Evidence map›Paper›PMID 38947019›Full record

ArticleResearch square2024

A prognostic matrix gene expression signature defines functional glioblastoma phenotypes and niches.

Monika Vishnoi, Zeynep Dereli, Zheng Yin, Elisabeth K Kong, Meric Kinali, Kisan Thapa, Ozgun Babur, Kyuson Yun, Nourhan Abdelfattah, Xubin Li and 4 more

Abstract readPreprint
In one paragraph

Article in Research square, 2024. 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
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Monika VishnoiDepartment of Neurosurgery, Houston Methodist Research Institute, Houston, TX, 77030 USA.
Zeynep DereliDepartment of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Zheng YinDepartment of Systems Medicine and Bioengineering, Houston Methodist Neal Cancer Center, Houston, TX, 77030 USA.
Elisabeth K KongDepartment of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Meric KinaliComputer Science, College of Science and Mathematics, University of Massachusetts Boston, Boston, MA, 02125.
Kisan ThapaComputer Science, College of Science and Mathematics, University of Massachusetts Boston, Boston, MA, 02125.
Ozgun BaburComputer Science, College of Science and Mathematics, University of Massachusetts Boston, Boston, MA, 02125.
Kyuson YunDepartment of Neurology, Houston Methodist Research Institute, Houston, TX, 77030 USA.
Nourhan AbdelfattahDepartment of Neurology, Houston Methodist Research Institute, Houston, TX, 77030 USA.
Xubin LiDepartment of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Behnaz BozorguiDepartment of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Mary C Farach-CarsonDepartment of Diagnostic and Biomedical Sciences, School of Dentistry, The University of Texas Health Science Center at Houston, Houston, TX, 77054, USA.
Robert C RostomilyDepartment of Neurosurgery, Houston Methodist Research Institute, Houston, TX, 77030 USA.
Anil KorkutDepartment of Bioinformatics and Computational Biology, MD Anderson Cancer Center, Houston, TX 77030, USA.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIANE BODURKA · 1985 to 2026
$290.8M
Microfluidic Device to Profile Chemosensitivity in Glioma Slice CulturesR01CA181445 · NCI · UNIVERSITY OF WASHINGTON · PI FOLCH, ALBERT · 2014 to 2025
$5.3M
Mechanistic maps of adaptive responses to therapeutic stress to optimize combination therapies.U01CA253472 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI KORKUT, ANIL, LIANG, HAN · 2021 to 2025
$2.6M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA181445NCI NIH HHS U01 CA253472
6 · The paper itself

Abstract

Background: Interactions among tumor, immune, and vascular niches play major roles in driving glioblastoma (GBM) malignancy and treatment responses. The composition, heterogeneity, and localization of extracellular core matrix proteins (CMPs) that mediate such interactions, however, are not well understood. Methods: Here, through computational genomics and proteomics approaches, we analyzed the functional and clinical relevance of CMP expression in GBM at bulk, single cell, and spatial anatomical resolution. Results: We identified genes encoding CMPs whose expression levels categorize GBM tumors into CMP expression-high (M-H) and CMP expression-low (M-L) groups. CMP enrichment is associated with worse patient survival, specific driver oncogenic alterations, mesenchymal state, infiltration of pro-tumor immune cells, and immune checkpoint gene expression. Anatomical and single-cell transcriptome analyses indicate that matrisome gene expression is enriched in vascular and leading edge/infiltrative niches that are known to harbor glioma stem cells driving GBM progression. Finally, we identified a 17-gene CMP expression signature, termed Matrisome 17 (M17) signature that further refines the prognostic value of CMP genes. The M17 signature is a significantly stronger prognostic factor compared to Conclusion: The matrisome gene expression signature provides a robust stratification of GBM patients by survival and potential biomarkers of functionally relevant GBM niches that can mediate mesenchymal-immune cross talk. Patient stratification based on matrisome profiles can contribute to selection and optimization of treatment strategies.

Indexed as

genomicsGlioblastomamatrisomemesenchymal-immune cross talktumor microenvironment

Identifiers

PMID38947019
PMCPMC11213219

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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.