Evidence map›Paper›PMID 39946540›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

A clinically relevant model and method to study necrosis as a driving force in glioma restructuring and progression.

Jiabo Li, Ling-Kai Shih, Steven M Markwell, Cheryl L Olson, David P Sullivan, Constadina Arvanitis, James L Ross, Nicolas G Lam, Hannah Nuszen, Dolores Hambardzumyan and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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 registry

The 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 literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Jiabo Li *Department of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.ORCID 0000-0002-9288-9673
Ling-Kai Shih *Department of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
Steven M MarkwellDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.ORCID 0000-0003-4017-5430
Cheryl L OlsonDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
David P SullivanDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
Constadina ArvanitisDepartment of Cell and Developmental Biology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
James L RossDepartment of Microbiology and Immunology, Emory Vaccine Center, Emory University, Atlanta, GA 30322.
Nicolas G LamDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.ORCID 0000-0001-7146-1523
Hannah NuszenDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
Dolores HambardzumyanDepartments Oncological Sciences and Neurosurgery, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.ORCID 0000-0003-1975-4665
Oren J BecherJack Martin Division of Pediatric Hematology-Oncology, Mount Sinai Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Daniel J BratDepartment of Pathology, Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.ORCID 0000-0002-0633-6563

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Devalingam Mahalingam · 1993 to 2026
$153.9M
STINGing GBM: A First-in- Man Clinical Trial in Surgical Resectable Recurrent GBMP50CA221747 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Hui Zhang · 2018 to 2026
$21.4M
Modeling the Glioblastoma Microenvironment to Uncover Progression Mechanisms and Therapeutic TargetsR01CA247905 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BRAT, DANIEL J · 2020 to 2024
$2.5M
Identification and targeting of mechanisms specific to glioma stem cells in glioblastomaR01CA214928 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BRAT, DANIEL J · 2018 to 2022
$1.8M
Olympus FV1000MPE Multiphoton MicroscopeS10OD010398 · OD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHEW, TENG-LEONG · 2012 to 2012
$551k
Aging Exacerbates Neutrophil Persistence and Negatively Impacts Stroke OutcomesR21AG086751 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BATRA, AYUSH, SULLIVAN, DAVID PATRICK · 2024 to 2024
$440k
HHS | NIH | National Cancer Institute (NCI) P30CA060553HHS | NIH | National Cancer Institute (NCI) P50CA221747HHS | NIH | National Cancer Institute (NCI) R01CA214928HHS | NIH | National Cancer Institute (NCI) R01CA247905HHS | NIH | NIH Office of the Director (OD) 1S10OD010398-01NCI NIH HHS P30 CA060553NCI NIH HHS P50 CA221747NCI NIH HHS R01 CA214928NCI NIH HHS R01 CA247905NIA NIH HHS R21 AG086751NIH HHS S10 OD010398
6 · The paper itself

Abstract

All glioblastoma (GBM) molecular subsets share the common trait of accelerated progression following necrosis, which cannot be adequately explained by cellular proliferation arising from accumulated genetic alterations. Counter to dogma that "cancer outgrows its blood supply," we suggest that development of necrosis is not merely a consequence of aggressive neoplastic growth but could be a contributing force causing tumor microenvironment (TME) restructuring and biologic progression. Mechanisms related to necrotic contributions are poorly understood due to a lack of methods to study necrosis as a primary variable. To reveal spatiotemporal changes related to necrosis directly, we developed a mouse model and methodology designed to induce clinically relevant thrombotic vaso-occlusion within GBMs in an immunocompetent RCAS/tv-a mouse model to study TME restructuring by intravital microscopy and demonstrate its impact on glioma progression. Diffuse high-grade gliomas are generated by introducing RCAS-PDGFB-RFP and RCAS-Cre in a

Indexed as

Brain NeoplasmsGlioblastomaGliomaNecrosisAnimalsDisease Models, AnimalDisease ProgressionHumansMiceMice, TransgenicTumor Microenvironmentglioblastomaglioma stem cellmouse modelnecrosistumor-associated macrophage

Identifiers

PMID39946540
PMCPMC11848380

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.