Evidence map›Paper›PMID 30680510›Full record

ArticleJournal of neuro-oncology2019

EGFR amplification and classical subtype are associated with a poor response to bevacizumab in recurrent glioblastoma.

Koos E Hovinga, Heather J McCrea, Cameron Brennan, Jason Huse, Junting Zheng, Yoshua Esquenazi, Katherine S Panageas, Viviane Tabar

Abstract read
In one paragraph

Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 3 pooled it
–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

29 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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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.

Koos E HovingaDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY, 10065, USA.ORCID http://orcid.org/0000-0002-1415-8189
Heather J McCreaDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY, 10065, USA.
Cameron BrennanDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY, 10065, USA.
Jason HuseDepartment of Pathology, M.D. Anderson Cancer Center, Houston, TX, USA.
Junting ZhengDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Yoshua EsquenaziDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY, 10065, USA.
Katherine S PanageasDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Viviane TabarDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY, 10065, USA. tabarv@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Radiation Damage Repair in the Brain via Human ES cellsR21NS046045 · NINDS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI TABAR, VIVIANE · 2003 to 2004
$413k
NCI NIH HHS P30 CA008748NINDS NIH HHS R21 NS046045
6 · The paper itself

Abstract

purposeThe highly vascular malignant brain tumor glioblastoma (GBM) appears to be an ideal target for anti-angiogenic therapy; however, clinical trials to date suggest the VEGF antibody bevacizumab affects only progression-free survival. Here we analyze a group of patients with GBM who received bevacizumab treatment at recurrence and are stratified according to tumor molecular and genomic profile (TCGA classification), with the goal of identifying molecular predictors of the response to bevacizumab.

methodsWe performed a retrospective review of patients with a diagnosis of glioblastoma who were treated with bevacizumab in the recurrent setting at our hospital, from 2006 to 2014. Treatment was discontinued by the treating neuro-oncologists, based on clinical and radiographic criteria. Pre- and post-treatment imaging and genomic subtype were available on 80 patients. We analyzed time on bevacizumab and time to progression. EGFR gene amplification was determined by FISH.

resultsPatients with classical tumors had a significantly shorter time on bevacizumab than mesenchymal, and proneural patients (2.7 vs. 5.1 vs. 6.4 and 6.0 months respectively, p = 0.011). Classical subtype and EGFR gene amplification were significantly associated with a shorter time to progression both in univariate (p < 0.001 and p = 0.007, respectively) and multivariate analysis (both p = 0.010).

conclusionEGFR gene amplification and classical subtype by TCGA analysis are associated with significantly shorter time to progression for patients with recurrent GBM when treated with bevacizumab. These findings can have a significant impact on decision-making and should be further validated prospectively.

Indexed as

AdultAgedAged, 80 and overAntineoplastic Agents, ImmunologicalBevacizumabBiomarkers, TumorBrain NeoplasmsErbB ReceptorsFemaleFollow-Up StudiesGene AmplificationGlioblastomaHumansMaleMiddle AgedNeoplasm Recurrence, LocalAntineoplastic Agents, ImmunologicalBevacizumabBiomarkers, TumorEGFR protein, humanErbB ReceptorsBevacizumabClassicalEGFRGlioblastomaMesenchymalProneural

Identifiers

PMID30680510
PMCPMC6752204

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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.