Evidence map›Paper›PMID 22583806›Full record

ArticleMolecular cancer2012

Galectin-1, a gene preferentially expressed at the tumor margin, promotes glioblastoma cell invasion.

L Gerard Toussaint, Allan E Nilson, Jennie M Goble, Karla V Ballman, C David James, Florence Lefranc, Robert Kiss, Joon H Uhm

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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  18. Tumor Cell Invasion in Glioblastoma.International journal of molecular sciences · 2020
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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 5 institutions in 2 countries.

L Gerard ToussaintThe Texas Brain and Spine Institute, Bryan, TX 77807, USA. Gtoussaint@medicine.tamhsc.edu
Allan E Nilson
Jennie M Goble
Karla V Ballman
C David James
Florence Lefranc
Robert Kiss
Joon H Uhm
Mayo Clinic in Arizona · USUniversité Libre de Bruxelles · BEMayo Clinic · USNeurological Surgery · USTexas A&M Health Science Center · US

Funding

Research Training Program in Neuro-OncologyT32NS007494 · NINDS · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2002 to 2014
$1.4M
NINDS NIH HHS T32 NS 07494
6 · The paper itself

Abstract

backgroundHigh-grade gliomas, including glioblastomas (GBMs), are recalcitrant to local therapy in part because of their ability to invade the normal brain parenchyma surrounding these tumors. Animal models capable of recapitulating glioblastoma invasion may help identify mediators of this aggressive phenotype.

methodsPatient-derived glioblastoma lines have been propagated in our laboratories and orthotopically xenografted into the brains of immunocompromized mice. Invasive cells at the tumor periphery were isolated using laser capture microdissection. The mRNA expression profile of these cells was compared to expression at the tumor core, using normal mouse brain to control for host contamination. Galectin-1, a target identified by screening the resulting data, was stably over-expressed in the U87MG cell line. Sub-clones were assayed for attachment, proliferation, migration, invasion, and in vivo tumor phenotype.

resultsExpression microarray data identified galectin-1 as the most potent marker (p-value 4.0 x 10-8) to identify GBM cells between tumor-brain interface as compared to the tumor core. Over-expression of galectin-1 enhanced migration and invasion in vitro. In vivo, tumors expressing high galectin-1 levels showed enhanced invasion and decreased host survival.

conclusionsIn conclusion, cells at the margin of glioblastoma, in comparison to tumor core cells, have enhanced expression of mediators of invasion. Galectin-1 is likely one such mediator. Previous studies, along with the current one, have proven galectin-1 to be important in the migration and invasion of glioblastoma cells, in GBM neoangiogenesis, and also, potentially, in GBM immune privilege. Targeting this molecule may offer clinical improvement to the current standard of glioblastoma therapy, i.e. radiation, temozolomide, anti-angiogenic therapy, and vaccinotherapy.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationExtracellular MatrixGalectin 1Gene Expression ProfilingGlioblastomaHumansMiceMice, NudeNeoplasm InvasivenessTransplantation, HeterologousGalectin 1

Identifiers

PMID22583806
PMCPMC3407025
OpenAlexW2137087689

What OpenQuestion holds

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LicenceCC BY
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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.