<unk>  causes regional effects by compression, invasion, and destruction of brain parenchyma, arterial and venous hypoxia, competition for nutrients, release of metabolic end products (e.g., free radicals, altered electrolytes, neurotransmitters), and release and recruitment of cellular mediators (e.g., cytokines) that disrupt normal parenchymal function. Secondary clinical sequelae may be caused by elevated intracranial pressure attributable to direct mass effect, increased blood volume, or increased cerebrospinal fluid volume. Molecular alterations A genome-wide pattern of DNA copy-number alterations (CNAs) has been uncovered, which is correlated with a patient’s survival and response to treatment. This pattern identifies among glioblastoma as well as lower-grade<unk>  patients a subtype, where the CNA genotype is correlated with an approximately one-year survival phenotype.
Astrocytoma
Oligoastrocytoma
Hemangiopericytoma
Ameloblastoma
Schwannoma
Glioma
Schwannomatosis
Hemangioblastoma