Progression as exemplified by human astrocytic tumors.
The last 10 years has seen major improvements in our understanding of the genetic anomalies that lie behind the development and progression of human astrocytic tumors. The least aggressive astrocytomas frequently show loss of wild type p53 as well as losses of alleles from a number of regions of the genome. The genes targeted have yet to be identified. The most aggressive tumors, the glioblastomas, show mutations affecting the cellular mechanisms controlling entry into the S-phase of the cell cycle. The picture has become more complex as regards the mechanisms targeted. The heterogeneous genetic abnormalities reported previously in individual tumors of the same type have become easier to understand with the realization that they represent the mutation of different genes that code for components of the same cellular control mechanisms. There remain many routes to explore before we understand in detail the molecular mechanisms behind the phenotype of these tumors.
Collins
V P
VP
Division of Clinical Molecular Pathology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK.
D001254:Astrocytoma / Q000145:classification / Q000235:genetics* / Q000473:pathology*; D001932:Brain Neoplasms / Q000145:classification / Q000235:genetics* / Q000473:pathology*; D002453:Cell Cycle; D018450:Disease Progression; D005909:Glioblastoma / Q000145:classification / Q000235:genetics / Q000473:pathology; D006801:Humans; D009154:Mutation / Q000235:genetics; D009857:Oncogenes / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology
D016159:Tumor Suppressor Protein p53