Evidence map›Paper›PMID 27713131›Full record

ArticleOncotarget2016

Discovery of cell surface vimentin targeting mAb for direct disruption of GBM tumor initiating cells.

Hyangsoon Noh, Jun Yan, Sungguan Hong, Ling-Yuan Kong, Konrad Gabrusiewicz, Xueqing Xia, Amy B Heimberger, Shulin Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Effects ofMarine drugs · 2025
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  3. Exploring vimentin expression and its protein interactors across diverse cancer types via the cancer genome atlas datasets: a comprehensive analysis.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
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  11. Membrane-Anchored and Tumor-Targeted IL12 (attIL12)-PBMC Therapy for Osteosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
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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

8 authors at 2 institutions in 1 country.

Hyangsoon NohDepartment of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jun YanDepartment of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Sungguan HongDepartment of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
Ling-Yuan KongDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Konrad GabrusiewiczDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Xueqing XiaDepartment of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Amy B HeimbergerDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Shulin LiDepartment of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Tropism Enhanced Oncolytic Adenovirus for the Treatment of Brain TumorsP50CA127001 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Juan Fueyo · 2008 to 2026
$41.2M
Gene-Product Auto-Targeting to Tumor VesselsR01CA120895 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, SHULIN · 2007 to 2025
$4.8M
Fgl-2 targeted therapy for reversing multi-modality immune suppressionR01CA203493 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HEIMBERGER, AMY BETH, LI, SHULIN · 2016 to 2020
$1.8M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA127001NCI NIH HHS R01 CA120895NCI NIH HHS R01 CA203493
6 · The paper itself

Abstract

Intracellular vimentin overexpression has been associated with epithelial-mesenchymal transition, metastasis, invasion, and proliferation, but cell surface vimentin (CSV) is less understood. Furthermore, it remains unknown whether CSV can serve as a therapeutic target in CSV-expressing tumor cells. We found that CSV was present on glioblastoma multiforme (GBM) cancer stem cells and that CSV expression was associated with spheroid formation in those cells. A newly developed monoclonal antibody against CSV, 86C, specifically and significantly induced apoptosis and inhibited spheroid formation in GBM cells in vitro. The addition of 86C to GBM cells in vitro also led to rapid internalization of vimentin and decreased GBM cell viability. These findings were associated with an increase in caspase-3 activity, indicating activation of apoptosis. Finally, treatment with 86C inhibited GBM progression in vivo. In conclusion, CSV-expressing GBM cells have properties of tumor initiating cells, and targeting CSV with the monoclonal antibody 86C is a promising approach in the treatment of GBM.

Indexed as

AnimalsAntibodies, MonoclonalApoptosisCaspase 3Cell Line, TumorCell ProliferationGlioblastomaHumansMiceNeoplastic Stem CellsSpheroids, CellularVimentinAntibodies, MonoclonalCaspase 3Vimentincancer therapeutic targetcell surface vimentinglioblastoma multiformetumor initiating cells

Identifiers

PMID27713131
PMCPMC5342141
OpenAlexW2528328324

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.