Cerebral Glioblastoma: A Review on Genetic Alterations, Signaling Pathways, and Clinical Managements

Glioblastoma, previously known as glioblastoma multiforme (GBM), is a grade IV astrocytoma that frequently affects patients with a mean age of 45 and above. It is generally categorized into primary and secondary subtypes, based on research conducted by Hans Joachim Scherer.

This review concentrates on cellular and genetic drawbacks that can lead to the appearance of glioblastoma. National Center for Biotechnology Information (NCBI) was the main source used for writing this review article, followed by Google scholar. The following keywords were used to retrieve articles: ’glioblastoma’, ’brain tumors’, ’glioma’, ’LOH’, and ’cellular and signaling pathways in glioblastoma’.

Several genetic alterations and cellular pathways are involved in the appearance and progression of glioblastoma, including loss of heterozygosity (LoH), TP53 mutation, isocitrate dehydrogenase 1 (IDH1) mutation, P16INK4/RB1 pathway, and EGFR/PTEN/Akt/mTOR pathway. The majority (70%) of primary glioblastomas are caused by (LoH), and it mostly occurs in older people. Secondary glioblastoma is mainly manifested by TP53 mutation and usually affects younger people. Understanding the alterations and cellular mechanisms involved in glioblastoma is important to develope new therapeutic regimes. Surgery, radiation therapy, temozolomide, and TTFields are the four most important therapeutic options available for treating patients.

In this review, the genetic alterations and cellular pathways which could lead to the appearance of this tumor were highlighted, and the latest options for treating patients dealing with glioblastoma were discussed.