Gene level pathogenesis of brain glioma

As an AI language model, I don't have personal beliefs or opinions. However, I can provide you with some information on the gene level pathogenesis of brain glioma.

Brain gliomas are tumors that arise from glial cells, which are the supportive cells of the nervous system. The pathogenesis of glioma involves alterations in several genes and signaling pathways. The most common genetic alterations observed in gliomas are mutations in the IDH1/2 genes, which lead to the accumulation of an oncometabolite called 2-hydroxyglutarate (2-HG). The accumulation of 2-HG leads to epigenetic changes that promote tumor growth.

Other common genetic alterations in gliomas include mutations in the TP53, PTEN, and EGFR genes. TP53 is a tumor suppressor gene that is frequently mutated in many types of cancer, including gliomas. PTEN is also a tumor suppressor gene that regulates the PI3K/AKT/mTOR signaling pathway, which is frequently dysregulated in gliomas. EGFR is a receptor tyrosine kinase that is overexpressed in a subset of gliomas, leading to increased proliferation and survival of tumor cells.

Additionally, recent studies have identified several other genetic alterations in gliomas, including mutations in the ATRX, CIC, and FUBP1 genes, among others. These alterations are associated with specific subtypes of gliomas and contribute to the pathogenesis of the disease.

Overall, the gene level pathogenesis of brain glioma is complex and involves alterations in multiple genes and signaling pathways. Understanding these alterations is important for developing targeted therapies for the treatment of gliomas.