Evidence map›Paper›PMID 24148564›Full record

ArticleMolecular cancer2013

R-RAS2 overexpression in tumors of the human central nervous system.

Sylvia Gutierrez-Erlandsson, Pedro Herrero-Vidal, Marcos Fernandez-Alfara, Susana Hernandez-Garcia, Sandra Gonzalo-Flores, Alberto Mudarra-Rubio, Manuel Fresno, Beatriz Cubelos

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  14. R-Ras GTPases Signaling Role in Myelin Neurodegenerative Diseases.International journal of molecular sciences · 2020
    Review
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  16. Article
  17. R-Ras1 and R-Ras2 Are Essential for Oligodendrocyte Differentiation and Survival for Correct Myelination in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    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

8 authors at 3 institutions in 1 country.

Sylvia Gutierrez-Erlandsson
Pedro Herrero-Vidal
Marcos Fernandez-Alfara
Susana Hernandez-Garcia
Sandra Gonzalo-Flores
Alberto Mudarra-Rubio
Manuel Fresno
Beatriz CubelosCentro de Biología Molecular Severo Ochoa, Departamento de Biología Molecular, Universidad Autónoma de Madrid, Madrid 28049, Spain. bcubelos@cbm.uam.es.
Centro de Biología Molecular Severo Ochoa · ESCentro Nacional de Biotecnología · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant tumors of the central nervous system (CNS) are the 10th most frequent cause of cancer mortality. Despite the strong malignancy of some such tumors, oncogenic mutations are rarely found in classic members of the RAS family of small GTPases. This raises the question as to whether other RAS family members may be affected in CNS tumors, excessively activating RAS pathways. The RAS-related subfamily of GTPases is that which is most closely related to classical Ras and it currently contains 3 members: RRAS, RRAS2 and RRAS3. While R-RAS and R-RAS2 are expressed ubiquitously, R-RAS3 expression is restricted to the CNS. Significantly, both wild type and mutated RRAS2 (also known as TC21) are overexpressed in human carcinomas of the oral cavity, esophagus, stomach, skin and breast, as well as in lymphomas. Hence, we analyzed the expression of R-RAS2 mRNA and protein in a wide variety of human CNS tumors and we found the R-RAS2 protein to be overexpressed in all of the 90 CNS cancer samples studied, including glioblastomas, astrocytomas and oligodendrogliomas. However, R-Ras2 was more strongly expressed in low grade (World Health Organization grades I-II) rather than high grade (grades III-IV) tumors, suggesting that R-RAS2 is overexpressed in the early stages of malignancy. Indeed, R-RAS2 overexpression was evident in pre-malignant hyperplasias, both at the mRNA and protein levels. Nevertheless, such dramatic changes in expression were not evident for the other two subfamily members, which implies that RRAS2 is the main factor triggering neural transformation.

Indexed as

AdolescentAdultAgedBrain NeoplasmsFemaleGene ExpressionGliomaHumansMaleMembrane ProteinsMiddle AgedMonomeric GTP-Binding ProteinsRNA, MessengerTissue Array AnalysisYoung AdultMembrane ProteinsMonomeric GTP-Binding ProteinsRNA, MessengerRRAS2 protein, human

Identifiers

PMID24148564
PMCPMC3900289
OpenAlexW2112659448

What OpenQuestion holds

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LicenceCC BY
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.