Neuro-oncology最新文献

{"title":"Identifying appropriate external control datasets in support of future glioblastoma clinical trials leveraging external data.","authors":"Rifaquat Rahman, Steffen Ventz, Robert Redd, Geoffrey Fell, Yujue Tan, Peter Orio, Kirk Tanner, Patrick Y Wen, Lorenzo Trippa","doi":"10.1093/neuonc/noaf031","DOIUrl":"https://doi.org/10.1093/neuonc/noaf031","url":null,"abstract":"<p><strong>Background: </strong>Recent interest in leveraging external data for clinical trial design and analysis in glioblastoma has raised questions on the identification of appropriate data to use as external controls for future trials. We perform a comprehensive analysis assessing candidate sources of external data and comparing clinical trial and real-world datasets in newly diagnosed glioblastoma.</p><p><strong>Methods: </strong>Individual patient-level data (PLD) from several clinical trials, a large academic institutional database and a registry (National Cancer Database) were used for analysis of patients receiving standard of care radiation with concurrent and adjuvant temozolomide. Data summaries from randomized trials 2012-2022 were analyzed to account for trials without available PLD. Multivariable modeling was employed to compare survival across datasets.</p><p><strong>Results: </strong>In total, 8 datasets with PLD for 3061 patients with newly diagnosed glioblastoma treated with standard chemoradiation were analyzed. Patients on trials were younger (age<60:64% vs. 48%,p<0.001) and had higher KPS (KPS>90:58% vs. 48%,p<0.001) compared to non-trial patients. Patients in clinical trials exhibited inferior survival relative to non-trial patients (HR 1.30,95%CI 1.13-1.48,p<0.001) after adjustment for age, sex, KPS, extent of resection and MGMT methylation status. In assessment of data summaries of 19 randomized trials, there was no detectable time-trend toward improved outcomes 2012-2022.</p><p><strong>Conclusions: </strong>In newly diagnosed glioblastoma patients treated with standard of care chemoradiation, there were significant differences between trial datasets and real-world datasets but no evidence of a trial effect benefit from trial participation. After adjustment of relevant covariates, there was no evidence of temporal drift of improved survival over the last decade.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of LDOC1 by chromatin compaction in mesenchymal tumor cells is required for PFA1 ependymoma growth.","authors":"Graziella Ribeiro de Sousa, Annaliese J Calzadilla, Enrique Grimaldo, Andrew M Donson, Lays Martin Sobral, Kendra M Jones, Tian Liu, Vladimir Amani, Sujatha Venkataraman, Nathan A Dahl, Jean M Mulcahy Levy, Tzu Phang, Rajeev Vibhakar, Todd Hankinson, Michael Handler, Elvis Terci Valera, Nicholas K Foreman, Andrea M Griesinger","doi":"10.1093/neuonc/noaf029","DOIUrl":"https://doi.org/10.1093/neuonc/noaf029","url":null,"abstract":"<p><strong>Background: </strong>Posterior fossa molecular subtype A (PFA) ependymoma occurs in young children and is the deadliest subtype of pediatric ependymoma. High-risk subtypes with chromosome 1q+ and/or 6q- exhibit significantly poorer outcome compared to wild-type PFA. However, 50% of wild-type PFA patients relapse and there is a high risk of gaining chromosome 1q at recurrence. We previously found constitutively active NF-κB, through loss of LDOC1, led to chronic IL-6 secretion and an overall immunosuppressive tumor microenvironment in the higher risk wild-type PFA ependymoma subset (PFA1).</p><p><strong>Methods: </strong>In this study, we delineate the mechanistic consequences of LDOC1 loss in PFA1, using our PFA ependymoma in vitro and in vivo models under normoxia and hypoxia conditions.</p><p><strong>Results: </strong>We noted chromatin compaction by H3K27me3 at the LDOC1 loci results in loss of LDOC1 gene expression. Restoration of LDOC1 was sufficient to reduce proliferation, NF-κB signaling and significant decrease in IL-6 secretion. Furthermore, tumors implanted with LDOC1- transduced cells in vivo were out competed by non-transduced cells, suggesting loss of LDOC1 is required for PFA tumor growth.</p><p><strong>Conclusion: </strong>These findings shed further light on the biology of PFA1 ependymoma and the role LDOC1 loss has on the tumor and immunobiology of high risk pediatric ependymoma.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular subtypes of adamantinomatous craniopharyngiomas.","authors":"Wenhao An, Shouwei Li, Yihua An, Zhixiong Lin","doi":"10.1093/neuonc/noaf030","DOIUrl":"https://doi.org/10.1093/neuonc/noaf030","url":null,"abstract":"<p><p>Adamantinomatous craniopharyngioma (ACP) is the most common benign tumor in the sellar region of children and originates from embryonic remnants. Owing to its unique location and frequent tight adhesion to and invasion of surrounding structures, the ACP poses significant challenges for neurosurgical treatment. Traditionally, the core treatment for ACPs has been surgical resection supplemented with radiotherapy in cases of residual or recurrent tumors. As a result, ACP classification has been based primarily on the tumor's relationship with surrounding anatomical and histological structures, guiding the selection of surgical approaches and the prevention of complications. Moreover, efforts to explore pharmacological treatments for ACP have yielded varying results across different cases, creating confusion among researchers. This variability also suggests the possibility of different molecular subtypes within ACPs, despite being driven by a single gene mutation. With advancements in molecular biological studies, such as ACP RNA sequencing, whole-exome sequencing, and methylation analysis, along with the discovery of interactions between different molecular pathways within ACP, researchers have been continuously exploring the molecular subtyping of ACP and predicting the efficacy of targeted therapies on the basis of these subtypes. This review focuses on summarizing and synthesizing the molecular mechanisms and potential subtypes of ACP, aiming to provide theoretical support for future research on the molecular subtyping of ACP.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intrathecal Sintilimab for Leptomeningeal Metastases of Non-small Cell Lung Cancer Failed from Targeted Therapy and Intrathecal Chemotherapy (LMIS study).","authors":"Chengjuan Fan, Yuanyuan Hu, Chong Teng, Yanju Lv, Xiaowei Song, Weixi Shen, Qiuying Jiang, Dayong Huang, Lina Du, Guohua Wang, Yang Du, Siqi Man, Zhichao Zhang, Jing Zhang, Li Li, Tao Xin","doi":"10.1093/neuonc/noaf025","DOIUrl":"https://doi.org/10.1093/neuonc/noaf025","url":null,"abstract":"<p><strong>Backgroud: </strong>Leptomeningeal metastases (LMs) are serious complications of non-small cell lung cancer (NSCLC). This study aimed to investigate the safety and efficacy of intrathecal immune checkpoint inhibitors (ICIs) in treating NSCLC-LM.</p><p><strong>Methods: </strong>We conducted this prospective phase 1 study (ChiCTR2200062245) using a traditional \"3 + 3\" design with intrathecal sintilimab (dose escalation 10mg, 20mg, 30mg, and 40mg) for NSCLC-LM patients who had progressed from targeted therapy and intrathecal pemetrexed. The primary study endpoints were safety and recommended dose, and the secondary endpoints included clinical response rate, progression-free survival (PFS), intracranial progression-free survival (iPFS), and overall survival (OS).</p><p><strong>Results: </strong>No dose-limiting toxicity was found at 10mg, 20mg, 30mg, and 40mg for intrathecal sintilimab. Therefore, sintilimab 40mg was recommended for intrathecal injection. A total of 19 patients were enrolled in this study. The median age at diagnosis of LM was 53 years. The overall incidence of adverse events (AEs) was 68.4%, and rash (n=4, 21.1%) was the most common AEs, which returned to normal after symptomatic treatment. As 1 patient was lost to follow-up and 18 patients could be evaluated for efficacy, the clinical response rate was 38.9% (7/18). Median PFS was 3.5 months (95% CI: 2.7-4.2 months), median iPFS was 3.5 months (95% CI: 1.3-5.6 months), and median OS was 11.5 months (95% CI: 0.0-25.4 months).</p><p><strong>Conclusions: </strong>Intrathecal ICIs for NSCLC-LM patients are safe, and the recommended dose of sintilimab is 40mg. Intrathecal sintilimab for NSCLC-LM failed from multi-line therapies, showed potential effectiveness in some patients, and is worthy for further study.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GBMPurity: A Machine Learning Tool for Estimating Glioblastoma Tumour Purity from Bulk RNA-seq Data.","authors":"Morgan P H Thomas, Shoaib Ajaib, Georgette Tanner, Andrew J Bulpitt, Lucy F Stead","doi":"10.1093/neuonc/noaf026","DOIUrl":"10.1093/neuonc/noaf026","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) presents a significant clinical challenge due to its aggressive nature and extensive heterogeneity. Tumour purity, the proportion of malignant cells within a tumour, is an important covariate for understanding the disease, having direct clinical relevance or obscuring signal of the malignant portion in molecular analyses of bulk samples. However, current methods for estimating tumour purity are non-specific and technically demanding. Therefore, we aimed to build a reliable and accessible purity estimator for GBM.</p><p><strong>Methods: </strong>We developed GBMPurity, a deep-learning model specifically designed to estimate the purity of IDH-wildtype primary GBM from bulk RNA-seq data. The model was trained using simulated pseudobulk tumours of known purity from labelled single-cell data acquired from the GBmap resource. The performance of GBMPurity was evaluated and compared to several existing tools using independent datasets.</p><p><strong>Results: </strong>GBMPurity outperformed existing tools, achieving a mean absolute error of 0.15 and a concordance correlation coefficient of 0.88 on validation datasets. We demonstrate the utility of GBMPurity through inference on bulk RNA-seq samples and observe reduced purity of the Proneural molecular subtype relative to the Classical, attributed to the increased presence of healthy brain cells.</p><p><strong>Conclusions: </strong>GBMPurity provides a reliable and accessible tool for estimating tumour purity from bulk RNA-seq data, enhancing the interpretation of bulk RNA-seq data and offering valuable insights into GBM biology. To facilitate the use of this model by the wider research community, GBMPurity is available as a web-based tool at: https://gbmdeconvoluter.leeds.ac.uk/.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IRS2 as a driver of brain metastasis in colorectal cancer: a potential target for novel therapeutic strategies.","authors":"Inbal Greenberg, Fayhaa Khair, Keren Merenbakh-Lamin, Ethan Sokol, Anat Klein Goldberg, Dor Simkin, Avishay Spitzer, Moshe Benhamou, Shai Bar-Shira, Michal Raz, Rachel Grossman, Eilam Yeini, Paula Ofek, Tomer Meirson, Ronit Satchi-Fainaro, Hadas Reuveni, Tami Rubinek, Ido Wolf","doi":"10.1093/neuonc/noaf028","DOIUrl":"https://doi.org/10.1093/neuonc/noaf028","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) ranks as the fourth most common cause of brain metastasis (BM), with its incidence on the rise. However, the molecular mechanisms driving the formation of these lesions from CRC remain unclear.</p><p><strong>Methods: </strong>We analyzed the FoundationOne genomic database, which includes over 35,000 CRC samples from both local and metastatic sites. The role of insulin receptor substrate 2 (IRS2) in CRC brain tropism was investigated using various in vitro (co-culture systems and 3D sphere formation assays), in vivo (intracranial and subcutaneous mouse models), and ex vivo (CRC Patient-Derived Explants (PDE)) models. The molecular and metabolic effects of IRS2 were examined through RNA sequencing and Seahorse analysis. The therapeutic potential of a combined treatment with NT219, an IRS2 inhibitor, and 5-fluorouracil (5-FU) was assessed using our CRC BM mouse model.</p><p><strong>Results: </strong>Our research reveals a distinctive genomic profile of CRC BM and highlights the role of IRS2 in promoting CRC BM. IRS2 mediates its effect by modulating the β-catenin and oxidative phosphorylation (OXPHOS) pathways. We developed a mouse model of BM from CRC and demonstrated that treatment with the IRS2 inhibitor NT219, in combination with 5-FU, significantly suppresses BM development and prolongs survival.</p><p><strong>Conclusions: </strong>Our work underscores the unique role of IRS2 in facilitating CRC brain adaptation and suggests a novel therapeutic strategy for CRC patients with BM.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor cells upregulate neurotransmitter GABA in the choroid plexus through STAT6-Bestrophin1 signaling, promoting leptomeningeal dissemination.","authors":"Diganta Das, Mukund Iyer, Brooke Nakamura, Saman Sedighi, Angela Hsu, Camelia Danilov, Peter S LaViolette, Jennifer Connelly, Frances Chow, Josh Neman","doi":"10.1093/neuonc/noaf027","DOIUrl":"https://doi.org/10.1093/neuonc/noaf027","url":null,"abstract":"<p><strong>Background: </strong>Leptomeningeal dissemination (LMD) occurs when tumor cells interact with choroid plexus epithelium (CPE) to gain access to cerebrospinal fluid (CSF) in the brain's meninges and ventricular system. This disease is particularly devastating for patients due to our limited understanding and few therapeutic options. The leptomeningeal CSF is a nutritionally deprived microenvironment for tumor cells. Despite this, LMD tumor cells survive by taking up and metabolizing the neurotransmitter GABA from the CSF. However, we currently lack evidence on how CSF-GABA levels are altered and how tumor cells communicate with the choroid plexus epithelium to increase GABA levels in the LMD microenvironment. Herein, we examined the interactions between CPEs and tumor cells that make CSF more hospitable to LMD growth.</p><p><strong>Methods: </strong>We utilized primary choroid plexus, breast cancer cell and patient-derived breast and lung to brain metastatic cells along with in-vivo modeling along with STAT6 inhibitor and IL13 gene knockdown.</p><p><strong>Results: </strong>We show breast and lung cancer cells derived-IL13 activates STAT6 signaling in choroid plexus. Subsequently, choroid plexus upregulates GABA-synthesizing enzyme GAD67 and GABA-permeable channel Bestrophin-1, all leading to elevated neurotransmitter GABA levels in the cerebrospinal fluid. Moreover, we show a significant reduction of Bestrophin1 in choroid plexus when tumor-derived IL13 is knocked down or when treated with brain permeable STAT6 specific inhibitor AS1517499, leading to increased survival.</p><p><strong>Conclusions: </strong>Overall, these findings reveal a novel STAT6-Bestrophin1-GABA axis in choroid plexus and its therapeutic targeting can lead to favorable outcomes in leptomeningeal disease.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular Vesicles Released by Glioblastoma Cancer Cells Drive Tumor Invasiveness via Connexin-43 Gap Junctions.","authors":"Matteo Tamborini, Valentino Ribecco, Elisabetta Stanzani, Arianna Sironi, Monica Tambalo, Davide Franzone, Elena Florio, Edoardo Fraviga, Chiara Saulle, Maria C Gagliani, Marco Pizzocri, Milena Mattioli, Katia Cortese, Jean X Jiang, Giuseppe Martano, Letterio S Politi, Marco Riva, Federico Pessina, Davide Pozzi, Simona Lodato, Lorena Passoni, Michela Matteoli","doi":"10.1093/neuonc/noaf013","DOIUrl":"https://doi.org/10.1093/neuonc/noaf013","url":null,"abstract":"<p><strong>Background: </strong>Although invasiveness is one of the major determinants of the poor glioblastoma (GBM) outcome, the mechanisms of GBM invasion are only partially understood. Among the intrinsic and environmental processes promoting cell-to-cell interaction processes, eventually driving GBM invasion, we focused on the pro-invasive role played by Extracellular Vesicles (EVs), a heterogeneous group of cell-released membranous structures containing various bioactive cargoes, which can be transferred from donor to recipient cells.</p><p><strong>Methods: </strong>EVs isolated from patient-derived GBM cell lines and surgical aspirates were assessed for their pro-migratory competence by spheroid migration assays, calcium imaging, and PYK-2/FAK phosphorylation. Brain invasiveness was investigated in human cortical organoids-based assembloids and in vivo orthotopic xenografts. EV molecular features were specified by multiplex bead-based flow cytometry.</p><p><strong>Results: </strong>Results unveil a self-sustaining mechanism triggering migration through autocrine release and engagement of a specific population of EVs of large size (L-EVs), isolated from either patient-derived cell lines or surgical aspirates. L-EVs act through modulation of calcium transients via Connexin 43-Gap Junctions (Cx43-GJ) and phospho-activation of PYK2. Pre-incubation with blocking antibodies targeting Cx43 hemichannels demonstrated a dose-dependent inhibition of the L-EV-mediated GBM migration. By exploiting patients' surgical aspirates, we show that only L-EVs deriving from tumoral cells, and not those with immune origin, promote tumor migration, impacting more prominently the tumoral cells with mesenchymal subtype.</p><p><strong>Conclusions: </strong>We demonstrate that L-EVs released by GBM cells, but not by the immune cells of the tumor microenvironment, represent a relevant and unique autocrine pro-migratory input for the tumor.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoparticle encapsulation enables systemic IGF-Trap delivery to inhibit intra-cerebral glioma growth.","authors":"Yinhsuan Michely Chen, Julien Chambon, Alexandre Moquin, Masakazu Hashimoto, Stephanie Perrino, Matthew Leibovitch, Yasmine Benslimane, Orçun Haçariz, Qin Yang, Ichiro Nakano, Brian Meehan, Janusz Rak, Stéphane Gagné, Pnina Brodt","doi":"10.1093/neuonc/noaf011","DOIUrl":"https://doi.org/10.1093/neuonc/noaf011","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma is an aggressive brain cancer with a 5-year survival rate of 5-10%. Current therapeutic options are limited, due in part to drug exclusion by the blood-brain barrier, restricting access of targeted drugs to the tumor. The receptor for the type 1 insulin-like growth factor (IGF-1R) was identified as a therapeutic target in glioblastoma. We previously reported that the intracerebral growth of glioma cells with reduced IGF-1R levels was inhibited. The objectives of this study were to evaluate the sensitivity of glioma cells to a novel IGF-axis inhibitor, the IGF-Trap, and optimize its delivery to the brain.</p><p><strong>Methods: </strong>We tested the effect of the IGF-Trap on the growth of the human glioma stem cells MES-1123 and U87 MG cells, and of murine GL261 cells in vivo, using subcutaneous and orthotopic implantation.</p><p><strong>Results: </strong>We show that the growth of glioma cells implanted subcutaneously or orthotopically in the brain was inhibited by systemic and direct intracerebral administration of IGF-Trap, respectively, resulting in increased survival. To increase the efficiency of systemic delivery to the brain, we encapsulated the IGF-Trap in trimethyl chitosan (TRIOZAN™) nanoparticles prior to intravenous injection. We found that nanoparticle encapsulation increased the uptake and retention of the IGF-Trap in the brain and resulted in an improved therapeutic effect against intra-cerebrally growing tumors.</p><p><strong>Conclusion: </strong>Our results identify the IGF-Trap as a potent inhibitor of intracerebral glioma growth and show that encapsulation in nanoparticles can improve delivery of biologics such as the IGF-Trap to the brain, thereby enhancing the therapeutic response.</p>","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: Maternal obesogenic diet operates at the tumor cell of origin to increase incidence and decrease latency of neurofibromatosis type 1 optic pathway glioma.","authors":"","doi":"10.1093/neuonc/noaf010","DOIUrl":"https://doi.org/10.1093/neuonc/noaf010","url":null,"abstract":"","PeriodicalId":19377,"journal":{"name":"Neuro-oncology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}