Abstract
| Originalsprog | Engelsk |
|---|---|
| Bogserie | Advances in Cancer Research |
| Vol/bind | 94 |
| Sider (fra-til) | 1-27 |
| Antal sider | 26 |
| ISSN | 0065-230X |
| DOI | |
| Status | Udgivet - 2005 |
Bibliografisk note
Keywords: Animals; Brain Neoplasms; Cell Cycle; Glioma; Humans; Mice; Signal TransductionAdgang til dokumentet
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I: Advances in Cancer Research, Bind 94, 2005, s. 1-27.
Publikation: Bidrag til tidsskrift › Review › peer review
}
TY - JOUR
T1 - Molecular mechanisms in gliomagenesis.
AU - Hulleman, Esther
AU - Helin, Kristian
N1 - Keywords: Animals; Brain Neoplasms; Cell Cycle; Glioma; Humans; Mice; Signal Transduction
PY - 2005
Y1 - 2005
N2 - Glioma, and in particular high-grade astrocytoma termed glioblastoma multiforme (GBM), is the most common primary tumor of the brain. Primarily because of its diffuse nature, there is no effective treatment for GBM, and relatively little is known about the processes by which it develops. Therefore, in order to design novel therapies and treatments for GBM, research has recently intensified to identify the cellular and molecular mechanisms leading to GBM formation. Modeling of astrocytomas by genetic manipulation of mice suggests that deregulation of the pathways that control gliogenesis during normal brain development, such as the differentiation of neural stem cells (NSCs) into astrocytes, might contribute to GBM formation. These pathways include growth factor-induced signal transduction routes and processes that control cell cycle progression, such as the p16-CDK4-RB and the ARF-MDM2-p53 pathways. The expression of several of the components of these signaling cascades has been found altered in GBM, and recent data indicate that combinations of mutations in these pathways may contribute to GBM formation, although the exact mechanisms are still to be uncovered. Use of novel techniques including large-scale genomics and proteomics in combination with relevant mouse models will most likely provide novel insights into the molecular mechanisms underlying glioma formation and will hopefully lead to development of treatment modalities for GBM.
AB - Glioma, and in particular high-grade astrocytoma termed glioblastoma multiforme (GBM), is the most common primary tumor of the brain. Primarily because of its diffuse nature, there is no effective treatment for GBM, and relatively little is known about the processes by which it develops. Therefore, in order to design novel therapies and treatments for GBM, research has recently intensified to identify the cellular and molecular mechanisms leading to GBM formation. Modeling of astrocytomas by genetic manipulation of mice suggests that deregulation of the pathways that control gliogenesis during normal brain development, such as the differentiation of neural stem cells (NSCs) into astrocytes, might contribute to GBM formation. These pathways include growth factor-induced signal transduction routes and processes that control cell cycle progression, such as the p16-CDK4-RB and the ARF-MDM2-p53 pathways. The expression of several of the components of these signaling cascades has been found altered in GBM, and recent data indicate that combinations of mutations in these pathways may contribute to GBM formation, although the exact mechanisms are still to be uncovered. Use of novel techniques including large-scale genomics and proteomics in combination with relevant mouse models will most likely provide novel insights into the molecular mechanisms underlying glioma formation and will hopefully lead to development of treatment modalities for GBM.
U2 - 10.1016/S0065-230X(05)94001-3
DO - 10.1016/S0065-230X(05)94001-3
M3 - Review
C2 - 16095998
SN - 0065-230X
VL - 94
SP - 1
EP - 27
JO - Advances in Cancer Research
JF - Advances in Cancer Research
ER -