Evidence map›Paper›PMID 38060213›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2024

Functional Contribution and Clinical Implication of Cancer-Associated Fibroblasts in Glioblastoma.

Phillip M Galbo, Anne Tranberg Madsen, Yang Liu, Mou Peng, Yao Wei, Michael J Ciesielski, Robert A Fenstermaker, Sarah Graff, Cristina Montagna, Jeffrey E Segall and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Biomimetic Scaffold-Based 3D Models for Decoding Cancer Biology and Advancing Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  7. Pan-Cancer Analysis ofBiology · 2026
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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

13 authors at 3 institutions in 1 country.

Phillip M GalboDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0002-5391-598X
Anne Tranberg MadsenDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0001-9146-5943
Yang LiuDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0002-5804-0043
Mou PengDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0003-2953-5386
Yao WeiDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0002-1269-8421
Michael J CiesielskiDepartment of Neurosurgery, Roswell Park Comprehensive Cancer Center, Buffalo, New York.ORCID 0000-0002-3373-9421
Robert A FenstermakerDepartment of Neurosurgery, Roswell Park Comprehensive Cancer Center, Buffalo, New York.ORCID 0000-0003-0309-8130
Sarah GraffDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0002-4999-5454
Cristina MontagnaDepartment of Radiation Oncology, Rutgers University, New Brunswick, New Jersey.ORCID 0000-0003-2343-5851
Jeffrey E SegallDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0001-5425-9315
Simone SidoliDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0001-9073-6641
Xingxing ZangDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0001-5380-1942
Deyou ZhengDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0003-4354-5337
Albert Einstein College of Medicine · USRoswell Park Comprehensive Cancer Center · USRutgers, The State University of New Jersey · US

Funding

Tumor-expressed immune checkpoint B7x-mediated resistance to anti-CTLA-4 therapy.R01CA175495 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI ZANG, XINGXING · 2014 to 2025
$5.1M
A New Immune Checkpoint Pathway in Human Bladder CancerR01CA262132 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Xingxing Zang · 2023 to 2026
$2.4M
Leveraging Tumor Suppressor Inactivation for Osteosarcoma TherapyR01CA255643 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HOANG, BANG H · 2021 to 2024
$1.7M
NRSA Training CoreTL1TR002557 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MARANTZ, PAUL R · 2018 to 2022
$1.0M
Orbitrap Exploris 480 Basic SystemS10OD030286 · OD · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SIDOLI, SIMONE · 2021 to 2021
$600k
AOU NIH HHS 1S10OD030286AOU NIH HHS R01CA175495AOU NIH HHS R01CA255643AOU NIH HHS R01CA262132NCATS NIH HHS TL1 TR002557NCI NIH HHS R01 CA175495NCI NIH HHS R01 CA255643NCI NIH HHS R01 CA262132NIH HHS S10 OD030286
6 · The paper itself

Abstract

purposeThe abundance and biological contribution of cancer-associated fibroblasts (CAF) in glioblastoma (GBM) are poorly understood. Here, we aim to uncover its molecular signature, cellular roles, and potential tumorigenesis implications. EXPERIMENTAL

designWe first applied single-cell RNA sequencing (RNA-seq) and bioinformatics analysis to identify and characterize stromal cells with CAF transcriptomic features in human GBM tumors. Then, we performed functional enrichment analysis and in vitro assays to investigate their interactions with malignant GBM cells.

resultsWe found that CAF abundance was low but significantly correlated with tumor grade, poor clinical outcome, and activation of extracellular matrix remodeling using three large cohorts containing bulk RNA-seq data and clinical information. Proteomic analysis of a GBM-derived CAF line and its secretome revealed fibronectin (FN1) as a critical candidate factor mediating CAF functions. This was validated using in vitro cellular models, which demonstrated that CAF-conditioned media and recombinant FN1 could facilitate the migration and invasion of GBM cells. In addition, we showed that CAFs were more abundant in the mesenchymal-like state (or subtype) than in other states of GBMs. Interestingly, cell lines resembling the proneural state responded to the CAF signaling better for the migratory and invasive phenotypes.

conclusionsOverall, this study characterized the molecular features and functional impacts of CAFs in GBM, alluding to novel cell interactions mediated by CAFs in the GBM microenvironment.

Indexed as

Cancer-Associated FibroblastsGlioblastomaCell Line, TumorCell MovementFibroblastsHumansProteomicsTumor Microenvironment

Identifiers

PMID38060213
PMCPMC10922678
OpenAlexW4389432331

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.