In one paragraphArticle in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
17 authors.
Antoni MartijaDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0003-4293-6002 Brianna N BristowDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0002-0411-916X Dakshesh RanaDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0009-0005-0932-1761 Savan BolluDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0009-0000-3467-6453 Elisa FazzariDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0001-5651-8587 Shivani BaisiwalaDepartment of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0001-5252-9940 Claudia V NguyenDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0002-4796-6182 Weihong GeDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0003-2218-6291 Ryan L KanDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0003-1162-8365 Daria J AzizadDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0009-0006-7015-9027 Matthew X LiDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0009-0009-0539-7389 Patricia R NanoDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0002-5507-2656 Heejin ChoDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0003-4041-8033 Travis PerrymanDepartment of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0009-0004-5247-8898 David A NathansonDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0000-0002-4919-9159 Kunal S PatelDepartment of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0002-9854-9178 Aparna BhaduriDepartment of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California, Los Angeles, CA, USA.ORCID 0000-0003-4625-6899 Funding
UCLA SPORE in Brain CancerP50CA211015 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI David A. Nathanson · 2017 to 2026
$25.2MTUMOR CELL SURFACES AND CHROMOSOMEST32CA009056 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gay M Crooks, David A. Nathanson · 1985 to 2026
$10.5MTraining Grant in Neurobehavioral GeneticsT32NS048004 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEARDEN, CARRIE E, OPHOFF, ROEL A · 2004 to 2025
$5.8MUCLA-Caltech Medical Scientist Training ProgramT32GM152342 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Olujimi A Ajijola, David Wayne Dawson · 2024 to 2026
$5.3MResearch Training in Cell and Molecular BiologyT32GM145388 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jorge Torres · 2022 to 2026
$5.2MNCI NIH HHS P50 CA211015NCI NIH HHS T32 CA009056NIGMS NIH HHS T32 GM145388NIGMS NIH HHS T32 GM152342NINDS NIH HHS T32 NS048004
6 · The paper itselfAbstract
Glioblastoma (GBM) is a devastating primary brain tumor with remarkable inter- and intra-tumoral heterogeneity. GBM cells assume a spectrum of neurodevelopmental-like phenotypes and co-opt normal neurophysiological processes, which include synaptic integration with their neuronal microenvironment. This is mediated by neuron-tumor synapses (NTS) that predominantly involve glutamatergic receptors, which drive calcium elevations that promote tumor proliferation and invasion. The exact relationship between synaptic signaling and tumor cell fate specification, however, remains largely unexplored. Here, we develop and leverage a synapse-optimized human organoid tumor transplantation (so-HOTT) model of GBM to decipher how glutamatergic signaling impacts GBM lineage trajectories. so-HOTT preserves patient tumor heterogeneity, features excitatory NTS, and enables clonal lineage tracing of tumor cells after NTS perturbations. Genetic and pharmacological inhibition of AMPA and kainate receptors in so-HOTT shifts tumor cell composition from neuronal fates toward progenitor-proximal astrocytic/mesenchymal states. This occurs through the attenuation of calcium signaling and reduced plasticity of malignant radial glia (RG)-like progenitors, a previously unrecognized target of NTS. Through the integration of inputs from the neuronal microenvironment into glutamatergic signaling, progenitor populations modulate their transcriptional programs and cell fate, ultimately shaping GBM tumor heterogeneity. Targeting synaptic input may thus constrain the heterogeneity that fuels GBM adaptation and therapeutic escape.
Identifiers
PMID42182350
PMCPMC13192883
What OpenQuestion holds
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LicenceCC BY-NC
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