**1. Introduction**

Glioblastoma multiforme (GBM) tumor occurs either as a primary tumor when it is formed de novo or a secondary tumor when the tumor progresses from grade II or III to grade IV. GBM is a diffuse and infiltrative tumor with a high mitotic activity, nuclear atypia, pleomor‐ phism, and necrosis. GBM is the most frequently occurring brain tumor (12–15%) and represents 50–60% of all astrocytomas. There are two variants of glioblastoma: Glioblastoma of giant cells and gliosarcoma. GBM affects the cerebral hemispheres, mostly the white substance of the cerebral hemispheres. GBM primary has a bad prognostic due to its molecu‐ lar heterogeneity. On the basis of its transcriptional subtype, GBM primary is also classified as neural, classical, and mesenchymal as well as proneural for GBM secondary. In GBM primary occurs the amplification of epidermal growth factor (EGF), and the *PTEN* gene is mutated in 45% of GBM primary cases, whereas in GBM secondary, the EGF amplification does not occur. The chromosome alteration in GBM involves a loss of the chromosome 10. The treatment for this kind of tumor after a safe surgical process also involves radiotherapy (RT) and the pharmacological treatment using the alkylating agent Temozolamide (TMZ), and different combinations of this agent with antitumor drugs such as the Bevacizumab. In spite of these treatments, there is a short survival period for GBM patients (14–18 months), which promotes the development of different clinical trials (II or III) to provide the patient a treatment with a better outcome. These new approaches are based on the molecular aspects of GBM to make the treatments more individualized.. This chapter describes the main GBM endocrine and molecular characteristics now known and makes a proposal on future treatments for GBM patients on the basis of these molecular characteristics.
