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

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dc.contributor.author Gutiérrez-Erlandsson, Sylvia
dc.contributor.author Herrero-Vidal, Pedro
dc.contributor.author Fernández-Alfara, Marcos
dc.contributor.author Hernández-García, Susana
dc.contributor.author Gonzalo-Flores, Sandra
dc.contributor.author Mudarra-Rubio, Alberto
dc.contributor.author Fresno, Manuel
dc.contributor.author Cubelos, Beatriz
dc.contributor.other UAM. Departamento de Biología Molecular es_ES
dc.date.accessioned 2014-06-30T10:16:09Z
dc.date.available 2014-06-30T10:16:09Z
dc.date.issued 2013-10-23
dc.identifier.citation Molecular Cancer 12.1 (2013): 127 en_US
dc.identifier.issn 1476-4598 es_ES
dc.identifier.uri http://hdl.handle.net/10486/660661
dc.description.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. en_US
dc.description.sponsorship This work was supported by grants SAF2012-31279 from the ‘Comisión Interministerial de Ciencia y Tecnología’ and the ‘Ramón y Cajal’ program (RYC-2010-06251, to B.C.). We also thank the Fundación Ramón Areces for its institutional support of the ‘Centro de Biología Molecular Severo Ochoa’. en_US
dc.format.extent 12 pag. es_ES
dc.format.mimetype application/pdf es_ES
dc.language.iso eng es_ES
dc.publisher BioMed Central en_US
dc.relation.ispartof Molecular Cancer en_US
dc.rights © 2013 Gutierrez-Erlandsson et al. es_ES
dc.subject.other RAS family proteins en_US
dc.subject.other R-RAS2 en_US
dc.subject.other CNS tumors en_US
dc.subject.other TC21 en_US
dc.title R-RAS2 overexpression in tumors of the human central nervous system en_US
dc.type article en
dc.subject.eciencia Biología y Biomedicina / Biología es_ES
dc.relation.publisherversion http://dx.doi.org/10.1186/1476-4598-12-127 es_ES
dc.identifier.doi 10.1186/1476-4598-12-127 es_ES
dc.identifier.publicationfirstpage 127 es_ES
dc.identifier.publicationissue 1 es_ES
dc.identifier.publicationlastpage 127 es_ES
dc.identifier.publicationvolume 12 es_ES
dc.relation.projectID Comunidad de Madrid. S2010/BMD-2332/INDISNET es_ES
dc.type.version info:eu-repo/semantics/publishedVersion es_ES
dc.rights.accessRights openAccess en
dc.authorUAM Cubelos Álvarez, Beatriz (263020)

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