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Primary glioblastomas with and without EGFR amplification: Relationship to genetic alterations and clinicopathological features

2009; Wiley; Volume: 30; Issue: 4 Linguagem: Inglês

10.1111/j.1440-1789.2009.01081.x

1440-1789

Rafael Benito, Rosario Gil‐Benso, Vicent Quilis-Quesada, Miguel Mínguez, Mariela Gregori-Romero, Pedro Roldán, José M. González-Darder, Miguel Cerdá‐Nicolás, Concha López‐Ginés,

Cancer Mechanisms and Therapy

NeuropathologyVolume 30, Issue 4 p. 392-400 Original Article Primary glioblastomas with and without EGFR amplification: Relationship to genetic alterations and clinicopathological features Rafael Benito, Rafael Benito Department of Pathology, University of Valencia, andSearch for more papers by this authorRosario Gil-Benso, Rosario Gil-Benso Department of Pathology, University of Valencia, andSearch for more papers by this authorVicente Quilis, Vicente Quilis Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorMiguel Perez, Miguel Perez Department of Pathology, University of Valencia, andSearch for more papers by this authorMariela Gregori-Romero, Mariela Gregori-Romero Department of Pathology, University of Valencia, andSearch for more papers by this authorPedro Roldan, Pedro Roldan Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorJose Gonzalez-Darder, Jose Gonzalez-Darder Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorMiguel Cerdá-Nicolas, Miguel Cerdá-Nicolas Department of Pathology, University of Valencia, andSearch for more papers by this authorConcha Lopez-Gines, Corresponding Author Concha Lopez-Gines Department of Pathology, University of Valencia, andConcha Lopez-Gines, PhD, Facultad de Medicina y Odontología. Avda. Blasco Ibañez, 15., Valencia. Spain. Email: [email protected]Search for more papers by this author Rafael Benito, Rafael Benito Department of Pathology, University of Valencia, andSearch for more papers by this authorRosario Gil-Benso, Rosario Gil-Benso Department of Pathology, University of Valencia, andSearch for more papers by this authorVicente Quilis, Vicente Quilis Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorMiguel Perez, Miguel Perez Department of Pathology, University of Valencia, andSearch for more papers by this authorMariela Gregori-Romero, Mariela Gregori-Romero Department of Pathology, University of Valencia, andSearch for more papers by this authorPedro Roldan, Pedro Roldan Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorJose Gonzalez-Darder, Jose Gonzalez-Darder Department of Neurosurgery, Hospital Clínico Universitario, Valencia, SpainSearch for more papers by this authorMiguel Cerdá-Nicolas, Miguel Cerdá-Nicolas Department of Pathology, University of Valencia, andSearch for more papers by this authorConcha Lopez-Gines, Corresponding Author Concha Lopez-Gines Department of Pathology, University of Valencia, andConcha Lopez-Gines, PhD, Facultad de Medicina y Odontología. Avda. Blasco Ibañez, 15., Valencia. Spain. Email: [email protected]Search for more papers by this author First published: 20 July 2010 https://doi.org/10.1111/j.1440-1789.2009.01081.xCitations: 30Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract Glioblastomas express a notable heterogeneity in both the histological and cell patterns with glial astrocytic differentiation. Primary glioblastoma, which is the most frequent presentation (90–95%), occurs mainly in older patients and arises de novo, without any clinical or histological evidence of a less malignant precursor lesion. EGFR amplification has been identified as a genetic hallmark of primary glioblastomas and occurs in 40–60% of cases. However, there exist primary glioblastomas without EGFR amplification/overexpression. The purpose of this study was to stabilize the association between cases with and without EGFR gene amplification with clinical and genetic parameters in 45 cases of primary glioblastomas. EGFR amplification was observed in 24 cases (53%), while in the remaining 21 cases (47%) this alteration was not displayed. And whereas EGFR was overexpressed in 79% of cases with EGFR amplification, only 33% of the cases without EGFR amplification showed overexpression. The amplification of EGFR was associated with amplifications in MDM2 and CDK4 and a higher percentage of cases with promoter methylation of INK4a. Only one case of glioblastoma with EGFR amplification presented TP53 mutation simultaneously. Seven remaining cases with TP53 mutations were glioblastomas without EGFR amplification. The INK4a, INK4b and ARF deletions were similar in the two groups. Primary glioblastomas with and without EGFR amplification did not show any significant differences in average survival. The genetic studies suggest the existence of molecular subtypes within primary glioblastoma that may, when fully defined, contribute toward the development of drugs that specifically target tumors with divergent genetic profiles. Citing Literature Volume30, Issue4August 2010Pages 392-400 RelatedInformation