Evidence map›Paper›PMID 29793116›Full record

ArticleNeoplasia (New York, N.Y.)2018

Patterns of Invasive Growth in Malignant Gliomas-The Hippocampus Emerges as an Invasion-Spared Brain Region.

Awais A Mughal, Lili Zhang, Artem Fayzullin, Andres Server, Yuping Li, Yingxi Wu, Rainer Glass, Torstein Meling, Iver A Langmoen, Trygve B Leergaard and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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  8. Remote Neuroinflammation in Newly Diagnosed Glioblastoma Correlates with Unfavorable Clinical Outcome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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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

11 authors at 3 institutions in 1 country.

Awais A MughalVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; SFI-CAST-Cancer Stem Cell Innovation Center, Oslo University Hospital, Oslo, Norway. Electronic address: awaisam@gmail.com.
Lili ZhangInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
Artem FayzullinVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Andres ServerSection of Neuroradiology, Department of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway.
Yuping LiNeurosurgical Research, Ludwig-Maximilian University of Munich, Munich, Germany.
Yingxi WuNeurosurgical Research, Ludwig-Maximilian University of Munich, Munich, Germany.
Rainer GlassNeurosurgical Research, Ludwig-Maximilian University of Munich, Munich, Germany.
Torstein MelingDepartment of Neurosurgery, Oslo University Hospital, and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Iver A LangmoenVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; SFI-CAST-Cancer Stem Cell Innovation Center, Oslo University Hospital, Oslo, Norway; Norwegian Center for Stem Cell Research, Department of Immunology and Transfusion Medicine, Oslo University Hospital, Norway.
Trygve B LeergaardDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Norway.
Einar O Vik-MoVilhelm Magnus Laboratory for Neurosurgical Research, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway; Department of Neurosurgery, Oslo University Hospital, and Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; SFI-CAST-Cancer Stem Cell Innovation Center, Oslo University Hospital, Oslo, Norway; Norwegian Center for Stem Cell Research, Department of Immunology and Transfusion Medicine, Oslo University Hospital, Norway.
Oslo University Hospital · NOUniversity of Oslo · NOInstitutt for Eksperimentell Medisinsk Forskning · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWidespread infiltration of tumor cells into surrounding brain parenchyma is a hallmark of malignant gliomas, but little data exist on the overall invasion pattern of tumor cells throughout the brain.

methodsWe have studied the invasive phenotype of malignant gliomas in two invasive mouse models and patients. Tumor invasion patterns were characterized in a patient-derived xenograft mouse model using brain-wide histological analysis and magnetic resonance (MR) imaging. Findings were histologically validated in a cdkn2a-/- PDGF-β lentivirus-induced mouse glioblastoma model. Clinical verification of the results was obtained by analysis of MR images of malignant gliomas.

resultsHistological analysis using human-specific cellular markers revealed invasive tumors with a non-radial invasion pattern. Tumors cells accumulated in structures located far from the transplant site, such as the optic white matter and pons, whereas certain adjacent regions were spared. As such, the hippocampus was remarkably free of infiltrating tumor cells despite the extensive invasion of surrounding regions. Similarly, MR images of xenografted mouse brains displayed tumors with bihemispheric pathology, while the hippocampi appeared relatively normal. In patients, most malignant temporal lobe gliomas were located lateral to the collateral sulcus. Despite widespread pathological fluid-attenuated inversion recovery signal in the temporal lobe, 74% of the "lateral tumors" did not show signs of involvement of the amygdalo-hippocampal complex.

conclusionsOur data provide clear evidence for a compartmental pattern of invasive growth in malignant gliomas. The observed invasion patterns suggest the presence of preferred migratory paths, as well as intra-parenchymal boundaries that may be difficult for glioma cells to traverse supporting the notion of compartmental growth. In both mice and human patients, the hippocampus appears to be a brain region that is less prone to tumor invasion.

Indexed as

AnimalsAnimals, Genetically ModifiedBrain NeoplasmsDisease Models, AnimalGliomaHeterograftsHippocampusHumansMagnetic Resonance ImagingMaleMiceMicroscopy, FluorescenceNeoplasm Invasiveness

Identifiers

PMID29793116
PMCPMC6030235
OpenAlexW2804047087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.