In one paragraphArticle in Neuro-oncology, 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
21 authors.
Elaheh HashemiDepartment of Neurological Surgery, University of California, San Francisco, California, USA.
Ravishkumar Lakshmi AkshayaDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0001-9646-5846 Lin WangDepartment of Neurological Surgery, University of California, San Francisco, California, USA.
Spencer BerglandDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0009-0009-8430-3546 Hadeesha PiyadasaDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0002-0276-6590 Jolene S RanekDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0002-0701-0565 Viva VoongDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0009-0002-2376-6781 Aditya KshirsagarDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0001-8926-9353 Anny ShaiDepartment of Neurological Surgery, University of California, San Francisco, California, USA.
Benjamin OberltonDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Anupam KumarDepartment of Neurological Surgery, University of California, San Francisco, California, USA.
Mitchel S BergerDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0003-1983-4892 Edward F ChangDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0003-2480-4700 Michael C OldhamDepartment of Neurological Surgery, University of California, San Francisco, California, USA.
Sean C BendallDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0003-1341-2453 Michael AngeloDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.ORCID 0000-0003-1531-5067 Shawn L Hervey-JumperDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0003-4699-260X Hideho OkadaDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0003-0076-9920 Aaron DiazDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0001-9059-9501 Joanna J PhillipsDepartment of Neurological Surgery, University of California, San Francisco, California, USA.ORCID 0000-0002-3789-8120 Funding
Tissue CoreP50CA097257 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2002 to 2026
$57.4MTraining Program in Translational Brain Tumor ResearchT32CA151022 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2010 to 2026
$6.6MAn informatics framework for single-cell multi-omics from clinical specimensR01LM013897 · NLM · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Aaron Antonio Diaz · 2022 to 2026
$1.8MRegulating the glioma immune microenvironmentR01NS131474 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joanna Phillips · 2024 to 2026
$1.8MPreclinical development of breakthrough immunotherapy for brain tumorsR35NS142982 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Hideho Okada · 2026 to 2026
$943kAlliance for Cancer Gene TherapyAmerican Brain Tumor Association Basic Research FellowshipCancer Research Society Postdoctoral FellowshipDepartment of Defense W81XWH-19-1-0348Karl Schmidt Oligodendroglioma Research Fund BRF2500040NCI NIH HHS P50 CA097257NCI NIH HHS T32 CA151022NIH HHS P50 CA097257NIH HHS P50CA097257NIH HHS R01LM013897NIH HHS R01 NS131474NIH HHS R35 1R35NS142982-01NIH HHS T32 CA151022NINDS NIH HHS R01 NS131474NINDS NIH HHS R35 NS142982NLM NIH HHS R01 LM013897Parker Institute for Cancer ImmunotherapyT.J. Martell FoundationUCSF Brain Tumor SPORE Biorepository
6 · The paper itselfAbstract
backgroundIn brain tumors, the immunosuppressive microenvironment leads to tumor aggressiveness and immunotherapy resistance. To identify factors that regulate the glioma-immune landscape, we took advantage of the disease trajectory of the MAPK-driven glioma, pleomorphic xanthoastrocytoma (PXA), which evolves from an immune-rich low-grade tumor to an aggressive glioma.
methodsUsing a multiomics approach that included single-nucleus RNA sequencing, spatial transcriptomics, and spatial proteomics, a cohort of 38 tumors, including 10 longitudinal pairs, was profiled.
resultsTumor progression was associated with transition to a more proliferative progenitor state and increased hypoxia. Hypoxic reprogramming of the immune landscape included increased TGF-β signaling and altered chemokine signaling, including decreased CXC-chemokine ligand 14 (CXCL14) and CXCL16-CXCR6 signaling important in immune cell recruitment and activation. The resulting immune landscape was spatially reorganized with reduced HLA class II expression, reduced CD8+ and CD4+ T cells, and dominated by immunosuppressive myeloid cells.
conclusionsHypoxia and chemokine signaling emerged as key components of the glioma-immune landscape that evolve with tumor progression. These findings identify potential therapeutic opportunities in PXA, and they argue that optimal immunomodulatory strategies in glioma will differ along the disease trajectory.
Indexed as
Brain NeoplasmsGliomaMitogen-Activated Protein KinasesTumor MicroenvironmentDisease ProgressionHumansMultiomicsSignal TransductionMitogen-Activated Protein KinasesCXCL16-CXCR6glioma-immune microenvironmentglioma multiomicsspatial proteomicstumor hypoxia
Identifiers
PMID42377256
PMCPMC13635575
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