title: Genetic modeling of glioma formation in mice.
abstract: In addition to the histological features that define gliomas, mutations and other alterations in gene expression and signal transduction are classically found in these tumors. Some of these alterations are likely to be the effects of the neoplastic phenotype, while others may be causative agents essential to the etiologic origin of the disease. The determination of whether specific genetic alterations, either individually or in combination, can serve as the etiology of gliomas requires modeling in animals with the fulfillment of Koch's postulates. Animal modeling studies not only provide information on the potential causes of glioma formation, they also identify novel candidate targets for therapy and provide tumor-bearing animals for preclinical trials. Recently, remarkable strides have been made in the generation of mouse models of the diffuse gliomas that provide unparalleled opportunities for advancing our knowledge of the etiology, maintenance, and treatment of this lethal class of tumors.
authors.affiliation: Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
authors.forename: Martin
authors.initials: M
authors.lastname: Begemann
authors.forename: Gregory N
authors.initials: GN
authors.lastname: Fuller
authors.forename: Eric C
authors.initials: EC
authors.lastname: Holland
mesh_terms: D000818:Animals; D001932:Brain Neoplasms / Q000235:genetics* / Q000503:physiopathology; D002453:Cell Cycle / Q000235:genetics; D019070:Cell Lineage / Q000235:genetics; D004195:Disease Models, Animal; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D018390:Gene Targeting / Q000379:methods; D005910:Glioma / Q000235:genetics* / Q000503:physiopathology; D051379:Mice; D008822:Mice, Transgenic / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics