| Animal models of cell cycle dysregulation and the pathogenesis of gliomas. | |
| | |
MedLine Citation:
|
PMID: 11407597 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Mutations in gliomas, for the most part, fall into two main categories. The first category of mutations affects genes that produce proteins which activate signal transduction pathways downstream of tyrosine kinase receptors; the second category disrupts the pathways leading to cell cycle arrest. Cell cycle arrest pathways normally maintain cells in the G1 phase of the cell cycle, preventing inappropriate proliferation. The role of disregulation of these pathways in tumor formation is currently the focus of many investigations. Studies carried out with astrocytes and other cell types indicate that these pathways may also function in maintenance of appropriate chromosome number and differentiated phenotype, and in acquisition of senescence. Genetically defined mouse models of gliomagenesis have been helpful in increasing our understanding of how cell cycle arrest pathways cooperate with alterations in signal transduction pathways to provoke tumor formation in many cell types, including glial cells. Various strategies for experimental cell cycle arrest disruption show minimal or no formation of gliomas. In contrast, gliomas are generated with a number of strategies that enhance signal transduction downstream of tyrosine kinase receptors. Experimental disruption of the cell cycle arrest pathways is required for gliomagenesis in some of these models, but not in others. Furthermore in some cases, although not required for gliomagenesis, disruption of the cell cycle arrest pathways appears to enhance glioma formation. The results of these mouse model experiments imply a potentially complex role for cell cycle arrest disruption in human gliomagenesis. |
| | |
Authors:
|
E C Holland |
Related Documents
:
|
1458027 - What is the minimum number of dedicated functions required for a basic cell cycle? 12909627 - The orc1 cycle in human cells: i. cell cycle-regulated oscillation of human orc1. 2906147 - Roles for the phosphatidylinositol cycle in early development. 8909137 - At the heart of the budding yeast cell cycle. 20238267 - Application of laser microdissection to study plant-fungal pathogen interactions. 2407597 - Igg subclass-containing cells in the human large bowel of normal controls, non-ibd coli... |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Journal of neuro-oncology Volume: 51 ISSN: 0167-594X ISO Abbreviation: J. Neurooncol. Publication Date: 2001 Feb |
Date Detail:
|
Created Date: 2001-06-15 Completed Date: 2001-10-25 Revised Date: 2005-11-17 |
Medline Journal Info:
|
Nlm Unique ID: 8309335 Medline TA: J Neurooncol Country: Netherlands |
Other Details:
|
Languages: eng Pagination: 265-76 Citation Subset: IM |
Affiliation:
|
Department of Neurosurgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. hollande@mskcc.org |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Cell Cycle / genetics Disease Models, Animal Gene Transfer Techniques Glioma / etiology, genetics* Mutation Proteins / genetics Signal Transduction / physiology Tumor Suppressor Protein p14ARF |
| Chemical | |
Reg. No./Substance:
|
0/Proteins; 0/Tumor Suppressor Protein p14ARF |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Mitogenic signaling and the relationship to cell cycle regulation in astrocytomas.
Next Document: Delivery of cell cycle genes to block astrocytoma growth.