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Eskişehir Osmangazi Üniversitesi, Tıp Fakültesi, Nöroşirürji Anabilim Dalı, Eskişehir The prognosis of glioblastoma is poor despite many treatment modalities including cytoreductive surgery. Glioblastoma is separated into two subgroups in the molecular basis as primary and secondary glioblastomas. The mutation of P53 tumor suppressor gene and the overexpression of “Platelet-derived growth factor receptors” (PDGFR) are known as the initial genetic changes in the formation of astrocytoma. The transformation of astrocytoma to anaplastic astrocytoma and secondary glioblastoma involves inactivation of a putative tumor suppressor gene on chromosome 19q, mutations or deletions of the retinoblastoma gene and the deletion of long arm of chromosome 10. The activation of epidermal growth factor receptor gene (EGFR), located on chromosome 7, the homozygous deletion of the p16, located on the short arm of chromosome 9, deforming of the equilibrium between MDM2-p53 proteins, the losses on 10p and 10q arms, and the genetic imbalances like PTEN mutation in the astrocytic stem cells may lead to the formation of primary glioblastoma de novo, The interactions between the regulator proteins on the cell cycle checkpoints, the role of the methylation of tumor suppressor genes and the activity of telomerase on the formation of glioblastoma, were discussed. Anahtar Kelimeler : Genetics, Glioblastoma multiforme, Primer, Secondary