tbuckley/cabot-search huggingface dataset:
Intracerebroventricular B7-H3-targeting CAR T cells for diffuse intrinsic pontine glioma: a phase 1 trial
Authors: Nicholas A. Vitanza, Rebecca Ronsley, Michelle Choe, Kristy Seidel, Wenjun Huang, Stephanie D. Rawlings-Rhea, Madison Beam, Leonel Steinmetzer, Ashley L. Wilson, Christopher Brown, Adam Beebe, Catherine Lindgren, Joshua A. Gustafson, Amy Wein, Susan Holtzclaw, Corrine Hoeppner, Hannah E. Goldstein, Samuel R. Browd, Jason S. Hauptman, Amy Lee, Jeffrey G. Ojemann, Erin E. Crotty, Sarah E. S. Leary, Francisco A. Perez, Jason N. Wright, Marta M. Alonso, Matthew D. Dun, Jessica B. Foster, Diana Hurst, Ada Kong, Alison Thomsen, Rimas J. Orentas, Catherine M. Albert, Navin Pinto, Colleen Annesley, Rebecca A. Gardner, On Ho, Sowmya Pattabhi, Juliane Gust, Jason P. Wendler, Julie R. Park, Michael C. Jensen
Journal: Nature Medicine (2025)

Abstract Diffuse intrinsic pontine glioma (DIPG) is a fatal central nervous system (CNS) tumor that confers a median survival of 11 months. As B7-H3 is expressed on pediatric CNS tumors, we conducted BrainChild-03, a single-center, dose-escalation phase 1 clinical trial of repetitive intracerebroventricular (ICV) dosing of B7-H3-targeting chimeric antigen receptor T cells (B7-H3 CAR T cells) for children with recurrent or refractory CNS tumors and DIPG. Here we report results from Arm C, restricted to patients with DIPG. The primary objectives were to assess feasibility and tolerability, which were both met. Secondary objectives included assessments of CAR T cell distribution and survival. A total of 23 patients with DIPG enrolled, and 21 were treated with repeated doses of ICV B7-H3 CAR T cells using intra-patient dose-escalation regimens without previous lymphodepletion. Concurrent tumor-directed therapy, including re-irradiation, was not allowed while on protocol therapy. We delivered a total of 253 ICV doses and established the highest planned dose regimen, DR4, which escalated up to 10 × 10 7 cells per dose, as the maximally tolerated dose regimen. Common adverse events included headache, fatigue and fever. There was one dose-limiting toxicity (intratumoral hemorrhage) during DR2. For all treated patients ( n = 21), the median survival from their initial CAR T cell infusion was 10.7 months and the median survival from diagnosis was 19.8 months with 3 patients still alive at 44, 45 and 52 months from diagnosis. Ultimately, this completed first-in-human trial shows that repetitive ICV dosing of B7-H3 CAR T cells in pediatric and young adult patients with DIPG is tolerable, including multiyear repeated dosing, and may have clinical efficacy that warrants further investigation on a multisite phase 2 trial. ClinicalTrials.gov registration: NCT04185038 .
Author Correction: Profibrotic monocyte-derived alveolar macrophages are expanded in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19
Authors: Joseph I. Bailey, Connor H. Puritz, Karolina J. Senkow, Nikolay S. Markov, Estefani Diaz, Emmy Jonasson, Zhan Yu, Suchitra Swaminathan, Ziyan Lu, Samuel Fenske, Rogan A. Grant, Hiam Abdala-Valencia, Ruben J. Mylvaganam, Amy Ludwig, Janet Miller, R. Ian Cumming, Robert M. Tighe, Kymberly M. Gowdy, Ravi Kalhan, Manu Jain, Ankit Bharat, Chitaru Kurihara, Ruben San Jose Estepar, Raul San Jose Estepar, George R. Washko, Ali Shilatifard, Jacob I. Sznajder, Karen M. Ridge, G. R. Scott Budinger, Rosemary Braun, Alexander V. Misharin, Marc A. Sala
Journal: Nature Immunology (2025)
Effects of early, late and self-selected time-restricted eating on visceral adipose tissue and cardiometabolic health in participants with overweight or obesity: a randomized controlled trial
Authors: Manuel Dote-Montero, Antonio Clavero-Jimeno, Elisa Merchán-Ramírez, Maddi Oses, Jon Echarte, Alba Camacho-Cardenosa, Mara Concepción, Francisco J. Amaro-Gahete, Juan M. A. Alcántara, Alejandro López-Vázquez, Rocío Cupeiro, Jairo H. Migueles, Alejandro De-la-O, Patricia V. García Pérez, Victoria Contreras-Bolivar, Araceli Muñoz-Garach, Ana Zugasti, Estrella Petrina, Natalia Alvarez de Eulate, Elena Goñi, Cristina Armendariz-Brugos, Maria T. González Cejudo, Jose L. Martín-Rodríguez, Fernando Idoate, Rafael Cabeza, Almudena Carneiro-Barrera, Rafael de Cabo, Manuel Muñoz-Torres, Idoia Labayen, Jonatan R. Ruiz
Journal: Nature Medicine (2025)
Single-dose suraxavir marboxil for acute uncomplicated influenza in adults and adolescents: a multicenter, randomized, double-blind, placebo-controlled phase 3 trial
Authors: Yeming Wang, Hong Wang, Yu Zhang, Anlin Ma, Dong Liu, Xiaoguang Li, Guoru Yang, Min Deng, Shaofang Wang, Yuanyuan Liu, Chuanmiao Liu, Fangqi Ge, Sikui Wang, Yunsong Yu, Ganzhu Feng, Zuke Xiao, Xing Li, Yilan Sun, Xuyan Chen, Zhaolong Cao, Yan Ding, Xiaoping Wu, Jun Wei, Bin Cao
Journal: Nature Medicine (2025)
Neoadjuvant anti-PD-1 alone or in combination with anti-TIGIT or an oncolytic virus in resectable stage IIIB–D melanoma: a phase 1/2 trial
Authors: Reinhard Dummer, Caroline Robert, Richard A. Scolyer, Janis M. Taube, Michael T. Tetzlaff, Alexander M. Menzies, Andrew Hill, Jean-Jacques Grob, David C. Portnoy, Celeste Lebbe, Muhammad A. Khattak, Jonathan Cohen, Gil Bar-Sela, Inderjit Mehmi, Ronnie Shapira-Frommer, Nicolas Meyer, Andrea L. Webber, Yixin Ren, Mizuho Fukunaga-Kalabis, Clemens Krepler, Georgina V. Long
Journal: Nature Medicine (2025)

Neoadjuvant immunotherapies have shown antitumor activity in melanoma. Substudy 02C of the global, rolling-arm, phase 1/2, adaptive-design KEYMAKER-U02 trial is evaluating neoadjuvant pembrolizumab (anti-PD-1) alone or in combination, followed by adjuvant pembrolizumab, for stage IIIB–D melanoma. Here we report results from the first three arms: pembrolizumab plus vibostolimab (anti-TIGIT), pembrolizumab plus gebasaxturev (coxsackievirus A21) and pembrolizumab monotherapy. Pathologic complete responses occurred in 10 of 26 patients (38%) with pembrolizumab plus vibostolimab, 7 of 25 (28%) with pembrolizumab plus gebasaxturev and 6 of 15 (40%) with pembrolizumab monotherapy. Major pathologic responses occurred in 13 (50%), 10 (40%) and 7 (47%) patients, respectively. Safety was manageable. Treatment-related adverse events occurred in 24 of 26 patients (92%) with pembrolizumab plus vibostolimab, 21 of 25 (84%) with pembrolizumab plus gebasaxturev and 12 of 15 (80%) with pembrolizumab monotherapy; grade 3 or 4 treatment-related adverse events occurred in 2 (8%), 7 (28%) and 1 (7%) patient in each arm, respectively. No deaths due to adverse events occurred. Exploratory objective responses per RECIST v1.1 were observed in 13 (50%), 8 (32%) and 4 (27%) patients, in each arm, respectively. In a post hoc analysis, scores for tumor mutational burden and an 18-gene T cell-inflamed gene expression profile were generally higher in patients with major pathologic response. Longer follow-up will provide insight into the incremental benefit of combining neoadjuvant pembrolizumab with other therapies in stage IIIB–D melanoma. ClinicalTrials.gov registration: NCT04303169 . In an ongoing adaptive-design trial exploring different combinations of neoadjuvant immunotherapies including the anti-PD-1 agent pembrolizumab, the anti-TIGIT agent vibostolimab and the oncolytic virus gebasaxturev, neoadjuvant pembrolizumab-based regimens elicited encouraging clinical responses in patients with resectable melanoma.
Intracerebroventricular anaerobic dopamine in Parkinson’s disease with l-dopa-related complications: a phase 1/2 randomized-controlled trial
Authors: Caroline Moreau, Pascal Odou, Julien Labreuche, Alexandre Demailly, Gustavo Touzet, Nicolas Reyns, Bastien Gouges, Alain Duhamel, Christine Barthelemy, Damien Lannoy, Natacha Carta, Benjamin Palas, Michèle Vasseur, Felix Marchand, Thomas Ollivier, Céline Leclercq, Camille Potey, Thavarak Ouk, Simon Baigne, Kathy Dujardin, Louise Carton, Anne Sophie Rolland, Jean Christophe Devedjian, Véronique Foutel, Dominique Deplanque, Matthieu Fisichella, David Devos
Journal: Nature Medicine (2025)

Continuous compensation for cerebral dopamine deficiency represents an ideal treatment for Parkinson's disease. Dopamine does not cross the digestive and blood–brain barriers and is rapidly oxidized. The new concept is the intracerebroventricular administration of anaerobic dopamine (A-dopamine) using an abdominal pump connected to a subcutaneous catheter implanted in the third ventricle, near the striatum. An open-label phase 1 study showed no serious adverse reactions induced by A-dopamine in 12 patients. A randomized, controlled, open-label, crossover phase 2 study of 1 month of A-dopamine versus 1 month of optimized oral antiparkinsonian therapy was conducted in 9 patients. The primary endpoint, a blinded assessment of the percentage over target (that is, time with dyskinesia or bradykinesia), recorded by home actimetry using a wristwatch, was significantly reduced on A-dopamine compared with that on oral treatment alone (P = 0.027), with a median within-patient difference of −10.4 (Hedge g = −0.62 (95% confidence interval: −1.43, −0.08)). Home diaries were also significantly improved. These initial data on the feasibility, safety and effects of this new device-assisted therapy suggest validation by a large randomized double-blind trial. ClinicalTrials.gov registration: NCT04332276 . A phase 1/2 clinical trial of a new device-assisted therapy in Parkinson's disease revealed that intracerebroventricular administration of anaerobic dopamine was safe and significantly reduced l-dopa-related complications.
Angiogenic factors versus fetomaternal Doppler for fetal growth restriction at term: an open-label, randomized controlled trial
Authors: Pablo Garcia-Manau, Erika Bonacina, Raquel Martin-Alonso, Lourdes Martin, Ana Palacios, Maria Luisa Sanchez-Camps, Cristina Lesmes, Ivan Hurtado, Esther Perez, Albert Tubau, Patricia Ibañez, Marina Alcoz, Nuria Valiño, Elena Moreno, Carlota Borrero, Esperanza Garcia, Eva Lopez-Quesada, Sonia Diaz, Jose Roman Broullon, Mireia Teixidor, Carolina Chulilla, Roser Ferrer-Costa, Maria M. Gil, Monica Lopez, Gemma M. Ramos-Forner, José Eliseo Blanco, Anna Moreno, Marta Lázaro-Rodríguez, Oscar Vaquerizo, Beatriz Soriano, Marta Fabre, Elena Gomez-Valencia, Ana Cuiña, Nicolas Alayon, Jose Antonio Sainz-Bueno, Angels Vives, Esther Esteve, Vanesa Ocaña, Miguel Ángel López, Anna Maroto, Elena Carreras, Manel Mendoza
Journal: Nature Medicine (2025)
The hepatic clock synergizes with HIF-1α to regulate nucleotide availability during liver damage repair
Authors: Linyuan Peng, Siliang Xiang, Tianzhi Wang, Mei Yang, Yajun Duan, Xiaoyu Ma, Su Li, Cong Yu, Xin Zhang, Haiyang Hu, Zuojun Liu, Jie Sun, Chunmeng Sun, Chen Wang, Baohua Liu, Zhongyuan Wang, Minxian Qian
Journal: Nature Metabolism (2025)
Multi-omics-based mapping of decidualization resistance in patients with a history of severe preeclampsia
Authors: Irene Muñoz-Blat, Raúl Pérez-Moraga, Nerea Castillo-Marco, Teresa Cordero, Ana Ochando, Sheila Ortega-Sanchís, Marcos Parras, Rogelio Monfort-Ortiz, Elena Satorres-Perez, Blanca Novillo, Alfredo Perales, Matthew Gormley, Sofia Granados-Aparici, Rosa Noguera, Beatriz Roson, Susan J. Fisher, Carlos Simón, Tamara Garrido-Gómez
Journal: Nature Medicine (2025)

Endometrial decidualization resistance (DR) is implicated in various gynecological and obstetric conditions. Here, using a multi-omic strategy, we unraveled the cellular and molecular characteristics of DR in patients who have suffered severe preeclampsia (sPE). Morphological analysis unveiled significant glandular anatomical abnormalities, confirmed histologically and quantified by the digitization of hematoxylin and eosin-stained tissue sections. Single-cell RNA sequencing (scRNA-seq) of endometrial samples from patients with sPE (n = 11) and controls (n = 12) revealed sPE-associated shifts in cell composition, manifesting as a stromal mosaic state characterized by proliferative stromal cells (MMP11 and SFRP4) alongside IGFBP1+ decidualized cells, with concurrent epithelial mosaicism and a dearth of epithelial–stromal transition associated with decidualization. Cell–cell communication network mapping underscored aberrant crosstalk among specific cell types, implicating crucial pathways such as endoglin, WNT and SPP1. Spatial transcriptomics in a replication cohort validated DR-associated features. Laser capture microdissection/mass spectrometry in a second replication cohort corroborated several scRNA-seq findings, notably the absence of stromal to epithelial transition at a pathway level, indicating a disrupted response to steroid hormones, particularly estrogens. These insights shed light on potential molecular mechanisms underpinning DR pathogenesis in the context of sPE. A multi-omics analysis of decidualization resistance, which is implicated in various gynecological and obstetric conditions, in patients with a history of severe preeclampsia revealed defects in the stroma, epithelium and epithelial-to-stromal transition, with findings validated in a separate replication cohort.
Deep CRISPR mutagenesis characterizes the functional diversity of TP53 mutations
Authors: Julianne S. Funk, Maria Klimovich, Daniel Drangenstein, Ole Pielhoop, Pascal Hunold, Anna Borowek, Maxim Noeparast, Evangelos Pavlakis, Michelle Neumann, Dimitrios-Ilias Balourdas, Katharina Kochhan, Nastasja Merle, Imke Bullwinkel, Michael Wanzel, Sabrina Elmshäuser, Julia Teply-Szymanski, Andrea Nist, Tara Procida, Marek Bartkuhn, Katharina Humpert, Marco Mernberger, Rajkumar Savai, Thierry Soussi, Andreas C. Joerger, Thorsten Stiewe
Journal: Nature Genetics (2025)

Abstract The mutational landscape of TP53 , a tumor suppressor mutated in about half of all cancers, includes over 2,000 known missense mutations. To fully leverage TP53 mutation status for personalized medicine, a thorough understanding of the functional diversity of these mutations is essential. We conducted a deep mutational scan using saturation genome editing with CRISPR-mediated homology-directed repair to engineer 9,225 TP53 variants in cancer cells. This high-resolution approach, covering 94.5% of all cancer-associated TP53 missense mutations, precisely mapped the impact of individual mutations on tumor cell fitness, surpassing previous deep mutational scan studies in distinguishing benign from pathogenic variants. Our results revealed even subtle loss-of-function phenotypes and identified promising mutants for pharmacological reactivation. Moreover, we uncovered the roles of splicing alterations and nonsense-mediated messenger RNA decay in mutation-driven TP53 dysfunction. These findings underscore the power of saturation genome editing in advancing clinical TP53 variant interpretation for genetic counseling and personalized cancer therapy.
Regulation of T Cell Glycosylation by MXene/β‐TCP Nanocomposite for Enhanced Mandibular Bone Regeneration
Authors: Fei Yu, Xing Zhao, Shuting Zhang, Wenxin Lu, Peilin Li, Wei Yang, Zhihe Zhao
Journal: Advanced Healthcare Materials (2025)

Immune-mediated bone regeneration driven by bone biomaterials offers a therapeutic strategy for repairing bone defects. Among 2D nanomaterials, Ti3C2Tx MXenes have garnered substantial attention for their potential in tissue regeneration. This investigation concentrates on the role of MXene nanocomposites in modulating the immune microenvironment within bone defects to facilitate bone tissue restoration. Ti3C2Tx MXenes are synthetized, incorporated into beta-tricalcium phosphate ceramics (β-TCP) nanocomposites (T-MXene), and their osteoinductive and immunomodulatory effects are evaluated. The effects of T-MXene-treated T-cells on bone marrow stromal cells (BMSCs) are explored. In addition, its therapeutic potential for bone regeneration is assessed in vivo using a critical-sized mandibular bone defect model. The underlying mechanisms by which T-MXene regulates T-cell differentiation and bone regeneration are explored via whole-transcriptome RNA sequencing. The scaffolds activate N-glycosylation in T cells, which possess anti-inflammatory and antioxidant effects, thereby inducing a pro-regenerative response. T-MXene increased the proportion of IL-4+ T cells among primary T cells and mandibular lymph nodes, ultimately promoting osteogenesis in BMSCs and injured mandibles. The distinctive function of MXene-based nanocomposites in osteoimmunomodulation provides a solid foundation for further exploration and application of MXenes as immune response modulators, potentially advancing their use in regenerative medicine.
Effect of exercise training on modulating the TH17/TREG imbalance in individuals with severe COPD: A randomized controlled trial
Authors: Juliana Tiyaki Ito, Luan Henrique Vasconcelos Alves, Luana de Mendonça Oliveira, Rafaella Fagundes Xavier, Regina Maria Carvalho-Pinto, Iolanda de Fátima Lopes Calvo Tibério, Maria Notomi Sato, Celso R. F. Carvalho, Fernanda Degobbi Tenorio Quirino dos Santos Lopes
Journal: Pulmonology (2025)

Background Chronic obstructive pulmonary disease (COPD) induces an imbalance in T helper (Th) 17/regulatory T (Treg) cells that contributes to of the dysregulation of inflammation. Exercise training can modulate the immune response in healthy subjects.
MgSO<sub>4</sub> as a novel hypothermia infusion solution promotes ischemic stroke recovery through Ca<sup>2+</sup> regulation of neurovascular units
Authors: Yang Zhang, Miaowen Jiang, Ming Wei, Chuanjie Wu, Yiming Huang, Baoying Song, Yi Xu, Hongkang Zhang, Yunong Shen, Di Wu, Yufeng Zheng, Ming Li, Xunming Ji
Journal: Theranostics (2025)

The neuroprotection of acute ischemic stroke (AIS) patients to alleviate the reperfusion injury is a long-standing problem. Although the intra-arterial selective cooling saline infusion (IA-SCSI) is a promising technique to improve the outcome of AIS, the clinical results are not sufficiently satisfactory. Magnesium-containing solutions such as magnesium sulfate (MgSO4) can protect cells by modulating the intracellular Ca2+ content in damaged cells, suggesting that they could be hypothermia infusion solution. In this study, we hypothesized that MgSO4, as a novel hypothermia infusion solution (IA-SCMI), can promote AIS recovery. Methods: First, IA-SCMI was performed in rats subjected to the middle cerebral artery occlusion. The effect of combined hypothermia and MgSO4 treatment on different neurovascular (NVU) cells after oxygen-glucose deprivation/reoxygenation (OGD/R) injury was examined. Results: Compared with the IA-SCSI or IA-MgSO4 infusion alone, IA-SCMI offered the best protective effect by improving neurological defects, and alleviating brain integrity damage and CBF reduction. Meanwhile, in vitro results revealed that the combination of hypothermia and MgSO4 provided maximum protection to the NVU cells, and this protective effect was mainly achieved through the regulation of Ca2+ homeostasis in different cells. Conclusion: MgSO4 may be a promising hypothermia infusion solution to facilitate the recovery of neurological function in AIS patients.
Oncogenic non-V600 mutations evade the regulatory machinery of RAF including the Cdc37/Hsp90 chaperone and the 14-3-3 scaffold
Authors: Xiaoyu Wan, Jiajun Yap, Junjun Chen, Yifan Li, Regina Faruk, Nazereth Tan Chor Boon, Yiying Ma, Yiting Lim, Karlina Bte Jubri, Jingyi Hu, Jimin Yuan, Ge Zhang, Quan Li, Yoon Sim Yap, Paula Lam, Mei Wang, Naiyang Fu, Jiancheng Hu
Journal: Theranostics (2025)

The Ser/Thr kinase RAF, particularly BRAF isoform is a dominant target of oncogenic mutations and many mutations have been identified in various cancers. However, how these mutations except V600E evade the regulatory machinery of RAF protein and hence trigger its oncogenicity remains unclear. Methods: In this study, we used mutagenesis, peptide affinity assay, immunoprecipitation, immunoblot, and complementary split luciferase assay as well as mouse xenograft tumour model to investigate how the function of RAF is cooperatively regulated by Cdc37/Hsp90 chaperones and 14-3-3 scaffolds and how this regulatory machinery is evaded by prevalent non-V600 mutations. Results: We found that Cdc37/Hsp90 chaperones engaged with mature BRAF proteins promoted together with 14-3-3 scaffolds a switch of BRAF proteins from active open dimers into inactive close monomers. Most non-V600 mutations were enriched on or around the Cdc37/Hsp90-binding segments of BRAF, which impair association of CDc37/Hsp90 chaperones with BRAF and hence trap BRAF in active open conformation favouring dimerization. These BRAF mutants with high dimer propensity sustained a prolonged ERK signaling, and were effectively targeted by RAF dimer breaker plx8394 in vitro and in vivo. In contrast, CRAF and ARAF existed as immature monomers highly packaged with Cdc37/Hsp90 chaperones, which will be released upon dimerization driven by RAS-GTP binding with their N-terminus as well as 14-3-3 scaffold association with their C-terminus. Mature CRAF and ARAF dimers also sustained a prolonged ERK signaling as non-V600 BRAF mutants by virtue of absence of the C-terminal Cdc37/Hsp90-binding segment. Conclusions: Cdc37/Hsp90 chaperones and 14-3-3 scaffolds cooperatively facilitate the switch of RAF proteins from open active dimers to close inactive monomers. Non-V600 mutations disrupt this regulatory machinery, and trap RAF in dimers, which could be targeted by RAF dimer breakers.
Tumor initiating cells escape tumor immunity via CCL8 from tumor-associated macrophages in mice
Authors: Shuang Chen, Chen-Song Huang, Kang Li, Maosheng Cheng, Caihua Zhang, Jianqi Xiong, Guoli Tian, Ruoxing Zhou, Rongsong Ling, Xiaochen Wang, Gan Xiong, Zhihui Zhang, Jieyi Ma, Yan Zhu, Bin Zhou, Liang Peng, Zhenwei Peng, Heping Li, Demeng Chen
Journal: Journal of Clinical Investigation (2025)

Tumor-initiating cells (TICs) play a key role in cancer progression and immune escape. However, how TICs evade immune elimination remains poorly characterized. Combining single-cell RNA sequencing (scRNA-seq), dual-recombinase-based lineage tracing, and other approaches, we identified a WNT-activated subpopulation of malignant cells that act as TICs in vivo. We found intensive reciprocal interactions between TICs and immune regulatory tumor-associated macrophages (Reg-TAMs) via GAS6-AXL/MERTK signaling pathways, which facilitated the immune escape of TICs. Our study employed chemical inhibitors and Axl/Mertk conditional double knockout mice to demonstrate that inhibiting the interaction between TIC-derived GAS6 and AXL/MERTK in Reg-TAMs reactivated anti-tumor immune responses. We identified CCL8 as a critical mediator of the GAS6/AXL/MERTK pathway, primarily by inhibiting regulatory T cell (Treg) infiltration into the tumor. Furthermore, the AXL/MERTK signaling blockade sensitized tumor cells to anti-PD-1 treatment. Thus, we elucidated a detailed mechanism by which TICs evade tumor immunity, providing insights into strategies to eradicate TICs that escape conventional immunotherapy.
Predicting recurrence of meningioma using DNA methylation for clinical practice
Authors: Karenna J Groff, Matija Snuderl
Journal: Neuro-Oncology (2025)

Journal Article Accepted manuscript Predicting recurrence of meningioma using DNA methylation for clinical practice Get access Karenna J Groff, Karenna J Groff Division of Neuropathology, Department of Pathology, NYU Langone Health and Grossman School of Medicine, New York, New York, USA https://orcid.org/0000-0002-6725-094X Search for other works by this author on: Oxford Academic PubMed Google Scholar Matija Snuderl Matija Snuderl Division of Neuropathology, Department of Pathology, NYU Langone Health and Grossman School of Medicine, New York, New York, USA Corresponding Author: Matija Snuderl, MD, Professor of Pathology, Director of Molecular Pathology, NYU Langone Health, Department of Pathology, 240 E 38th Street, 22nd Floor, New York, NY 10016, T: 646-501-5281, Fax: 212-263-7712, Email: [email protected] https://orcid.org/0000-0003-0752-0917 Search for other works by this author on: Oxford Academic PubMed Google Scholar Neuro-Oncology, noaf003, https://doi.org/10.1093/neuonc/noaf003 Published: 08 January 2025 Article history Received: 31 December 2024 Published: 08 January 2025