In silico Analysis of Transcription Factors Associated to Differentially Expressed Genes in Irradiated Glioblastoma Cell Lines

Glioblastoma multiforme (GBM) is one of the most frequent tumors in the central nervous system and the most malignant tumor among gliomas. In the past two decades, cytogenetic and molecular genetic studies have identified a number of recurrent chromosomal abnor‐ malities and genetic alterations in malignant gliomas, particularly in GBM [1]. It was already described that GBM harbors combinations of the following genetic alterations: loss of heter‐ ozygozity of 10q, EGFR amplification, TP53 mutations, p16INK4a deletion and PTEN muta‐ tions [2]. New integrative genomics studies provided a comprehensive view of the complicated genomic landscape of GBM, revealing a set of core signaling pathways com‐ monly activated in GBM involving TP53, RB, and RTK (receptor tyrosine kinase) pathways [3, 4]. The majority of GBM tumors present genetic alterations in all three pathways, which helps to stimulate cell proliferation and enhance cell survival while allowing tumor cells to escaping from cell-cycle checkpoints, senescence, and apoptosis. This approach also identi‐ fied previously unknown genetic alterations in IDH1/2, NF1, ERBB2, and NFKBIA genes [1].