Evidence map›Paper›PMID 28766870›Full record

ArticleAdvanced healthcare materials2017

Extracellular Hyaluronic Acid Influences the Efficacy of EGFR Tyrosine Kinase Inhibitors in a Biomaterial Model of Glioblastoma.

Sara Pedron, Jacob S Hanselman, Mark A Schroeder, Jann N Sarkaria, Brendan A C Harley

Open access · greenAbstract read
In one paragraph

Article in Advanced healthcare materials, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
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

32 citing papers in PubMed, 59 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Sara PedronCarl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Urbana, IL, 61801, USA.
Jacob S HanselmanCarl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Urbana, IL, 61801, USA.
Mark A SchroederDepartment of Radiation Oncology, Mayo Clinic, 200 First Street Southwest, Rochester, MN, 55905, USA.
Jann N SarkariaDepartment of Radiation Oncology, Mayo Clinic, 200 First Street Southwest, Rochester, MN, 55905, USA.
Brendan A C HarleyCarl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Urbana, IL, 61801, USA.ORCID http://orcid.org/0000-0001-5458-154X
University of Illinois Urbana-Champaign · USMayo Clinic · US

Funding

Biomimetic Hydrogel Niches to Study the Malignant Phenotype of Glioblastoma MultiformeR01CA197488 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI HARLEY, BRENDAN A. · 2016 to 2020
$2.2M
NCI NIH HHS R01 CA197488
6 · The paper itself

Abstract

3D biomaterial models have potential to explore the influence of the tumor microenvironment on aberrant signaling pathways and compensatory signals using patient-derived cells. Glioblastoma (GBM) tumors are highly heterogeneous, with both cell composition and extracellular matrix biophysical factors seen as key regulators of malignant phenotype and treatment outcomes. Amplification, overexpression, and mutation of the epidermal growth factor receptor (EGFR) tyrosine kinase have been identified in 50% of GBM patients. Here, hyaluronic acid (HA) decorated methacrylamide-functionalized gelatin (GelMA) hydrogels are used to examine the synergies between microenvironmental factors and a model EGFR tyrosine kinase inhibitor (TKI) using patient-derived xenograft cells. The in vitro behavior of 3 patient-derived xenografts that reflect a clinically relevant range of EGFR variants is characterized: GBM10 (EGFR, wild type), GBM12 (EGFR+), and GBM6 (EGFRvIII). GelMA hydrogels support xenograft culture; cells remain viable, active, respond to matrix-immobilized HA, and upregulate genes associated with matrix remodeling and tumor growth. Interestingly, matrix-immobilized HA alters the response of GBM cells to a model tyrosine kinase inhibitor, erlotinib. While constitutively activated EGFRvIII cells are sensitive to TKI in gelatin hydrogels, hyaluronic acid mediated adhesive signaling interacts with EGFRvIII signaling to increase cell metabolic activity, increase soluble hyaluronic acid synthesis, and modify response to erlotinib exposure.

Indexed as

AcrylamidesAnimalsBiocompatible MaterialsBrain NeoplasmsCell ProliferationErbB ReceptorsErlotinib HydrochlorideExtracellular MatrixGelatinGlioblastomaHumansHyaluronic AcidHydrogelsMatrix Metalloproteinase 2MiceMice, NudeAcrylamidesBiocompatible MaterialsErbB ReceptorsErlotinib HydrochlorideGelatinHyaluronic AcidHydrogelsMatrix Metalloproteinase 2methacrylamidePhosphatidylinositol 3-KinasesProtein Kinase InhibitorsEGFRglioblastomahyaluronanpatient-derived tumor cellstumor microenvironment

Identifiers

PMID28766870
PMCPMC5726872
OpenAlexW2739871743

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Registered trials

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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.