Journal of Neuro-Oncology

BackgroundIn an era characterized by rapid progression in neurosurgical technologies, traditional tools such as the non-navigated two-dimensional intraoperative ultrasound (nn-2D-IOUS) risk being overshadowed. Against this backdrop, this study endeavors to provide a comprehensive and rigorous assessment of the clinical efficacy and surgical relevance of nn-2D-IOUS, specifically in the context of glioma resections. MethodsThis retrospective study undertaken at a single center evaluated 99 consecutive, non-selected patients diagnosed with both high-grade and low-grade gliomas. The primary objective was to assess the proficiency of nn-2D-IOUS in generating satisfactory image quality, identifying residual tumor tissue, and its influence on the extent of resection. To validate these results, early postoperative MRI data served as the reference standard. ResultsThe nn-2D-IOUS exhibited a high level of effectiveness, successfully generating good quality images in 79% of the cases evaluated. With a sensitivity rate of 68% and a perfect specificity of 100%, nn-2D-IOUS unequivocally demonstrated its utility in intraoperative tumor detection. Notably, in cases where total tumor removal was the surgical objective, a resection exceeding 95% of the initial tumor volume was achieved in 86% of patients. Additionally, in cases where residual tumor was not detected by nn-2D-IOUS, the mean volume of undetected tumor tissue was remarkably minimal, averaging at 0.29 cm3. ConclusionOur study provides compelling evidence supporting the invaluable role and efficacy of nn-2D-IOUS in glioma surgery. The results underscore the potential of harnessing traditional, cost-effective technologies such as nn-2D-IOUS to achieve enhanced surgical outcomes, even in the face of more advanced alternatives. These insights carry significant implications, particularly for resource-constrained settings, emphasizing the importance of optimizing the use of existing tools to improve patient care in a practical and efficient manner.

IntroductionInteractions between cancer cells and their microenvironment are central to tumor formation. Regional microenvironmental variability in the brain may offer insight into essential factors in tumorigenesis. Surprisingly, a granular assessment of regional patterns of gliomagenesis has not been undertaken in the molecular era. ObjectiveTo quantitatively establish the anatomical distribution of the major molecular subtypes of adult diffuse glioma. MethodsWe retrospectively analyzed a consecutive series of 204 IDH-mutant and 200 IDH- wildtype gliomas. Tumor volumes were segmented, normalized, and assigned to a brain location using a standardized neuroanatomic atlas. An independent and external validation cohort of 190 IDH-mutant and 227 IDH-wildtype gliomas was used to assess reproducibility. Microarray expressions from the Allen Human Brain Atlas were utilized to analyze transcriptomic differences between hotspots and coldspots of IDH-mutant gliomas. Results50.5% (103/204) of IDH-mutant tumors arose with the superior and middle frontal gyri indicating a 3.1-fold regional enrichment relative to the volume of these gyri (p<0.001). Only 0.5% (1/204) of IDH-mutant tumors arose with the occipital gyri indicating a 23.4-fold regional scarcity relative to volume (p<0.001). 9.5% (19/200) of IDH-wildtype tumors arose in the superior temporal gyrus with a 2.1-fold enrichment (p=0.01) and 6% (12/200) in the hippocampus with a 6-fold enrichment (p<0.001). IDH-mutant and wildtype tumors were enriched by 4 and 4.5-fold respectively in the insula (both p<0.001). Both IDH-mutant astrocytomas and oligodendrogliomas were significantly enriched in the SFG (39.2% and 40.2% respectively; both p<0.001), but 23.5% (24/102) of astrocytomas occurred disproportionately higher in the insula compared to oligodendrogliomas (p<0.001). These enrichment patterns were reproduced in an independent validation cohort of 417 glioma patients. Transcriptomic analysis comparing the lobar hotspot (frontal lobe) to the coldspot (occipital lobe) revealed frontal enrichment of cholesterol (NES=1.78) and fatty acid (NES=1.94) metabolism pathways, paralleling the observed regional enrichment of IDH-mutant gliomas. ConclusionsThis study reveals striking regional differences in glioma incidence, identifying key hotspots in the brain for gliomagenesis that vary based on tumor molecular subtype. Metabolic differences across cortical regions raise the possibility that regional metabolic differences may contribute to the observed vulnerability of specific regions to gliomagenesis. These findings provide a framework for investigating additional microenvironmental factors that drive human glioma formation.

Background and Objectives: Recurrence following burr-hole drainage of chronic subdural haematoma (cSDH) occurs in 10-25% of cases, sustained by neovascularisation of the subdural neomembrane supplied by the middle meningeal artery (MMA). MMA embolisation reduces recurrence; whether incidental burr-hole intersection of MMA branches during drainage confers similar benefit is unknown. Methods: We performed a multicentre retrospective cohort study of consecutive adults undergoing burr-hole drainage for cSDH at two UK tertiary neurosurgical centres. Postoperative thin-slice CT was used to classify burr-hole intersection of the underlying MMA groove (no hit, distal-branch hit or main-branch hit) and measure perpendicular burr-hole-to-MMA-groove distance. Co-primary outcomes were radiological recurrence and recurrence requiring intervention. Patient-clustered multivariable logistic regression adjusted for prespecified clinical covariates and treating site. Results: 227 patients (284 operated hemispheres) were included. Radiological recurrence decreased from 34.4% with no branch hit to 22.9% with main-branch intersection, with the gradient confined predominantly to unilateral cSDH. Main-branch intersection was associated with lower adjusted odds of radiological recurrence in unilateral cSDH (adjusted OR 0.30, 95% CI 0.11- 0.81; P = .018), with a similar but non-significant association in the overall cohort (adjusted OR 0.53, 95% CI 0.26-1.07; P = .075). Burr-hole-to-MMA-groove distance demonstrated a more consistent association: in the overall cohort, each 5-mm increase independently increased the odds of radiological recurrence (adjusted OR 1.38, 95% CI 1.04-1.82; P = .025). In unilateral cSDH, each 5-mm increase was independently associated with both radiological recurrence (adjusted OR 1.45, 95% CI 1.03-2.04; P = .034) and recurrence requiring intervention (adjusted OR 1.52, 95% CI 1.05-2.20; P = .027). Conclusion: Main-branch intersection of the middle meningeal artery during routine burr-hole surgery is associated with lower recurrence of unilateral cSDH, while the accompanying burr-hole-to-MMA-groove distance gradient provides biologically plausible support for a dose-response relationship. Together, these findings provide mechanistic rationale for prospective evaluation of intentional neuronavigation-guided MMA targeting (BURR-MMA; NCT07549893).

PurposeTo evaluate the association between surgically acquired neurological deficits and mortality among patients who underwent surgical resection of brain metastases. MethodsPatients who underwent surgical resection of brain metastases at our institution between 2011 and 2019 were included. Surgically acquired neurological deficits were defined as dysarthria/aphasia, ataxia, hemiparesis, and visual field loss. A Cox proportional hazards model adjusting for potential confounders was constructed to evaluate whether surgically acquired neurological deficits were independently associated with a higher risk of overall mortality. ResultsA total of 153 patients were included in the analysis. 3.3% (5 patients) had a surgically acquired neurological deficit. On univariate time-to-event analysis, there was no statistically significant association between the development of a surgically acquired neurological deficit and mortality (HR=1.12; 95% CI=0.15, 8.24; p=0.910). On multivariate time-to-event analysis adjusting for potential confounders, there was also no statistically significant association between the development of a surgically acquired neurological deficit and mortality (HR=1.53; 95% CI=0.20, 11.9; p=0.683). ConclusionThe development of a surgically acquired neurological deficit was not associated with overall mortality. Although this conclusion differs from other studies in the literature, the goal of surgical resection remains unchanged - to resect as much tumor as possible while still preserving neurological function.

BackgroundBrain tumors can present as focal neurologic deficits (reflecting the tumor location) or generalized symptoms due to increased intracranial pressure. Occasionally, brain tumors can be found incidentally in asymptomatic patients or in patients with unrelated symptoms who undergo brain imaging. The term incidentaloma is used to refer to these imaging abnormalities. ObjectiveThe object of this study was to examine the prevalence and correlates of asymptomatic glioma in a large epidemiological study of brain tumors. MethodsThe analysis was based on a large series of patients with glioma (N = 1989) enrolled in a multicenter clinic-based epidemiologic study between 2005 and 2017. Patients were considered asymptomatic from the tumor, and thus as having an incidentally detected glioma (IDG), if the tumor was diagnosed during workup of injury or unrelated medical condition. ResultsA total of 32 of 1989 (1.6%) patients were asymptomatic at diagnosis. The leading indication for brain imaging in IDG was non-workplace injuries followed by medical workup for unrelated conditions. IDG was more prevalent in patients younger than 50 years of age (2.6% vs 1.0%). IDG was also more common in patients with low grade gliomas (4.7% for WHO grade II and 1.5% for WHO grade III) vs glioblastomas (0.6% in WHO grade IV). ConclusionThe present data suggest that gliomas may be found incidentally, especially among low grade gliomas. Studies of IDG may be useful as a proxy for early detection of tumor as a means to improve patient survival.

Genome-wide DNA methylation aberrations are pervasive and associated with clinicopathological features across pituitary tumors (PT) subtypes. The feasibility to detect CpG methylation abnormalities in circulating cell-free DNA (cfDNA) has been reported in central nervous system tumors other than PT. Here, we aimed to profile and identify methylome-based signatures in the serum of patients harboring PT (n =13). Our analysis indicated that serum cfDNA methylome from patients with PT are distinct from the counterparts in patients with other tumors (gliomas, meningiomas, colorectal carcinomas, n =134) and nontumor conditions (n = 4). Furthermore, the serum methylome patterns across PT was associated with functional status and adenohypophyseal cell lineage PT subtypes, recapitulating epigenetic features reported in PT-tissue. A machine learning algorithm using serum PT-specific signatures generated a score that distinguished PT from non-PT conditions with 100% accuracy in our validation set. These preliminary results underpin the potential clinical application of a liquid biopsy-based DNA methylation profiling as a noninvasive approach to identify clinically relevant epigenetic markers that can be used in the management of PT.

ObjectiveThis paper seeks to quantify the normalized expression of transcripts FOXM1*3, VEGF, CD133, and MGMT and their relation with the histopathological and molecular diagnosis and with the probability of estimating tumor progression-free survival of gliomas. MethodsA cohort of patients was made up of patients aged over 18 years with a histological and molecular diagnosis of gliomas from the year 2011 to 2018. The patients had a complete tumor resection. Patients with high-grade glioma received adjuvant management (temozolamide and radiotherapy). Clinical and imaging follow-up was carried out periodically to identify the time of progression free survival (PFS). ResultsNinety-one patients (age range, 18-85 years) comprised the study cohort with a predominance of males. The expression of FOXM1*3, VEGF, and CD133 allowed the differentiation of astrocytomas grade II from GBM. ROC curves proved statistically significant in the GBM model (p < 0.05), demonstrating greatest sensitivity with FOXM1*3 (91%), and greatest specificity with VEGF (93%). The age-adjusted Cox multivariate model established that a PFS50% of 25 months corresponds to a median value of 5.3 for VEGF and 0.42 for CD133. ConclusionsThe normalized expression of transcripts FOXM1*3, VEGF, and CD133 allow us to estimate the probability of PFS, especially in gliomas grades II and IV; likewise, their overexpression defines the diagnosis of GBM. AuthorshipO_LISubstantial contributions to conception and design (IAFR, BNR, MARF, GG, IG), acquisition of data (IAFR, BNR, MARF, IFE, LCP, JCM, SOS, JAC, CRA), analysis and interpretation of data (IAFR, BNR, MARF, JCM, SOS, CEN, HMG, IG). C_LIO_LIDrafting the article (IAFR, BNR, MARF, IFE, LCP, SOS, JAC, IG), revising it critically for important intellectual content (IAFR, JCM, CEN, GG, HMG, CRA, IG) C_LIO_LIFinal approval of the version to be published (IAFR, BNR, MARF, IFE, LCP, JCM, SOS, JAC, CEN, GG, HMG, CRA, IG). C_LI

BackgroundNRCAM, a neuronal cell adhesion molecule, has been implicated in glioma biology through splicing alterations reported by prior studies. However, the relative contributions of genomic and epigenetic mechanisms to NRCAM dysregulation in gliomas remain unclear. MethodsWe analyzed glioma datasets from The Cancer Genome Atlas (TCGA) using UCSC Xena and cBioPortal. Copy number variation (CNV), DNA methylation (Illumina 450K arrays), and mutation profiles were assessed for NRCAM. Kaplan Meier survival analyses were performed with Xena, stratifying patients by copy number status and methylation state. Correlations between mutation burden and fraction genome altered were evaluated using Spearman and Pearson methods. ResultsSomatic mutations in NRCAM were rare across TCGA gliomas. In contrast, CNV and methylation changes were frequent and clinically relevant. Copy number gains at the NRCAM locus were associated with significantly shorter overall survival, while higher methylation of NRCAM correlated with improved survival outcomes. NRCAM mutation count did not show a linear correlation with fraction genome altered (FGA), suggesting these alterations are largely independent of overall genomic instability. The findings highlight copy number imbalance and epigenetic regulation as predominant mechanisms of NRCAM dysregulation. ConclusionNRCAM is recurrently dysregulated in gliomas through copy number alterations and DNA methylation, both of which stratify patient survival. Together with previously reported splicing deregulation, these data suggest that NRCAM functions as a multilayered regulator of glioma progression. NRCAM methylation may represent a prognostic biomarker, while therapeutic modulation of NRCAM warrants further investigation.

The understanding of glioma disease has been evolving drastically with dedicated research into the genetic and molecular profiling of glioma tumour tissue. Molecular biomarkers have gained progressive and substantial importance in providing diagnostic information, leading to groundbreaking changes in the tumour classification system, criteria and taxonomy standardised by the 2016 and 2021 editions of the World Health Organization Classification of Tumours of the Central Nervous Systems guidelines (WHO-2016 and WHO-2021, respectively). Some of the insights into glioma disease derived from extensive research on open-source multi-omics databases, such as the Cancer Genome Atlas (TCGA). However, given the substantial changes in glioma classification, retrospective databases may harbour outdated diagnostic annotations, suboptimal for further research. Here we propose two methods for updating the tumour classification of TCGA glioma samples in accordance with WHO-2016 and WHO-2021 guidelines through the integration of curated molecular profiling information. Our methods allowed for the diagnostic update of 98% and 87% of evaluated TCGA glioma cases according to WHO-2016 and -2021, respectively, and highlighted changes in patient-specific diagnosis across both guidelines editions. Our reclassification pipelines are provided in software R, facilitating direct reproduction or tailoring upon new releases of WHO guidelines.

Background: Extent of resection remains central to meningioma management, yet Simpson grading is subjective and may not reflect measurable postoperative residual disease. We compared surgeon-reported Simpson grade, report-derived radiological grading, and residual tumour volumetry across a multicentre cohort. Methods: We performed a retrospective study across two tertiary neurosciences centres comprising four hospitals, including patients undergoing primary cranial meningioma resection from 2006 to 2025. Postoperative magnetic resonance imaging (MRI) reports were harmonised using weakly supervised natural language processing based on term frequency-inverse document frequency (TF-IDF) and a linear support vector machine classifier. Residual tumour volume was segmented from contrast-enhanced postoperative MRI and log-transformed. Concordance between Simpson and radiological gross-total/subtotal resection classification was assessed using absolute agreement and prevalence-adjusted bias-adjusted kappa (PABAK). Cox models assessed recurrence-free survival, with bootstrap validation and anatomical and scan-timing sensitivity analyses. Results: Among 912 patients, recurrence or residual progression occurred in 281. Surgical-radiological agreement was substantial but imperfect (absolute agreement 74%; PABAK 0.61), with lower agreement in skull-base and parafalcine-parasagittal tumours. In adjusted models, recurrence hazard increased with Simpson grade (hazard ratio 1.54, 95% confidence interval 1.37-1.72), radiological grade (1.92, 1.68-2.20), and log-transformed residual volume (1.20, 1.16-1.24; all p<0.0005). Optimism corrected concordance increased from Simpson grade to radiological grade and log-volumetry (0.692, 0.733, and 0.748), with this ranking preserved across sensitivity analyses. Conclusions: Imaging-based postoperative residual disease measures outperformed Simpson grade. TF-IDF-assisted report-derived grading provides a scalable bridge to volumetry, while quantitative residual volume offers the strongest prognostic representation.

Glioblastomas integrate into the brain globally, where they provoke neuronal hyperactivity to enhance tumor growth and invasion. Communication of glioblastomas with neurons is not only present locally, but has preclinically been shown to extend towards the contralateral hemisphere through white matter tracts. However, it remains unknown how the distant hyperactivity that is often found in patients relates to structural embedding of the tumor into the larger brain network. 29 newly diagnosed IDH-wildtype glioblastoma patients and 25 age and sex matched healthy controls were included. To define structural tumor embedding, we overlayed each patient-specific tumor mask with a normative structural connectome obtained from diffusion MRI. We identified the average number of streamlines intersecting the tumor, extracting the tumors average tract density ( Lesion-Tract Density Index, L-TDI). For a subgroup of patients (n = 17), we determined structural embedding directly from diffusion scans and subsequent tractography. To identify regions connecting to the tumor, we seeded from each patients tumor rim outside FLAIR hyperintensities in the white matter to the 210 cortical regions of the Brainnetome atlas. We then counted the number of tumor-connecting regions, termed PATNET hereafter. Finally, participants underwent eyes-closed resting-state magnetoencephalography. We used broadband power as a proxy for neuronal spiking activity of each cortical region. To capture deviant brain activity in tumor and non-tumor regions, we regionally standardized broadband values using controls. We then sought to establish an association of deviant peritumor activity with both L-TDI and PATNET. Subsequently, we investigated whether tumor-connected regions showed more deviant activity than unconnected regions. Finally, we explored the clinical relevance of L-TDI and PATNET. Greater structural tumor embedding significantly related to more deviant peritumor activity (rhoLTDI= 0.47, PLTDI = .010; rhoPATNET = 0.54, PPATNET = .024), with larger tumors showing greater embedding and more hyperactivity than smaller tumors. Furthermore, distant tumor-connected regions showed more hyperactivity than unconnected regions, but only in patients with peritumor hyperactivity (F(1,15) = 11.02, P =.005). Finally, higher PATNET associated with lower KPS (U = 61.5, P = .015). Glioblastomas structural embedding explains hyperactivity around the tumor and in distant cortical regions, such that distant hyperactivity occurs primarily when there is tumor hyperactivity and the region is structurally connected to the tumor. Moreover, patient-specific tumor embedding relates to functional status.

ObjectivePituitary neuroendocrine tumors (PitNETs) are common intracranial neoplasms that can exhibit invasive behavior, leading to increased morbidity, recurrence, and resistance to treatment. Identifying biomarkers associated with tumor invasiveness could improve early diagnosis and guide therapeutic interventions. This systematic review evaluates molecular biomarkers linked to PitNET invasiveness and explores the potential of radiolabeling for noninvasive detection. MethodsA systematic search of PubMed and Embase databases was conducted to identify studies evaluating molecular markers associated with invasive PitNETs. Biomarkers were selected based on their proposed role in tumor invasion, and evidence supporting their clinical relevance was summarized. Additionally, existing radiolabeling techniques for biomarker detection were reviewed. ResultsFive key biomarker groups were identified: matrix metalloproteinases (MMPs), urokinase plasminogen activator (uPA) system, myosin 5A (MYO5A), vascular endothelial growth factor (VEGF), and survivin. MMPs were strongly linked to extracellular matrix degradation and invasion, while uPA facilitated invasion via MMP activation. MYO5A and survivin were implicated in epithelial-mesenchymal transition and tumor motility, and VEGF promoted angiogenesis. Radiolabeling techniques for MMPs, uPA/uPAR, VEGF, and survivin demonstrated feasibility for imaging tumor invasiveness, though limitations such as non-specific tracer accumulation remain. ConclusionsThis review highlights the potential of molecular biomarkers in predicting PitNET invasiveness and the emerging role of radiolabeled probes in noninvasive imaging. Future research should focus on validating these biomarkers in longitudinal studies and refining radiolabeling techniques to improve diagnostic accuracy and therapeutic targeting of invasive PitNETs.

Robot-assisted hematoma puncture has seen significant development in primary hospitals across the country. Sino Plan software system is the core of the intelligent surgical robot, independently developed by Sinovation.We conducted a comparative study of imaging indicators, such as residual hematoma volume and hematoma clearance rate, as well as prognostic indicators, in patients who underwent hematoma puncture at our hospital over a 9-year period, before and after the introduction of Sino Plan.The results indicated that following the application of Sino Plan, the hematoma clearance rate was significantly enhanced, and the residual hematoma volume was markedly reduced. Regarding patient prognosis, there was no significant difference in GCS scores between the two groups, but the incidence of adverse prognostic events was lower in patients where Sino Plan was utilized.In conclusion, this 9-year retrospective analysis at our hospital reveals that Sino Plan offers distinct advantages. However, its application in certain special cases suggests that further improvements to the software are warranted to better meet the demands of more specific clinical scenarios.

BackgroundCraniotomy is one of the most resource-intensive neurosurgical procedures, yet comparative information on its cost-effectiveness across different pathologies is limited. Differences in surgical techniques such as decompressive versus standard craniotomy, awake versus asleep resections, and endoscopic versus open approaches have major implications for outcomes and healthcare expenditure. This systematic review synthesizes the available economic evidence on craniotomy procedures applied to traumatic, neoplastic, congenital, inflammatory, and vascular conditions. MethodsA systematic search was performed in PubMed, Scopus, and Web of Science (July 6, 2025) in accordance with PRISMA 2020 guidelines (PROSPERO registration ID:CRD420251167810). Studies from 2010 onward were included if they reported comparative cost-effectiveness or cost-utility data for craniotomy approaches in any neurosurgical pathology. Two reviewers independently screened records and extracted data into predefined Excel templates encompassing demographic, clinical, and economic variables. Outcomes included mortality, complications, hospital and ICU stay, and incremental cost-effectiveness ratio (ICER). All cost values were reported as in the primary studies; no currency conversion or inflation adjustment was performed because of heterogeneity across {pound}, {euro}, and $ datasets. Methodological quality was assessed using the JBI tool, and the certainty of evidence was graded via GRADE. ResultsFrom 831 citations, 11 studies (1 RCT, 10 retrospective cohorts) met inclusion criteria, including 19145 participants (11123 craniotomy cases). Pathologies included traumatic acute subdural hematoma (taSDH), chronic SDH, gliomas, vascular aneurysms, colloid cysts, and craniosynostosis. O_LITrauma (Pyne et al., 2024): Craniotomy yielded lower total NHS costs ({pound} 48,509 vs {pound} 53,573) and higher QALYs (0.471 vs 0.336), dominating decompressive craniectomy (ICER {approx} {pound} 14,783/QALY). C_LIO_LINeoplasm: Among glioma series (Eseonu 2017; Sarikonda 2025), awake craniotomy reduced annual cost by 30 % compared to asleep approach with similar or better functional outcomes. Beaumont 2022 reported 52.6 % lower inpatient cost for endoscopic colloid cyst resection. C_LIO_LICongenital (Garber 2017): Endoscopic strip craniectomy averaged 21,203 versus 45,078 for open vault reconstruction (p < 0.001) with shorter LOS (1.8 vs 4.2 days) and fewer revisions (1 % vs 6-8 %). C_LIO_LIVascular (Lauzier 2023): Endovascular repair incurre 24578 v.s 39737 for open craniotomy while maintaining comparable morbidity. C_LIO_LINon-traumatic emergencies (Malmivaara 2011): Mean cost {euro} 5,000/QALY across diagnoses with 53 % overall mortality, acceptable under European thresholds. C_LI Across all pathologies, craniotomy was cost-effective or cost-dominant in 73 % of analyses. Quality assessment (JBI score 7-9/10) indicated moderate-to-high quality. According to GRADE (Table S3), the overall certainty was moderate, downgraded for currency inconsistency and study design heterogeneity. ConclusionsBased on current evidence, craniotomy and its minimally invasive derivatives appear to be cost effective in the setting of most neurosurgical domains. RCT-level data in trauma and convergent cohort findings in tumors, aneurysms, and craniosynostosis indicate that reduced length of stay, decreased incidence of complications, and avoidance of secondary operations collectively enhance cost-utility. As health systems pivot toward value-based models, these findings reinforce that surgical refinement and patient-centered selection are key to maximizing both clinical and economic outcomes in cranial surgery.

IntroductionPituitary adenomas with cavernous sinus invasion represent a challenging subset of intracranial tumors. The presence of cavernous sinus invasion complicates surgical resection and increases the risk of recurrence and postoperative complications. Endoscopic endonasal surgery (EES) has emerged as a promising alternative to traditional microscopic transsphenoidal surgery, offering enhanced visualization and reduced collateral damage. This meta-analysis aims to evaluate the efficacy and safety of EES in the treatment of pituitary adenomas with cavernous sinus invasion, focusing on remission rates, gross total resection (GTR), recurrence rates, and complications. MethodsA comprehensive literature search was conducted through PubMed, Scopus, Embase, and CENTRAL databases until August 2025, following PRISMA guidelines. Studies meeting eligibility criteria, including human studies published in English and involving adult patients with pituitary adenomas and cavernous sinus invasion treated with EES, were included. Data extraction focused on patient demographics, tumor characteristics, surgical outcomes, and complications. Statistical analysis was performed using a random-effects model, and subgroup analysis was conducted based on factors such as tumor size, Knosp grade, and hormonal subtype. ResultsA total of 27 studies involving 3,591 patients were included. The pooled remission rate was 60% (95% CI: 49% to 71%), with substantial variability across studies. The pooled residual tumor rate was 15% (95% CI: 11% to 19%), and the recurrence rate was 8% (95% CI: 6% to 11%). The incidence of cerebrospinal fluid (CSF) leaks was 9% (95% CI: 3% to 14%), while the rates of ICA injury and cranial nerve injury were extremely low (0.00% and 0.01%, respectively). Subgroup analyses revealed higher remission rates in macroadenomas (68%) compared to microadenomas (33%), and GH-secreting tumors showed higher endocrinological remission rates compared to ACTH-secreting tumors. ConclusionEndoscopic endonasal surgery demonstrates moderate efficacy in the treatment of pituitary adenomas with cavernous sinus invasion, with favorable remission and resection rates. However, substantial variability across studies emphasizes the need for further standardization of surgical techniques and patient selection criteria. The procedure is generally safe, with low rates of serious complications such as ICA injury and cranial nerve damage. Further prospective studies are needed to optimize patient management and evaluate long-term outcomes, including recurrence and quality of life.

D-2-hydroxyglutarate (D-2-HG) is a well-established oncometabolite of isocitrate dehydrogenase (IDH) mutant gliomas. While prior studies have demonstrated that D-2-HG is elevated in the cerebrospinal fluid (CSF) of patients with IDH-mutant gliomas1,2, no study has determined if CSF D-2-HG can provide a plausible method to evaluate therapeutic response. We are obtaining CSF samples from consenting patients during their disease course via intra-operative collection and Ommaya reservoirs. D-2-HG and D/L-2-HG consistently decreased following tumor resection and throughout chemoradiation in patients monitored longitudinally. Our early experience with this strategy demonstrates the potential for intracranial CSF D-2-HG as a monitoring biomarker for IDH-mutant gliomas.

For pediatric patients with central nervous system (CNS) tumors, primary treatment often involves neurosurgical tumor resection. Accurate diagnosis is crucial to perform the best-suited extent of resection. Since two years, Sturgeon, an AI-based validated intraoperative nanopore sequencing tool, has been fully integrated with frozen section analyses as standard of care in our nationwide centralized pediatric oncology hospital. This care evaluation is the first to demonstrate the impact of Sturgeon on neurosurgical decision-making. Sturgeon delivered correct diagnoses in 82 out of 94 consecutive patients (87.2%, <90 minutes), no diagnosis in 11.7% and 1 incorrect diagnosis. The diagnosis obtained by Sturgeon supported the intended surgical strategy (85.7%) or changed the strategy (14.3%) toward a more aggressive or limited resection. This resulted in only 3.2% second-look surgeries. In conclusion, intraoperative use of Sturgeon provides essential guidance toward the most optimal neurosurgical strategy and thereby has great potential to contribute to better clinical outcome.

ObjectiveThe most prevalent central nervous system (CNS) neoplasm arising from glial cells is glioma, which diffusely invades brain tissue. Among gliomas, Glioblastoma (GBM) is a glioma of the highest grade and associated with a grim prognosis, with a median overall survival of 15 months with and 3-4 months without therapy. We examined how clinical variables and molecular profiles may have affected overall survival (OS) at Sina Hospital in Tehran over the past ten years. MethodsA retrospective study was conducted at Sina Hospital in Tehran, Iran, and examined patients [&ge;] 11 years with confirmed glioma diagnoses between 2012 and 2020. We evaluated the correlation between OS in GBM patients and sociodemographic as well as clinical factors, including age, gender, extent of tumor resection, tumor location, chemo/radiotherapy, and molecular profiling based on IDH1, MGMT, TERT, and EGFR status. Kaplan-Meier and multivariate Cox regression models were used to assess patient survival. ResultsFollowing a comprehensive evaluation of medical records, 186 patients were enrolled in the study. The median OS was 20 months, with a 2-year survival rate of 62.5%. Among the 132 patients with available IDH measurements, 105 (79.5%) exhibited IDH1 wild-type tumors. Of the 132 patients with assessed MGMT methylation, 94 (71.2%) had MGMT methylated tumors. TERT promoter methylation was detected in 112 out of 132 cases (84.8%), while no methylation was observed in 20 cases (15.2%). Analyses using multivariable models revealed that age at histological grade (P < 0.0001), adjuvant radiotherapy (P < 0.014), IDH1 status (P < 0.026), and TERT promoter status (P < 0.030) were independently associated with OS. ConclusionThe findings of this study demonstrate that patients with higher tumor histological grades who had received adjuvant radiotherapy, exhibited IDH1 mutations, or presented with TERT promoter mutations, experienced improved OS. The median survival time was 20 months, with 15.6% and 46.9% of patients surviving at 12 and 24 months, respectively.

BackgroundGlioblastoma (GBM) progression is strongly influenced by its microenvironment, yet the contribution of white-matter injury-associated extracellular matrix (ECM) remodeling to human disease remains unclear. Experimental models show that glioma cells induce axonal injury and glial-scar-like ECM responses that accelerate tumor growth. MethodsWe curated an ECM Organization Signature reflecting injury-associated matrix remodeling and applied it to bulk RNA-sequencing data from TCGA-GBM. ECM scores were analyzed alongside wound-healing, microglia/TAM activation, and neuronal integrity signatures. Kaplan-Meier curves and age-adjusted Cox models assessed prognostic significance. ResultsECM organization, wound-healing, and microglia/TAM activation formed a coherent injury-response axis inversely correlated with neuronal programs. ECM-high tumors showed significantly different overall survival compared with ECM-low tumors (log-rank p = 0.023). In an age-adjusted Cox model, ECM remodeling independently predicted mortality (HR = 1.23, p = 0.0156). ConclusionWhite-matter injury-associated ECM remodeling is a prominent, clinically meaningful transcriptional state in human GBM and identifies a prognostic microenvironmental subtype.

IntroductionThe assessment of vestibular schwannoma (VS) requires a standardized measurement approach as growth is a key element in defining treatment strategy for VS. Volumetric measurements offer higher sensitivity and precision, but existing methods of segmentation, are labour-intensive, lack standardisation and are prone to variability and subjectivity. A new core set of measurement indicators reported consistently, will support clinical decision-making and facilitate evidence synthesis. This systematic review aimed to identify indicators used in 1) magnetic resonance imaging (MRI) acquisition and 2) measurement or 3) growth of VS. This work is expected to inform a Delphi consensus. MethodsSystematic searches of Medline, Embase and Cochrane Central were undertaken on 4th October 2024. Studies that assessed the evaluation of VS with MRI, between 2014 and 2024 were included. ResultsThe final dataset consisted of 102 studies and 19001 patients. Eighty-six (84.3%) studies employed post contrast T1 as the MRI acquisition of choice for evaluating VS. Nine (8.8%) studies additionally employed heavily weighted T2 sequences such as constructive interference in steady state (CISS) and FIESTA-C. Only 45 (44.1%) studies reported the slice thickness with the majority 38 (84.4%) choosing <3mm in thickness. Fifty-eight (56.8%) studies measured volume whilst 49 (48.0%) measured the largest linear dimension; 14 (13.7%) studies used both measurements. Four studies employed semi-automated or automated segmentation processes to measure the volumes of VS. Of 68 studies investigating growth, 54 (79.4%) provided a threshold. Significant variation in volumetric growth was observed but the threshold for significant percentage change reported by most studies was 20% (n = 18). ConclusionSubstantial variation in MRI acquisition, and methods for evaluating measurement and growth of VS, exists across the literature. This lack of standardization is likely attributed to resource constraints and the fact that currently available volumetric segmentation methods are very labour-intensive. Following the identification of the indicators employed in the literature, this study aims to develop a Delphi consensus for the standardized measurement of VS and uptake in employing a data-driven artificial intelligence-based measuring tools.