Gene expression analysis of aberrant signaling pathways in meningiomas
Entity
UAM. Departamento de CirugíaPublisher
Spandidos PublicationsDate
2013-07-01Citation
10.3892/ol.2013.1363
Oncology Letters 6.1 (2013): 275-279
ISSN
1792-1074 (print); 1792-1082 (online)DOI
10.3892/ol.2013.1363Funded by
This study was partially supported by Fondo de Investigaciones Sanitarias, Ministerio de Ciencia e Innovación, Spain, Grants PI‑08/1849 and PI‑10/1972; and by grant PI‑10‑045 from the Fundación Sociosanitaria de Castilla‑La Mancha, SpainSubjects
Gene expression arrays; Meningioma; Neurofibromin gene; Schwannoma; Signaling pathways; MedicinaAbstract
Examining aberrant pathway alterations is one method for understanding the abnormal signals that are involved in tumorigenesis and tumor progression. In the present study, expression arrays were performed on tumor-related genes in meningiomas. The GE Array Q Series HS-006 was used to determine the expression levels of 96 genes that corresponded to six primary biological regulatory pathways in a series of 42 meningiomas, including 32 grade I, four recurrent grade I and six grade II tumors, in addition to three normal tissue controls. Results showed that 25 genes that were primarily associated with apoptosis and angiogenesis functions were downregulated and 13 genes frequently involving DNA damage repair functions were upregulated. In addition to the inactivation of the neurofibromin gene, NF2, which is considered to be an early step in tumorigenesis, variations of other biological regulatory pathways may play a significant role in the development of meningioma
Files in this item
Google Scholar:Torres-Martín, Miguel
-
Martínez-Glez, Víctor
-
Peña-Granero, Carolina
-
Isla Guerrero, Alberto José
-
Lassaletta Atienza, Luis María
-
De Campos, José Maria
-
Pinto, Giovanny R.
-
Burbano, Rommel Rodríguez Rodríguez
-
Meléndez, Bárbara
-
Castresana, Javier Sáez
-
Rey, Juan Antonio
This item appears in the following Collection(s)
Related items
Showing items related by title, author, creator and subject.