OBJECTIVE:Meningiomas and gliomas are common adult brain tumors often linked to cognitive impairments. Meningiomas are frequently overlooked as a potential contributor to such impairments, due to their benign, extra-axial, and slow-growing nature. This systematic review compares the type and frequency of cognitive impairments associated with these brain tumors, prior to any therapeutic intervention. METHOD:Systematic search conducted in ProQuest, PubMed, Scopus, and Cochrane Library identified records on cognitive status of adults with untreated, nonrecurrent gliomas or meningiomas, published between January 01, 2000 and October 01, 2025. Studies using a comprehensive, test-based cognitive evaluation and strict exclusion criteria were included. RESULTS:Seventy studies (4,277 patients) with minimal risk of bias met the inclusion criteria. Although cross-study comparisons were hampered by heterogeneity in statistical thresholds, reported metrics, inclusion criteria, and neuropsychological assessments, the findings consistently indicated significant impairments across multiple cognitive domains, with comparable prevalence in gliomas and symptomatic meningiomas. Memory and executive impairments prevailed in gliomas, while executive and attentional impairments predominated in meningiomas. CONCLUSIONS:Cognitive impairments are highly prevalent in patients with symptomatic meningiomas or gliomas. While gliomas do not consistently result in a higher frequency of impairments, this review highlights slight differences in the cognitive domains affected. The role of tumor growth and intra-axial location in cognitive outcomes remains unclear. Comparative studies based on strict inclusion/exclusion criteria and comprehensive neuropsychological evaluations are essential for a better understanding of the pathophysiology of cognitive impairments associated with primary brain tumors. Existing guidelines should be followed to harmonize assessments and enable comparisons. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Breast cancer (BC) is the second leading cause of central nervous system (CNS) metastases, which include leptomeningeal metastasis (5%) and parenchymal brain metastasis (95%). Among BC subtypes, triple-negative breast cancer (TNBC) accounts for around 15-20% of all cases. This subtype is one of the most aggressive, with a higher risk of developing breast cancer brain metastases (BCBM). Brain metastases (BM) occur in approximately 10-30% of patients with advanced metastatic BC and are associated with poor prognosis. Recent studies suggest that cancer cells undergo metabolic reprogramming upon establishing in the brain, but the specific metabolic shifts remain unclear. This study aims to elucidate the metabolic signatures of BCBM xenograft cell lines by examining the expression of key genes involved in various metabolic pathways, with the ultimate goal of identifying novel therapeutic targets to hinder the progression of brain metastases. To achieve this, we developed a mouse model of brain metastasis by injecting human breast cancer cells (MDA-MB-231) intracranially into immunodeficient mice. These injections were repeated three successive times, allowing us to harvest xenografted BCBM cells that progressively adapted to the brain environment with each injection. Cancer cell lines represent an effective way of modelling the disease. The BCBM xenograft cells, named BR1/BR2/BR3 to refer to the number of passages in the brain, were molecularly characterized using FACS and Short Tandem Repeat (STR) analysis to ensure the purity of the cell lines. We conducted transcriptomic analysis based on RNA purification and quantification to explore the modifications between our various brain xenograft cell lines.Our in vivo models demonstrated increased tumour aggressiveness, as indicated by a significant decrease in mouse survival rates correlated with the number of cycles of intracranial injections (Log-rank test, p < 0.001). These findings suggest genotypic modifications in our BCBM xenograft cell lines. Based on Bulk RNA-sequencing database, the Principal Component Analysis (PCA) plot revealed similarities between the BR2 and BR3 cell lines, which differ markedly from the Parental and BR1 cell lines. Moreover, the heatmap of Euclidean distances between the samples, based on normalised DESeq2 gene expression, supports this observation by showing similar gene expression profiles between the BR2 and BR3 lines. By selecting the human Reactome gene sets (C2 collection - GSEA database) to generate a more detailed heatmap, we identified the metabolic pathways differentiating the Parental and BR1 cell lines from the BR2 and BR3 cell lines. These key pathways include the integration of energy metabolism, lipid metabolism, and nucleotide metabolism. The comparison of the overall gene expression in the Parental cells with the BR1, BR2 or BR3 cell lines by volcano plot confirms several up- and down-regulated genes, including those involved in lipid metabolism (significant results for an adjusted P-value < 0.05 and for a Log2(Fold Change) threshold of 1). Finally, RT-qPCR revealed significant upregulation of gene sets involved in the beta-oxidation pathway (Two-way ANOVA with Tukey’s Post Hoc test, p < 0.05), indicating a shift towards fatty acid metabolism during tumour progression in the brain. These findings suggest that metabolic adaptation is a critical feature of BCBM progression. To validate our results from the transcriptomic analysis, further proteomic and metabolomic analyses are required. These additional studies could pave the way for novel therapeutic strategies targeting specific metabolic pathways, potentially improving treatment outcomes for patients with BCBM. Citation Format: Julie Marin, Nadège Kindt, Sébastien Boutry, Lionel Larbanoix, Matteo Serra, Christos Sotiriou, Florence Lefranc, Fabrice Journé, Ghanem E Ghanem, Ahmad Awada. Metabolic Reprogramming in Breast Cancer Brain Metastasis Mouse Model: Insights from Transcriptomic Analysis [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2024; 2024 Dec 10-13; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(12 Suppl):Abstract nr P1-09-21.

Over the past decade, neuropathological diagnosis has undergone significant changes, integrating morphological features with molecular biomarkers. The molecular era has successfully refined neuropathological diagnostic accuracy; however, a substantial number of CNS tumor diagnoses remain challenging, particularly in children. DNA methylation classification has emerged as a powerful machine learning approach for clinical decision-making in CNS tumors. The aim of this study is to share our experience using DNA methylation classification in daily routine practice, illustrated through clinical cases. We employed a classification system to evaluate discrepancies between histo-molecular and DNA methylation diagnoses, with a specific focus on adult versus pediatric CNS tumors. In our study, we observed that 40% of cases fell into Class I, 47% into Class II, and 13% into Class III among the "matched cases" (>= 0.84). In other words, DNA methylation classification confirmed morphological diagnoses in 63% of adult and 23% of pediatric cases. Refinement of diagnosis was particularly evident in the pediatric population (65% vs. 21% for the adult population, p = 0.006). Additionally, we discussed cases classified with low calibrated scores. In conclusion, our study confirms that DNA methylation classification provides significant added-value for CNS tumors diagnosis, particularly in pediatric cases.

The inadequate vascularization seen in fast-growing solid tumors gives rise to hypoxic areas, fostering specific changes in gene expression that bolster tumor cell survival and metastasis, ultimately leading to unfavorable clinical prognoses across different cancer types. Hypoxia-inducible factors (HIF-1 and HIF-2) emerge as druggable pivotal players orchestrating tumor metastasis and angiogenesis, thus positioning them as prime targets for cancer treatment. A range of HIF inhibitors, notably natural compounds originating from marine organisms, exhibit encouraging anticancer properties, underscoring their significance as promising therapeutic options. Bioprospection of the marine environment is now a well-settled approach to the discovery and development of anticancer agents that might have their medicinal chemistry developed into clinical candidates. However, despite the massive increase in the number of marine natural products classified as ‘anticancer leads,’ most of which correspond to general cytotoxic agents, and only a few have been characterized regarding their molecular targets and mechanisms of action. The current review presents a critical analysis of inhibitors of HIF-1 and HIF-2 and hypoxia-selective compounds that have been sourced from marine organisms and that might act as new chemotherapeutic candidates or serve as templates for the development of structurally similar derivatives with improved anticancer efficacy.

Abstract Background: Central nervous system (CNS) metastases display molecular alterations that differ from primary tumors and metastatic sites, which might confer special CNS sensitivity for targeted treatments. Brain biopsies are an invasive approach and liquid biopsies (LB) are therefore being investigated as a potential tool for detecting these molecular alterations in cerebrospinal fluid (CSF) ctDNA. Methods: The BrainStorm program (NCT04109131) is an international, prospective, interventional study aiming to build a large clinico-pathological database to investigate the development of CNS metastases: (A) before the diagnosis; (B) at diagnosis; and (C) after the diagnosis of CNS metastases. Molecular landscape of CSFctDNA was analyzed and explored as a surrogate for CNS tumor tissue DNA using large next-generation sequencing panels in tumor tissue and tumor-informed targeted gene panels in LB (OncoDEEP®/OncoFOLLOW®) for patients (pts) included in Part (B). Results: As of October 2023, CSF was available for 30 out of 67 pts included in Part (B) of the study and analyses were performed for 12 matched extra-CNS tumor, plasma and CSF samples. The 12 cases were derived from pts with breast cancer (BC) (luminal n=6; triple negative (TN) n=2; HER2-positive n=4) and among them 4 pts were diagnosed with leptomeningeal metastases (LM). CSFctDNA was detectable in 7 out of the 12 CSF samples (58%) and in 3 out of 4 pts with LM (75%). In pts with detectable CSFctDNA, detection rate for known pathogenic molecular alterations was 80% (Table 1). No safety concerns from lumbar puncture were identified. Conclusion: The use of CSFctDNA as a surrogate for tumor tissue DNA in CNS metastases appears to be a feasible and safe approach. Clinically actionable alterations have been identified in CSFctDNA of pts with BC. Further results will be presented at a later stage. TABLE 1: NAND Table 1: Pathogenic molecular alterations in matched tumor, plasma and CSF from pts with detectable CSFctDNA Tumor type Extra-CNS tumor tissue Plasma CSF TNBC PIK3Ca pH1047R PIK3Ca pH1047R PIK3Ca pH1047R Luminal BC PIK3Ca Q546R PIK3Ca Q546R PIK3Ca Q546R Luminal (LM) None KRAS pG13D None Luminal BC BRCA2 p.Y1655, PIK3CA pE545K BRCA2 pY1655, PIK3CA pE545K BRCA2 pY1655, PIK3CA pE545K TNBC (LM) None None None Luminal (LM) ESR1 D538G, PIK3CA H1047R ESR1 D538G, PIK3CA H1047R ESR1 D538G, PIK3CA H1047R HER2-positive BC ErbB2 amplification None None Citation Format: Nuria Kotecki, Diogo Martins-Branco, Guilherme Nader-Marta, Andrea Gombos, Philippe Barthelemy, Anthony Gonçalves, Edith Borcoman, Florian Clatot, Stéphane Holbrechts, Eleonora Stephane de Maio D’Esposito, Claire Cheymol, Vincent Vanhaudenarde, François Duhoux, Caroline Duhem, Paul Clement, Lore Decoster, Hannelore Denys, Florence Lefranc, Jean-Luc Canon, Joseph Gligorov, Luca Arecco, Nadège Kindt, Ahmad Awada. CSFctDNA as a surrogate for tumor tissue DNA in BC pts with CNS metastases: First results from the Brainstorm program (Oncodistinct 006) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr CT202.

The management of primary central nervous system (PCNSL) is one of the most controversial topics in neuro-oncology because of the complexity of the disease and the limited number of controlled studies available. In 2021, given recent advances and the publication of practice-changing randomized trials, the European Association of Neuro-Oncology (EANO) created a multidisciplinary task force to update the previously published evidence-based guidelines for immunocompetent adult patients with PCNSL and added a section on immunosuppressed patients. The guideline provides consensus considerations and recommendations for the treatment of PCNSL, including intraocular manifestations and specific management of the elderly. The main changes from the previous guideline include strengthened evidence for the consolidation with ASCT in first-line treatment, prospectively assessed chemotherapy combinations for both young and elderly patients, clarification of the role of rituximab even though the data remain inconclusive, of the role of new agents, and the incorporation of immunosuppressed patients and primary ocular lymphoma. The guideline should aid the clinicians in everyday practice and decision making and serve as a basis for future research in the field.

Importance A potential relationship between meningioma and breast cancer was suggested 70 years ago. However, to date, no conclusive evidence is available on this topic. Objective To provide a comprehensive review of the literature on the association of meningioma with breast cancer, supported by a meta-analysis. Data Sources A systematic PubMed search was performed up to April 2023 to identify articles on the association of meningioma with breast cancer. The following key words were used strategically: meningioma , breast cancer , breast carcinoma , association , relation . Study Selection All studies reporting women diagnosed with meningioma and breast cancer were identified. The search strategy was not limited by study design or publication date but only included articles in English. Additional articles were identified via citation searching. Studies reporting a complete population of meningiomas or breast cancer patients throughout a specific study period and a proportion of patients with a second pathology could be used for the meta-analysis. Data Extraction and Synthesis Data extraction was performed by 2 authors in accordance with the Preferred Reporting Items for Systematic Reviews (PRISMA) statement. Meta-analyses regarding both populations were performed using a random-effects model. Risk of bias was assessed. Main Outcomes and Measures The main measures were whether there was an increased prevalence of breast cancer in female patients with meningioma and whether there was an increased prevalence of meningioma in female patients with breast cancer. Results A total of 51 retrospective studies (case reports, case series, and cancer registry reports) describing 2238 patients with both diseases were identified; 18 studies qualified for prevalence analyses and meta-analysis. The random-effects meta-analysis (13 studies) revealed a significantly greater prevalence of breast cancer in female patients with meningioma than in the overall population (odds ratio [OR], 9.87; 95% CI, 7.31-13.32). Meningioma incidence in patients with breast cancer (11 studies) was greater than that in the baseline population; however, the difference according to the random-effects model was not statistically significant (OR, 1.41; 95% CI, 0.99-2.02). Conclusions and Relevance This large systematic review and the meta-analysis on the association between meningioma and breast cancer found nearly 10-fold higher odds of breast cancer in female patients with meningioma compared with the general female population. These findings suggest that female patients with meningioma should be screened more intensively for breast cancer. Further research is required to identify the factors causing this association.

Task-based BOLD fMRI and DTI-fiber tracking have become part of the routine presurgical work-up of brain tumor patients in many institutions. However, their potential impact on both surgical treatment and neurologic outcome remains unclear, in despite of the high costs and complex implementation. We retrospectively investigated whether performing fMRI and DTI-ft preoperatively substantially impacted surgical planning and patient outcome in a series of brain tumor patients. We assessed (i) the quality of fMRI and DTI-ft results, by using a scale of 0–2 (0 = failed mapping; 1 = intermediate confidence; 2 = good confidence), (ii) whether functional planning substantially contributed to defining the surgical strategy to be undertaken (i.e., no surgery, biopsy, or resection, with or without ESM), the surgical entry point and extent of resection, and (iii) the incidence of neurological deficits post-operatively. Twenty-seven patients constituted the study population. The mean confidence rating was 1.9/2 for fMRI localization of the eloquent cortex and lateralization of the language function and 1.7/2 for DTI-ft results. Treatment strategy was altered in 33

Depressive symptoms are common among patients with glioblastoma, but patients are often not treated with antidepressants. There is only limited evidence on the association of antidepressant drug use with survival in glioblastoma. We performed a pooled analysis of patients treated within the CENTRIC, CORE, AVAglio and ACT‐IV trials to explore the relation of antidepressant drug use with progression‐free (PFS) and overall survival (OS) at baseline, at the start of maintenance therapy and at the start of maintenance cycle 4. We further assessed the association of antidepressant drugs with seizure, cognition, fatigue and a diagnosis of depression. Among more than 1700 patients, we found no significant association between the use of antidepressants at baseline or at the start of maintenance therapy and PFS or OS. However, we found OS, but not PFS, to be significantly worse in patients using antidepressants at the start of maintenance cycle 4. After adjustment for antiepileptic drug use and despite showing a trend for increased risk, seizures were not significantly associated with antidepressant drug use, nor was there a change in mini mental state examination (MMSE) scores or fatigue by antidepressant drug use at baseline. However, there was a significant positive association between antidepressant use at the start of maintenance treatment and fatigue during maintenance treatment. The association of antidepressant use at the start of maintenance cycle 4 with inferior OS of glioblastoma patients requires independent confirmation and further study. Further prospective trials should evaluate efficacy, side effects and associations with outcome of antidepressants in glioblastoma.

Abstract BACKGROUND Median survival with glioblastoma remains in the range of 12 months on population levels. Only few patients survive for more than 5 years. Patient and disease features associated with long-term survival remain poorly defined. METHODS European Organization for Research and Treatment of Cancer (EORTC) 1419 (ETERNITY) is a registry study supported by the Brain Tumor Funders Collaborative in the US and by the EORTC Brain Tumor Group. Patients with glioblastoma surviving at least 5 years from diagnosis were identified at 24 sites in Europe, US, and Australia. In patients with isocitrate dehydrogenase (IDH) wildtype tumors, prognostic factors were analyzed using the Kaplan-Meier method and the Cox proportional hazards model. A population-based reference cohort was obtained from the Cantonal cancer registry Zurich. RESULTS At the database lock of July 2020, 280 patients with histologically centrally confirmed glioblastoma (189 IDH wildtype, 80 IDH mutant, 11 incompletely characterized) had been registered. In the IDH wildtype population, median age was 56 years (range 24-78 years), 96 patients (50.8%) were female, 139 patients (74.3%) had tumors with O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. Median overall survival was 9.9 years (95% CI 7.9-11.9). Patients without recurrence experienced longer median survival (not reached) than patients with one or more recurrences (8.92 years) (p<0.001) and had a high rate (48.8%) of MGMT promoter unmethylated tumors. CONCLUSION s Freedom from progression is a powerful predictor of overall survival in long-term survivors with glioblastoma. Patients without relapse often have MGMT promoter-unmethylated glioblastoma and may represent a distinct subtype of glioblastoma.

ImportanceA potential relationship between meningioma and breast cancer was suggested 70 years ago. However, to date, no conclusive evidence is available on this topic. ObjectiveTo provide a comprehensive review of the literature on the association of meningioma with breast cancer, supported by a meta-analysis. Data SourcesA systematic PubMed search was performed up to April 2023 to identify articles on the association of meningioma with breast cancer. The following key words were used strategically: meningioma, breast cancer, breast carcinoma, association, relation. Study SelectionAll studies reporting women diagnosed with meningioma and breast cancer were identified. The search strategy was not limited by study design or publication date but only included articles in English. Additional articles were identified via citation searching. Studies reporting a complete population of meningiomas or breast cancer patients throughout a specific study period and a proportion of patients with a second pathology could be used for the meta-analysis. Data Extraction and SynthesisData extraction was performed by 2 authors in accordance with the Preferred Reporting Items for Systematic Reviews (PRISMA) statement. Meta-analyses regarding both populations were performed using a random-effects model. Risk of bias was assessed. Main Outcomes and MeasuresThe main measures were whether there was an increased prevalence of breast cancer in female patients with meningioma and whether there was an increased prevalence of meningioma in female patients with breast cancer. ResultsA total of 51 retrospective studies (case reports, case series, and cancer registry reports) describing 2238 patients with both diseases were identified; 18 studies qualified for prevalence analyses and meta-analysis. The random-effects meta-analysis (13 studies) revealed a significantly greater prevalence of breast cancer in female patients with meningioma than in the overall population (odds ratio [OR], 9.87; 95% CI, 7.31-13.32). Meningioma incidence in patients with breast cancer (11 studies) was greater than that in the baseline population; however, the difference according to the random-effects model was not statistically significant (OR, 1.41; 95% CI, 0.99-2.02). Conclusions and RelevanceThis large systematic review and the meta-analysis on the association between meningioma and breast cancer found nearly 10-fold higher odds of breast cancer in female patients with meningioma compared with the general female population. These findings suggest that female patients with meningioma should be screened more intensively for breast cancer. Further research is required to identify the factors causing this association.

2016 Background: Median survival with glioblastoma remains in the range of 12 months on population levels. Only few patients survive for more than 5 years. Patient and disease features associated with long-term survival remain poorly defined. Methods: European Organization for Research and Treatment of Cancer (EORTC) 1419 (ETERNITY) is a registry study supported by the Brain Tumor Funders Collaborative in the US and by the EORTC Brain Tumor Group. Patients with glioblastoma surviving at least 5 years from diagnosis were identified at 24 sites in Europe, US, and Australia. In patients with isocitrate dehydrogenase (IDH) wildtype tumors, prognostic factors were analyzed using the Kaplan-Meier method and the Cox proportional hazards model. A population-based reference cohort was obtained from the Cantonal cancer registry Zurich. Results: At the cut-off of July 2020, 280 patients with histologically centrally confirmed glioblastoma (189 IDH wildtype, 80 IDH mutant, 11 not otherwise specified) had been registered. In the IDH wildtype population, median age was 56 years (range 24-78 years), 96 patients (50.8%) were female, 139 patients (74.3%) had tumors with O 6 -methylguanine DNA methyltransferase ( MGMT) promoter methylation. Median overall survival was 9.9 years (95% CI 7.9–11.9). Patients without recurrence experienced longer median survival (not reached) than patients with one or more recurrences (8.92 years) (p<0.001) and had a high rate of MGMT promoter unmethylated tumors. Conclusions: Freedom from progression is a powerful predictor of overall survival in long-term survivors with glioblastoma. Never relapsing patients often have MGMT promoter-unmethylated glioblastoma and may represent a distinct subtype of glioblastoma. Clinical trial information: NCT03770468 .

Bevacizumab’s use in recurrent high-grade glioma is controversial. This study evaluates outcomes in recurrent high-grade glioma patients receiving bevacizumab alone or combined with chemotherapy as a late-line treatment. We retrospectively analyzed patients treated with bevacizumab alone or combined with chemotherapy for high-grade gliomas who showed tumor progression after multiple treatment attempts. Overall survival (OS) and progression-free survival (PFS) were analyzed with Kaplan–Meier curves. Predictors of PFS according to prognostic variables were assessed with regression analysis. Between 2010 and 2022, 31 consecutive patients received bevacizumab alone or combined with chemotherapy as a late-line treatment for recurrent high-grade gliomas. Of these patients, 14 (45.2

Posterior pituitary tumors (PPT) expressing thyroid transcription factor-1 (TTF-1) are extremely rare low-grade neoplasms. The recent discovery of BRAF mutations in these tumors offers a potential alternative treatment using targeted therapies. We present the case of a 57-year-old female with recurrent BRAFV600E-mutated TTF-1-positive PPT treated with a BRAF inhibitor monotherapy (dabrafenib) leading to tumor regression. After 18 months of uninterrupted treatment, ongoing radiological tumor regression was observed and the patient remained asymptomatic without any significant adverse event. BRAF inhibitor is potentially a valuable treatment option for recurrent TTF-1-positive PPT with BRAF mutation.

Background No systemic treatment has been established for meningioma progressing after local therapies. Methods This randomized, multicenter, open-label, phase II study included adult patients with recurrent WHO grade 2 or 3 meningioma. Patients were 2:1 randomly assigned to intravenous trabectedin (1.5 mg/m2 every 3 weeks) or local standard of care (LOC). The primary endpoint was progression-free survival (PFS). Secondary endpoints comprised overall survival (OS), objective radiological response, safety, quality of life (QoL) assessment using the QLQ-C30 and QLQ-BN20 questionnaires, and we performed tissue-based exploratory molecular analyses. Results Ninety patients were randomized (n = 29 in LOC, n = 61 in trabectedin arm). With 71 events, median PFS was 4.17 months in the LOC and 2.43 months in the trabectedin arm (hazard ratio [HR] = 1.42; 80% CI, 1.00-2.03; P = .294) with a PFS-6 rate of 29.1% (95% CI, 11.9%-48.8%) and 21.1% (95% CI, 11.3%-32.9%), respectively. Median OS was 10.61 months in the LOC and 11.37 months in the trabectedin arm (HR = 0.98; 95% CI, 0.54-1.76; P = .94). Grade ≥3 adverse events occurred in 44.4% of patients in the LOC and 59% of patients in the trabectedin arm. Enrolled patients had impeded global QoL and overall functionality and high fatigue before initiation of systemic therapy. DNA methylation class, performance status, presence of a relevant co-morbidity, steroid use, and right hemisphere involvement at baseline were independently associated with OS. Conclusions Trabectedin did not improve PFS and OS and was associated with higher toxicity than LOC treatment in patients with non-benign meningioma. Tumor DNA methylation class is an independent prognostic factor for OS.

Purpose Embolization of arteriovenous malformations (AVMs) before radiosurgery has been reported to negatively impact the obliteration rate. This study aims to assess treatment outcomes in a series of 190 patients treated by Gamma Knife radiosurgery (GKRS) for previously embolized AVMs. Methods The institutional database of AVMs was retrospectively reviewed between January 2004 and March 2018. The clinical and radiological data of patients treated with GKRS for previously embolized AVMs were analyzed. Predicting factors of obliteration and hemorrhage following GKRS were assessed with univariate and multivariate regression analyses. Results The mean AVM size was significantly reduced after embolization (p < 0.001). The obliteration rate was 78.4%. Multivariate analyses showed that a lower Spetzler-Martin grade (p = 0.035) and a higher marginal dose (p = 0.007) were associated with obliteration. Post-GKRS hemorrhages occurred in 14 patients (7.4%). A longer time between diagnosis and GKRS was the only factor associated with post-GKRS hemorrhages in multivariate analysis (p = 0.022). Complications related to the combined treatment were responsible for a new permanent neurological disability in 20 patients (10.5%), and a case of death (0.5%). Conclusions This study shows that the embolization of AVMs does not have a negative impact on the obliteration rate after radiosurgery. Embolization reduces the AVM size to a treatable volume by GKRS. However, the combined treatment results in an increased complication rate related to the addition of the risks of each treatment modality.