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Título
Heterogeneous EGFR, CDK4, MDM4, and PDGFRA Gene Expression Profiles in Primary GBM: No Association with Patient Survival.
Autor(es)
Assunto
Glioblastoma
Gene expression profile
Amplification
Intragenic deletions
heterogeneity
Fecha de publicación
2020-01-17
Editor
MDPI
Citación
González-Tablas, M., Arandia, D., Jara-Acevedo, M., Otero, Á., Vital, A. L., Prieto, C., ... & Tabernero, M. D. (2020). Heterogeneous EGFR, CDK4, MDM4, and PDGFRA gene expression profiles in primary GBM: no association with patient survival. Cancers, 12(1), 231. https://doi.org/10.3390/cancers12010231
Resumen
[EN]The prognostic impact of the expression profile of genes recurrently amplified in glioblastoma multiforme (GBM) remains controversial.
We investigated the RNA gene expression profile of epidermal growth factor receptor (EGFR), cyclin-dependent kinase 4 (CDK4), murine doble minute 4 (MDM4), and platelet derived growth factor receptor alpha (PDGFRA) in 83 primary GBM tumors vs. 42 normal brain tissue samples. Interphase FISH (iFISH) analysis for the four genes, together with analysis of intragenic deletions in EGFR and PDGFRA, were evaluated in parallel at the DNA level. As validation cohort, publicly available RNA gene expression data on 293 samples from 10 different GBM patient series were also studied.
At the RNA level, CDK4 was the most frequently overexpressed gene (90%) followed by EGFR (58%) and PDGFRA (58%). Chromosome 7 copy number alterations, i.e., trisomy (49%) and polysomy (44%), showed no clear association with EGFR gene expression levels. In turn, intragenic EGFR deletions were found in 39 patients (47%), including EGFRvIII (46%) in association with EGFRvIVa (4%), EGFRvII (2%) or other EGFR deletions (3%) and PDGFRA deletion of exons 8-9 was found in only two tumors (2%).
Overall, none of the gene expression profiles and/or intragenic EGFR deletions showed a significant impact on overall survival of GBM supporting the notion that other still unraveled features of the disease might play a more relevant prognostic role in GBM.
Descrição
Agradecimiento: el artículo está publicado en la revista Cancers [MDPI] y está disponible en: https://www.mdpi.com/2072-6694/12/1/231
URI
ISSN
2072-6694
Versión del editor
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