Evidence map›Paper›PMID 30158566›Full record

ArticleScientific reports2018

The Ras-related gene ERAS is involved in human and murine breast cancer.

Cristian Suárez-Cabrera, Bárbara de la Peña, Laura L González, Angustias Page, Mónica Martínez-Fernández, M Llanos Casanova, Jesús M Paramio, Alejandro Rojo-Sebastián, Gema Moreno-Bueno, Alicia Maroto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-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

10 citing papers in PubMed, 14 citations in OpenAlex.

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  8. The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?Frontiers in cell and developmental biology · 2020
    Review
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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

12 authors at 6 institutions in 3 countries.

Cristian Suárez-CabreraMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.
Bárbara de la PeñaMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.ORCID 0000-0001-9796-8015
Laura L GonzálezMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.
Angustias PageMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.ORCID 0000-0002-0231-8536
Mónica Martínez-FernándezMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.
M Llanos CasanovaMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.
Jesús M ParamioMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain.ORCID 0000-0001-7520-3177
Alejandro Rojo-SebastiánCentro de Investigación Biomédica en Red de Cáncer (CIBERONC), 28029, Madrid, Spain.
Gema Moreno-BuenoCentro de Investigación Biomédica en Red de Cáncer (CIBERONC), 28029, Madrid, Spain.
Alicia MarotoDepartment of Pathology, 12 de Octubre University Hospital, Madrid, Spain.
Ángel RamírezMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain. a.ramirez@ciemat.es.ORCID 0000-0001-7745-5108
Manuel NavarroMolecular Oncology Unit, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), 28040, Madrid, Spain. manuel.navarro@ciemat.es.ORCID 0000-0003-1118-8531
Research Institute Hospital 12 de Octubre · ESCentro de Investigación Biomédica en Red de Cáncer · ESCentro de Investigaciones Energéticas, Medioambientales y Tecnológicas · ESInstituto de Investigaciones Biomédicas Sols-Morreale · ESQueensland University of Technology · AUUniversidade de Santiago de Compostela · ES

Funding

Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) SAF-2015-66015-RMinistry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) CB/16/00228Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) CB16/12/00295Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PI16/00134Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PI16/00161Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PI17/00578Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PIE 15/00076Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) RD12/0036/0009
6 · The paper itself

Abstract

Although Ras genes are frequently mutated in human tumors, these mutations are uncommon in breast cancer. However, many breast tumors show evidences of Ras pathway activation. In this manuscript, we have analyzed and characterized mouse mammary tumors generated by random Sleeping Beauty transposon mutagenesis and identify ERAS -a member of the RAS family silenced in adult tissues- as a new gene involved in progression and malignancy of breast cancer. Forced expression of ERAS in human non-transformed mammary gland cells induces a process of epithelial-to-mesenchymal transition and an increase in stem cells markers; these changes are mediated by miR-200c downregulation. ERAS expression in human tumorigenic mammary cells leads to the generation of larger and less differentiated tumors in xenotransplant experiments. Immunohistochemical, RT-qPCR and bioinformatics analysis of human samples show that ERAS is aberrantly expressed in 8-10% of breast tumors and this expression is associated with distant metastasis and reduced metastasis-free survival. In summary, our results reveal that inappropriate activation of ERAS may be important in the development of a subset of breast tumors. These findings open the possibility of new specific treatments for this subset of ERAS-expressing tumors.

Indexed as

AnimalsBreast NeoplasmsCarcinogenesisCell DifferentiationCells, CulturedEpithelial CellsEpithelial-Mesenchymal TransitionHumansMiceNeoplasms, ExperimentalNeoplasm TransplantationOncogene Protein p21(ras)Transplantation, HeterologousERas protein, humanERas protein, mouseOncogene Protein p21(ras)

Identifiers

PMID30158566
PMCPMC6115423
OpenAlexW2888135192

What OpenQuestion holds

Textmetadata
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.