Worse Outcome in Primary Glioblastoma Multiforme With Concurrent Epidermal Growth Factor Receptor and p53 Alteration
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- Yolanda Ruano
- 1Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain
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- Teresa Ribalta
- 2Clínic Hospital, Barcelona University, August Pi i Sunyer Biomedical Research Unit, Barcelona, Spain
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- Ángel Rodríguez de Lope
- 3Department of Neurosurgery, Virgen de la Salud Hospital, Toledo, Spain
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- Yolanda Campos-Martín
- 1Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain
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- Concepción Fiaño
- 4Department of Pathology, Xeral-Cies Hospital Complex, Vigo, Spain
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- Elisa Pérez-Magán
- 1Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain
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- José-Luis Hernández-Moneo
- 3Department of Neurosurgery, Virgen de la Salud Hospital, Toledo, Spain
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- Manuela Mollejo
- 1Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain
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- Bárbara Meléndez
- 1Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain
説明
<jats:title>Abstract</jats:title> <jats:p>Primary glioblastoma multiforme (GBM), in contrast with secondary GBM, has been associated with the presence of EGFR amplification and absence of p53 mutation. In this study, we analyzed relevant molecular and clinical variables in 194 primary GBMs and tested them for survival analysis. Although most of the tumors showed a mutually exclusive pattern, concurrent alterations of EGFR and p53 were detected. Survival analysis of CDK4 amplification revealed a highly significant association with a worse clinical outcome (P = .01), whereas MDM2, CDK6, PTEN, and p21 were not associated with patient survival. Multivariate analysis including the significant clinical and molecular variables revealed CDK4 amplification, age, and radiotherapy to be markers with independent prognostic value. In addition, the primary GBM tumors showing simultaneous EGFR and p53 alterations were significantly associated with worse survival (P < .01). These results highlight the prognostic value of CDK4 amplification and of simultaneous EGFR-p53 alterations in the clinical outcome of patients with primary GBM.</jats:p>
収録刊行物
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- American Journal of Clinical Pathology
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American Journal of Clinical Pathology 131 (2), 257-263, 2009-02-01
Oxford University Press (OUP)