Evidence map›Paper›PMID 25598002›Full record

ArticleJournal of neurochemistry2015

Proteomic profiling of patient-derived glioblastoma xenografts identifies a subset with activated EGFR: implications for drug development.

Kristine E Brown, Gustavo Chagoya, Shawn G Kwatra, Timothy Yen, Stephen T Keir, Mary Cooter, Katherine A Hoadley, Ahmed Rasheed, Eric S Lipp, Roger Mclendon and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. GZ17-6.02 Inhibits the Growth of EGFRvIII+ Glioblastoma.International journal of molecular sciences · 2022
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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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

14 authors at 5 institutions in 2 countries.

Kristine E BrownSchool of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA.
Gustavo Chagoya
Shawn G Kwatra
Timothy Yen
Stephen T Keir
Mary Cooter
Katherine A Hoadley
Ahmed Rasheed
Eric S Lipp
Roger Mclendon
Francis Ali-Osman
Darell D Bigner
John H Sampson
Madan M Kwatra
Duke Medical Center · USDuke University · USJohns Hopkins University · USUniversity of North Carolina at Chapel Hill · USWake Forest University · US

Funding

Targeted Alpha-Particle Radiotheraphy of Brain Tumors with 211At-81C6 AntibodyP50CA190991 · NCI · DUKE UNIVERSITY · PI SAMPSON, JOHN H. · 2014 to 2023
$20.8M
Truncated NK1R in GBM: Pharmacology and Relationship with Patient SurvivalR21NS078642 · NINDS · DUKE UNIVERSITY · PI KWATRA, MADAN M · 2012 to 2013
$396k
NCI NIH HHS P50 CA190991NINDS NIH HHS R21 NS078642NINDS NIH HHS R21NS078642
6 · The paper itself

Abstract

The development of drugs to inhibit glioblastoma (GBM) growth requires reliable pre-clinical models. To date, proteomic level validation of widely used patient-derived glioblastoma xenografts (PDGX) has not been performed. In the present study, we characterized 20 PDGX models according to subtype classification based on The Cancer Genome Atlas criteria, TP53, PTEN, IDH 1/2, and TERT promoter genetic analysis, EGFR amplification status, and examined their proteomic profiles against those of their parent tumors. The 20 PDGXs belonged to three of four The Cancer Genome Atlas subtypes: eight classical, eight mesenchymal, and four proneural; none neural. Amplification of EGFR gene was observed in 9 of 20 xenografts, and of these, 3 harbored the EGFRvIII mutation. We then performed proteomic profiling of PDGX, analyzing expression/activity of several proteins including EGFR. Levels of EGFR phosphorylated at Y1068 vary considerably between PDGX samples, and this pattern was also seen in primary GBM. Partitioning of 20 PDGX into high (n = 5) and low (n = 15) groups identified a panel of proteins associated with high EGFR activity. Thus, PDGX with high EGFR activity represent an excellent pre-clinical model to develop therapies for a subset of GBM patients whose tumors are characterized by high EGFR activity. Further, the proteins found to be associated with high EGFR activity can be monitored to assess the effectiveness of targeting EGFR. The development of drugs to inhibit glioblastoma (GBM) growth requires reliable pre-clinical models. We validated proteomic profiles using patient-derived glioblastoma xenografts (PDGX), characterizing 20 PDGX models according to subtype classification based on The Cancer Genome Atlas (TCGA) criteria, TP53, PTEN, IDH 1/2, and TERT promoter genetic analysis, EGFR amplification status, and examined their proteomic profiles against those of their parent tumors. Proteins found to be associated with high EGFR activity represent potential biomarkers for GBM monitoring.

Indexed as

AgedAged, 80 and overAnimalsAntineoplastic AgentsBrain NeoplasmsDNA Mutational AnalysisErbB ReceptorsFemaleGene Expression ProfilingGenomicsGlioblastomaHumansMaleMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsErbB ReceptorsEGFRglioblastomaRPPAsignalingxenografts

Identifiers

PMID25598002
PMCPMC4514443
OpenAlexW2111559859

What OpenQuestion holds

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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.