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Growth Factor Expression in Central Nervous System Tumours

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Modification of Radiation Response

Part of the book series: Medical Radiology ((Med Radiol Radiat Oncol))

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Abstract

Central nervous system (CNS) tumour pathogenesis probably is a multi-step process in which tumour suppressor gene inactivation and oncogene activation and overexpression play a part, along with alterations in cell cycle progression, abnormalities in signal transduction pathways, glial cell invasion, and angiogenesis (Nagane et al. 1997; Ueki et al. 2002). The role of growth factors in this process has increasingly been studied over the last few years. This chapter summarizes the available data, usually derived from adult patients, and discusses their limitations as well as their potential influence on future therapeutic strategies. One of the most common types of brain tumours, malignant gliomas, may arise via a number of apparently distinct molecular pathways, illustrated in Table 11.1. For example, glioblastoma multiforme (GBM) can be divided into at least two distinct genetic subsets: those characterized by p53 mutations and allelic loss of chromosome 17p in the absence of epidermal growth factor receptor (EGFR) gene amplification, and those with EGFR gene amplification but no p53 mutations or chromosome 17p loss. Tumours with p53 mutations occur primarily in younger patients and those with EGFR gene amplification arise primarily in older patients (Louis 1996). Molecular classification of gliomas is a major challenge in the effort to improve therapeutic decisions.

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Nieder, C., Andratschke, N., Schlegel, J. (2003). Growth Factor Expression in Central Nervous System Tumours. In: Nieder, C., Milas, L., Ang, K.K. (eds) Modification of Radiation Response. Medical Radiology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-55613-5_11

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  • DOI: https://doi.org/10.1007/978-3-642-55613-5_11

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-62670-8

  • Online ISBN: 978-3-642-55613-5

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