Neuro-oncology advances最新文献

{"title":"Encorafenib plus binimetinib in patients with BRAF-mutated melanoma brain metastases: Results from the BECARE (GEM-2002) trial.","authors":"Pablo Cerezuela-Fuentes, Miguel-Angel Berciano-Guerrero, Eva Muñoz-Couselo, Pedro Sanchez Mauriño, Regina García Galindo, Lourdes Gutiérrez Sanz, José Balsalobre Yago, Teresa Puértolas, Carlos Aguado, Silvia Sequero, Guillermo Crespo, Cristina Aguayo, Enrique Espinosa, Pedro López, Rafael López Castro, Joaquín Fra Rodríguez, Gretel Benítez, Alberto Jacobo Cunquero-Tomás, Alfonso Berrocal, Ainara Soria","doi":"10.1093/noajnl/vdag252","DOIUrl":"10.1093/noajnl/vdag252","url":null,"abstract":"<p><strong>Background: </strong>Encorafenib plus binimetinib (EB) is a standard treatment for BRAF^V600-mutated melanoma brain metastasis (MBM). However, there is limited evidence of EB use in MBM from clinical trials, and real-world data are scarce. This study aimed to determine the effectiveness and safety of EB in BRAF^V600-mutated MBM.</p><p><strong>Methods: </strong>BECARE-GEM-2002 was a retrospective study conducted in 24 hospitals in Spain, including patients treated according to standard clinical practice with EB as the 1st line or 2nd line of treatment after progression to immunotherapy, regardless of symptoms and corticosteroid use. Patients had measurable intracranial disease (≥5 mm on CT scan). Previous treatment with BRAF/MEK inhibitors was not allowed.</p><p><strong>Results: </strong>Between 2021 and 2025, 60 patients were included, 52 (86.7%) treated upfront and 8 (13.3%) after immune checkpoint inhibitors (ICIs) progression. The ORR was 58.3% (95% confidence interval [CI], 44.9-70.9), 65.4% (95% CI, 44.3-82.8) in asymptomatic, and 52.9% (95% CI, 35.1-70.2) in symptomatic MBM. Radiotherapy (RT) was administered prior to EB in 7 patients (11.7%) and concurrently in 17 (28.3%). Patients receiving RT showed an ORR of 76% (95% CI, 54.9-90.6). The median PFS was 7.4 months (95% CI, 6.2-9.7) and median OS was 10.6 months (95% CI, 9.2-15.0). Treatment-related adverse events of grade ≥3 were reported in 12 patients (20%), the most frequent being transaminitis (6.7%) and gastrointestinal hemorrhage (3.3%).</p><p><strong>Conclusions: </strong>EB was safely administered in the real world and showed clinically significant benefit in patients with BRAF^V600-mutant MBM, regardless of brain symptoms. The potential role of RT should be explored in prospective trials.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag252"},"PeriodicalIF":4.6,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13648201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149140022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Value-based assessment of repeat surgery for recurrent glioma: A real-world quality-adjusted survival analysis.","authors":"Wanyu Qiao, Chen Luo, Tian Gan, Shuai Wu, Xian Xie, Jinsong Wu, Hugues Duffau, Jie Zhang, Ye Yao","doi":"10.1093/noajnl/vdag251","DOIUrl":"https://doi.org/10.1093/noajnl/vdag251","url":null,"abstract":"<p><strong>Background: </strong>Reoperation for recurrent glioma is widely practiced, yet clinical decision-making remains challenging due to substantial trade-offs between survival gain and postoperative functional burden. High-quality real-world evidence integrating survival and quality-of-life outcomes to inform reoperation decisions remains limited.</p><p><strong>Methods: </strong>We conducted a retrospective real-world cohort study of 1304 patients with recurrent glioma treated between 2010 and 2018. Propensity score matching was applied to balance baseline characteristics. Survival outcomes, quality-adjusted life years (QALYs), functional status, and prognostic factors associated with reoperation benefit were evaluated.</p><p><strong>Results: </strong>In the 1:1 propensity-matched cohort (140 reoperation vs 140 non-reoperation), reoperation was associated with a mean gain of 9.6 months in quality-adjusted life years (QALYs) and a 521-day longer overall survival. Postoperative functional status showed short-term improvement. In the glioblastoma subgroup, reoperation was associated with a numerical gain of 3.5 QALY months, although the confidence interval crossed zero, alongside a 218-day gain in overall survival. Predictive models based on preoperative characteristics demonstrated good discrimination in identifying patients likely to derive survival benefit beyond 6 months.</p><p><strong>Conclusion: </strong>This study provides real-world evidence that carefully selected patients with recurrent glioma may derive quality-adjusted survival benefits from reoperation, thereby supporting individualized surgical decision-making. These findings have implications for value-based surgical decision-making in recurrent glioma, particularly in healthcare systems where balancing survival benefit against functional outcomes and resource use is increasingly important.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag251"},"PeriodicalIF":4.6,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linac-based stereotactic radiosurgery for brain metastases: Survival and salvage treatment in a contemporary cohort of 3893 patients.","authors":"Drew T Bergman, Mitchell I Parker, Henry Walch, Åse Ballangrud, Michalis Aristophanous, Melissa Zinovoy, Brandon S Imber, Gustav Cederquist, Christopher Jackson, Connor J Kinslow, Anthony Abaya, John J Cuaron, James Janopaul-Naylor, Atif Khan, Zachary R Moore, Boris A Mueller, Jacob Y Shin, Divya Yerramilli, Yoshiya Yamada, Yao Yu, Luke R G Pike","doi":"10.1093/noajnl/vdag242","DOIUrl":"10.1093/noajnl/vdag242","url":null,"abstract":"<p><strong>Background: </strong>Real-world outcomes after stereotactic radiosurgery (SRS) for brain metastases across the full burden spectrum are limited. We tested whether overall survival (OS) in higher-burden lesion groups is non-inferior to a 5-10 lesion reference and characterized salvage patterns, including whole-brain radiotherapy (WBRT).</p><p><strong>Methods: </strong>A total of 3893 consecutive patients received linac-based SRS (1-5 fractions) at seven sites of an NCI-designated cancer center network (2017-2026), stratified by lesion count (1, 2-4, 5-10, 11-20, >20). Multivariable Cox regression used 5-10 as reference; pre-specified non-inferiority testing (margin HR 1.30, one-sided α = 0.025) compared higher-burden groups. Cumulative incidences of salvage interventions used death as the competing event.</p><p><strong>Results: </strong>Median age 65 years; median follow-up 41.2 months. 77% had 1-4, 17% had 5-10, and 6% had >10 lesions (maximum 140). Median OS was 16.2, 11.0, 8.2, 8.7, and 6.5 months for the 1, 2-4, 5-10, 11-20, and >20 groups. OS was significantly better for 1 (HR 0.62, 0.55-0.69) and 2-4 (HR 0.81, 0.73-0.90) versus 5-10; non-inferiority was met for 11-20 (<i>P</i> < .001) but not >20 (<i>n</i> = 41, <i>P</i> = .20). CNS-directed systemic therapy was strongly protective (HR 0.62, 0.57-0.68); 21.7% of patients with ≤20 lesions survived ≥30 months. 12-month salvage WBRT incidence was 2.9%-6.3%; 24-month incidence was 6.7% versus 41.7% for a third SRS course.</p><p><strong>Conclusions: </strong>OS plateaued from 5 through 20 lesions, with non-inferiority to the 5-10 reference established for 11-20; the >20 group (<i>n</i> = 41) was underpowered and showed a directionally worse estimate that could not exclude a clinically meaningful decrement. Salvage WBRT was uncommon across all lesion-count groups (24-month cumulative incidence ≤7.3%; >90% of patients received no salvage WBRT), even after multiple SRS courses. These data support an SRS-first strategy guided by clinical factors rather than fixed lesion-count thresholds.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag242"},"PeriodicalIF":4.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical factors associated with leptomeningeal disease in patients with melanoma brain metastasis.","authors":"Merve Hasanov, Christina A Faraj, Denai R Milton, Subhiksha Srinivasan, Eric A Goethe, Ian E McCutcheon, Jeffrey S Weinberg, Isabella C Glitza Oliva, Sherise D Ferguson","doi":"10.1093/noajnl/vdag232","DOIUrl":"10.1093/noajnl/vdag232","url":null,"abstract":"<p><strong>Background: </strong>Leptomeningeal disease (LMD) is a severe manifestation of metastatic cancer with limited treatment options and a poor prognosis. Melanoma has one of the highest rates of leptomeningeal spread among solid tumors. Given the associated morbidity and mortality, identifying clinical factors linked to LMD in patients with melanoma brain metastases (MBM) is crucial.</p><p><strong>Methods: </strong>We conducted a retrospective study of 829 MBM patients diagnosed at MD Anderson Cancer Center (2009-2018). The primary outcome measure was time from MBM to LMD. Cumulative incidence of LMD was determined using the competing risks method, where death was the competing risk. Differences in cumulative incidences were assessed using Gray's test, and associations between measures of interest and cumulative incidence were determined using proportional sub-distribution hazards models.</p><p><strong>Results: </strong>Among 829 patients, 129 (16%) developed LMD (median follow-up: 12.1 months, range: 0.0-156.2 months). Median time from MBM diagnosis to LMD was 5.5 months. Of those with known mutation status (<i>n</i> = 713), BRAF V600 mutation was present in 74% of patients who developed LMD versus 50% in those who did not (<i>P</i> < .001). Multivariable analysis (MVA) showed BRAF V600 mutation (<i>P</i> = .009) and craniotomy (<i>P</i> = .035) were associated with the development of LMD. In a sub-analysis of BRAF V600 mutant patients (<i>n</i> = 380), MVA revealed that primary melanoma site (upper extremity vs head/neck) and number of MBMs at diagnosis were associated with LMD development.</p><p><strong>Conclusion: </strong>LMD is a dire consequence of advanced melanoma, yet the clinical features associated with its development are not fully characterized. Identifying clinical predictors may guide management of high-risk populations.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag232"},"PeriodicalIF":4.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallium maltolate causes genomic instability to enhance glioblastoma response to radiation and temozolomide.","authors":"Joan N Whittier, Stephenson B Owusu, John Cooke, Jann N Sarkaria, Michael S Petronek","doi":"10.1093/noajnl/vdag246","DOIUrl":"https://doi.org/10.1093/noajnl/vdag246","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) represents the most common and aggressive central nervous system malignancy where overall survival is a dismal 14.6 months despite an aggressive standard of care treatment regimen that includes maximally safe surgical resection, radiotherapy, and temozolomide. It has recently been established that GBM tumors have increased transferrin receptor expression and iron content which corresponds with worse patient prognosis. This has led to the hypothesis that iron metabolism is a viable therapeutic target. An emergent therapeutic strategy to target GBM iron metabolism is gallium maltolate (GaM), which is an orally bioavailable form of Ga³⁺ that functions as a redox inactive iron mimic to disrupt iron metabolism. As mitochondrial iron metabolism serves as a central connection point between iron and DNA metabolism, the goal of this study was to determine if GaM could disrupt this system.</p><p><strong>Methods: </strong>The effects of GaM on GBM cells were interrogated using conventional techniques including colony formation assays to assess clonogenicity, alkaline comet assays to evaluate DNA damage induction, and Mito-FerroGreen analysis to evaluate mitochondrial iron content. The effects of GaM on tumor growth in vivo were evaluated using a subcutaneous flank xenograft model system to determine the induction of DNA damage and an orthtopic model system to evaluate the combinatorial effects of GaM, radiation, and temozolomide on murine survival.</p><p><strong>Results: </strong>This study uncovered that maintenance of high mitochondrial iron content corresponds with increased proliferative capacity in GBM cells. This study also shows that GaM can deplete mitochondrial iron to induce DNA damage both in vitro and in a subcutaneous xenograft model. Furthermore, GaM enhances the efficacy of radiation and temozolomide when delivered concomitant and adjuvantly in an orthotopic GBM model system.</p><p><strong>Conclusion: </strong>These results suggest that GaM warrants further consideration for use in combination with standard of care GBM therapy.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag246"},"PeriodicalIF":4.6,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13652141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage migration inhibitory factor is a potential therapeutic target for cisplatin induced peripheral neuropathy in breast cancer.","authors":"Hya El-Baroudy, Bhadrapriya Sivakumar, Ximena Mejia Delgadillo, Nishi Bamania, Isabelle Monsman, Shubham Dwivedi, Bari Chowdhury, Jay Patel, Nickson Joseph, Snigdha Pathak, Sandra Mitzkus, Hanrong Li, Shahid Ahmed, Anand Krishnan","doi":"10.1093/noajnl/vdag243","DOIUrl":"https://doi.org/10.1093/noajnl/vdag243","url":null,"abstract":"<p><strong>Background: </strong>Cisplatin (CP) is a potent chemotherapy drug used for the management of several cancers. However, the use of CP is associated with painful peripheral neuropathy. Effective therapies are currently unavailable for CP-induced peripheral neuropathy (CisIPN). Given the known association between pro-inflammatory cytokines and CisIPN, we explored the role of the pro-inflammatory cytokine, the macrophage migration inhibitory factor (MIF), in CisIPN.</p><p><strong>Methods: </strong>CisIPN was induced in normal and breast cancer mouse models. Circulating MIF levels in CisIPN mice were examined using ELISA. The effect of MIF inhibition on CisIPN severity was evaluated using small molecule inhibitors. Mechanical and cold sensitivities of CisIPN mice were examined using Von Frey filament and cold acetone assays. Macrophage infiltration and expression of MIF in dorsal root ganglia (DRG) and sciatic nerves of CisIPN mice were examined using immunostaining. Molecular changes downstream of MIF were examined in Schwann Cells (SCs) using western blot.</p><p><strong>Results: </strong>Circulating MIF levels were increased in CisIPN mice, indicating a potential role for MIF in CisIPN. Pharmacological inhibition of MIF suppressed the mechanical hypersensitivity component associated with CisIPN, substantiating a facilitatory role for MIF in CisIPN. There was no significant change observed in macrophage abundance in DRGs and sciatic nerves of CisIPN mice. ELISA, immunostaining, and western blot assays indicated that sensory neurons and SCs are potential sources for increased MIF in CisIPN. We also found fluctuations in ERK1/2 signaling downstream of MIF in SCs, suggesting it as a potential mechanism underlying MIF-dependent facilitation of CisIPN.</p><p><strong>Conclusions: </strong>Overall, our results indicate that MIF facilitates CisIPN, suggesting its potential role as a therapeutic target for CisIPN.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag243"},"PeriodicalIF":4.6,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Permeabilization of tumor margins in brain macrometastases using a type-1 receptor selective tumor necrosis factor mutein.","authors":"Vanessa A Johanssen, Claire Bristow, Sandra J Campbell, Daniel C Anthony, Mark R Middleton, Nicola R Sibson","doi":"10.1093/noajnl/vdag239","DOIUrl":"https://doi.org/10.1093/noajnl/vdag239","url":null,"abstract":"<p><strong>Background: </strong>Brain metastasis remains a major clinical challenge. The blood-brain barrier, which persists in the margins even in late-stage macrometastases, is a major impediment to effective drug delivery, surgery, or radiotherapy. The aim of this study was to determine whether a mutein of human tumor necrosis factor (TNF) that is selective for the TNFR1 receptor could increase permeabilization in the margins of brain metastases, enabling better delineation and more complete treatment.</p><p><strong>Methods: </strong>Intracerebral xenograft mouse models of breast cancer (MDA231Br-GFP), melanoma (H1_DL2), and lung cancer (SEBTA) brain metastasis were used to test the efficacy of the TNF mutein (mutTNF) in permeabilizing the margins of well-established macrometastases. Changes in tumor permeabilization were assessed in vivo by gadolinium-enhanced magnetic resonance imaging (MRI) and ex vivo by IgG immunohistochemistry.</p><p><strong>Results: </strong>Tumor margin permeabilization was increased following mutTNF treatment in all 3 models. The MDA231Br-GFP model showed a significant increase in the extent of both gadolinium enhancement (<i>P</i> < 0.01) and IgG extravasation (<i>P</i> < 0.05), whilst significant effects were detected by MRI alone in the SEBTA (<i>P</i> < 0.01) and H1_DL2 (<i>P</i> < 0.05) models. Although a strong trend toward increased IgG extravasation was found in the SEBTA model (<i>P</i> = 0.076). Consistent with these findings, the models showed differing degrees of both infiltration and vascular TNFR1 expression at the margins (MDA231Br-GFP > SEBTA > H1_DL2), suggesting a greater sensitivity to mutTNF with increasing marginal invasiveness.</p><p><strong>Conclusions: </strong>This work demonstrates the potential of TNFR1-selective mutTNF as an adjuvant strategy to improve tumor margin delineation and enhance therapeutic access in brain metastases.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag239"},"PeriodicalIF":4.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Exploring relationships between abnormal within-network functional connectivity, preoperative brain tumor variables, and neuropsychological test scores.","authors":"","doi":"10.1093/noajnl/vdag227","DOIUrl":"https://doi.org/10.1093/noajnl/vdag227","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/noajnl/vdag084.].</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag227"},"PeriodicalIF":4.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148914921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Siglec/sialic-acid axis in glioblastoma: Glycome-mediated immune evasion and emerging therapeutic platforms.","authors":"David Lee, William ElNemer, Omar Selim, Parth Patel, Sara Freeman, Hasan Slika, Fnu Ruchika, Henry Brem, Christopher Jackson, Betty M Tyler","doi":"10.1093/noajnl/vdag234","DOIUrl":"https://doi.org/10.1093/noajnl/vdag234","url":null,"abstract":"<p><p>Despite encouraging advances in cancer immunotherapy, several malignancies leverage resistance pathways to escape the effects of treatment. Abnormal cell signaling and cytokine secretion modulated by cancer cells promote a tumor microenvironment (TME), wherein the efficacy of infiltrating immune cells is diminished. There is increasing evidence that alteration of the glycosylation profile of some TMEs is a key factor in exhausting the immune response. The sialic-acid/Siglec axis has received attention for its suspected involvement in this context through both preclinical study and several clinical trials. Against this backdrop, glioblastoma (GBM) is a well-established immune-suppressive tumor with disappointing responses to most traditional immunotherapies. Recent studies have suggested that GBM can exploit the sialic-acid/Siglec axis to promote immune evasion and resistance to traditional immune checkpoint inhibitors. This review examines all presently identified Siglec interactions and the current state of Siglec-centered therapies with respect to GBM.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag234"},"PeriodicalIF":4.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13626132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnosis and treatment decision of an IDH-mutant glioma through CSF-based cfDNA sequencing.","authors":"Eve Fouarge, Rouzbeh Banan, Sebastian Curt Schulz, Martin Jakobs, Marianne Schell, Felix Sahm, Tobias Kessler","doi":"10.1093/noajnl/vdag240","DOIUrl":"https://doi.org/10.1093/noajnl/vdag240","url":null,"abstract":"<p><p>Classification of tumors of the central nervous system currently requires tumor tissue analysis for histology and molecular markers, according to the 2021 WHO Classification of Tumors of the Central Nervous System. Cerebrospinal fluid (CSF)-based cell-free DNA (cfDNA) sequencing detects these defining molecular alterations and allows for accurate diagnosis and WHO-analogue tumor classification. We hereby report the case of a female patient with an IDH-mutant glioma, TERT promoter mutant, NEC, in whom <i>IDH1</i> and <i>TERT</i> promoter mutations were identified in CSF after an initially non-informative tissue histology, then confirmed through tissue-based molecular analysis. The patient was initially treated with vorasidenib, an IDH inhibitor, which was then switched to a procarbazine-CCNU chemotherapy due to clinical worsening under initial therapy. CSF-based cfDNA sequencing is a promising tool for minimally invasive diagnosis of tumors of the CNS in situations in which tissue biopsy is challenging or non-informative.</p>","PeriodicalId":94157,"journal":{"name":"Neuro-oncology advances","volume":"8 1","pages":"vdag240"},"PeriodicalIF":4.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13599777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}