High-grade<unk> s are highly vascular tumors and have a tendency to infiltrate diffusely. They have extensive areas of necrosis and hypoxia. Often, tumor growth causes a breakdown of the blood–brain barrier in the vicinity of the tumor. As a rule, high-grade<unk> s almost always grow back even after complete surgical excision, so are commonly called recurrent cancer of the brain. Conversely, low-grade<unk> s grow slowly, often over many years, and can be followed without treatment unless they grow and cause symptoms. Several acquired (not inherited) genetic mutations have been found in<unk> s. Tumor suppressor protein 53 (p53) is mutated early in the disease. p53 is the "guardian of the genome", which, during DNA and cell duplication, makes sure the DNA is copied correctly and destroys the cell (apoptosis) if the DNA is mutated and cannot be fixed. When p53 itself is mutated, other mutations can survive. Phosphatase and tensin homolog (PTEN), another tumor suppressor gene, is itself lost or mutated. Epidermal growth factor receptor, a growth factor that normally stimulates cells to divide, is amplified and stimulates cells to divide too much. Together, these mutations lead to cells dividing uncontrollably, a hallmark of cancer. In 2009, mutations in IDH1 and IDH2 were found to be part of the mechanism and associated with a less favorable prognosis.
Glioma
Gliosis
Glioblastoma
Astrocytoma
Meningioma
Malignant meningioma
Ameloblastoma
Coma