle number, and patient selection are uncertain. Eligibility requires confirmed elevated somatostatin receptor expression on recent SPECT/CT or PET/CT, adequate kidney, liver, and bone marrow function, and suitable performance status. Because PRRT should be given only in specialized centers with multidisciplinary experience, an independent review can clarify whether these criteria are met. Diagnostic Detectives Network provides independent expert second opinions. ## Source Information **Original article title:** Radioligand Therapy in Meningiomas: Today's Evidence, Tomorrow's Possibilities. **Authors:** Sipka G, Apro K, Farkas I, Bakos A, Dobi A, Hideghety K, Pavics L, Dosa S, Radics B, Balazsfi M, Barzo P, Szolikova M, Besenyi Z. **Affiliations:** Department of Nuclear Medicine and Theranostics, University of Szeged, Hungary; Department of Oncotherapy, University of Szeged, Hungary; Department of Pathology, University of Szeged, Hungary; Department of Neurosurgery, University of Szeged, Hungary; Mediso Ltd., Budapest, Hungary **Journal:** Cancers 2026, 18, 297 **Publication details:** Received: 19 December 2025; Revised: 14 January 2026; Accepted: 16 January 2026; Published: 18 January 2026 **DOI:** https://doi.org/10.3390/cancers18020297 **Keywords:** meningioma; Lu-DOTATATE; PRRT; theranostic *This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and should not replace consultation with a qualified healthcare provider. Patients should discuss their individual treatment options with their medical team.* --- Publisher: Diagnostic Detectives Network (https://diagnosticdetectives.com) — independent multi-expert medical second opinions, worldwide, private-pay. Author byline: Anton Titov, MD, PhD. Contact: https://diagnosticdetectives.com/pages/contact Canonical page: https://diagnosticdetectives.com/products/radioligand-therapy-for-meningiomas-what-todays-evidence-shows-and-what-the-future-may-hold