Evidence map›Paper›PMID 30219696›Full record

ArticleTranslational oncology2018

Inhibition of Radiation and Temozolomide-Induced Invadopodia Activity in Glioma Cells Using FDA-Approved Drugs.

Clarissa A Whitehead, Hong P T Nguyen, Andrew P Morokoff, Rodney B Luwor, Lucia Paradiso, Andrew H Kaye, Theo Mantamadiotis, Stanley S Stylli

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 25 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

8 authors at 1 institution in 1 country.

Clarissa A WhiteheadDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Hong P T NguyenDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Andrew P MorokoffDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; Department of Neurosurgery, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Rodney B LuworDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Lucia ParadisoDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Andrew H KayeDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; Department of Neurosurgery, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Theo MantamadiotisDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; Department of Microbiology & Immunology, School of Biomedical Sciences, The University of Melbourne, Parkville VIC 3010, Victoria, Australia.
Stanley S StylliDepartment of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; Department of Neurosurgery, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia. Electronic address: stanley.stylli@mh.org.au.
The Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most common primary central nervous system tumor in adults is the glioblastoma multiforme (GBM). The highly invasive nature of GBM cells is a significant factor resulting in the inevitable tumor recurrence and poor patient prognosis. Tumor cells utilize structures known as invadopodia to faciliate their invasive phenotype. In this study, utilizing an array of techniques, including gelatin matrix degradation assays, we show that GBM cell lines can form functional gelatin matrix degrading invadopodia and secrete matrix metalloproteinase 2 (MMP-2), a known invadopodia-associated matrix-degrading enzyme. Furthermore, these cellular activities were augmented in cells that survived radiotherapy and temozolomide treatment, indicating that surviving cells may possess a more invasive phenotype posttherapy. We performed a screen of FDA-approved agents not previously used for treating GBM patients with the aim of investigating their "anti-invadopodia" and cytotoxic effects in GBM cell lines and identified a number that reduced cell viability, as well as agents which also reduced invadopodia activity. Importantly, two of these, pacilitaxel and vinorelbine tartrate, reduced radiation/temozolomide-induced invadopodia activity. Our data demonstrate the value of testing previously approved drugs (repurposing) as potential adjuvant agents for the treatment of GBM patients to reduce invadopodia activity, inhibit GBM cell invasion, and potentially improve patient outcome.

Identifiers

PMID30219696
PMCPMC6140414
OpenAlexW2891777242

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.