Expression of Mutant p53 Proteins Implicates a Lineage Relationship between Neural Stem Cells and Malignant Astrocytic Glioma in a Murine Model

Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elus...

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Published inCancer cell Vol. 15; no. 6; pp. 514 - 526
Main Authors Wang, Yuan, Yang, Jiong, Zheng, Huarui, Tomasek, Gerald J., Zhang, Peng, McKeever, Paul E., Lee, Eva Y.-H.P., Zhu, Yuan
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 02.06.2009
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Abstract Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2 + transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
AbstractList Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell-of-origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2 + transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2 + transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2 super(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
Author McKeever, Paul E.
Zhu, Yuan
Zhang, Peng
Tomasek, Gerald J.
Zheng, Huarui
Wang, Yuan
Yang, Jiong
Lee, Eva Y.-H.P.
AuthorAffiliation 1 Division of Molecular Medicine and Genetics, Department of Internal Medicine and Cell & Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109
2 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109
3 Departments of Developmental and Cell Biology and Biological Chemistry, University of California, Irvine, CA 92697
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– name: 2 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109
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Snippet Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these...
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SubjectTerms Animals
Astrocytes - pathology
Astrocytes - physiology
Astrocytoma - metabolism
Astrocytoma - pathology
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cell Differentiation
Cell Lineage - physiology
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
CELLCYCLE
Corpus Callosum - metabolism
Corpus Callosum - pathology
Disease Models, Animal
Mice
Mice, Knockout
Multipotent Stem Cells - pathology
Multipotent Stem Cells - physiology
Mutation
Neurons - pathology
Neurons - physiology
Signal Transduction - physiology
STEMCELL
Tumor Suppressor Protein p53 - biosynthesis
Tumor Suppressor Protein p53 - genetics
Title Expression of Mutant p53 Proteins Implicates a Lineage Relationship between Neural Stem Cells and Malignant Astrocytic Glioma in a Murine Model
URI https://dx.doi.org/10.1016/j.ccr.2009.04.001
https://www.ncbi.nlm.nih.gov/pubmed/19477430
https://search.proquest.com/docview/20616263
https://pubmed.ncbi.nlm.nih.gov/PMC2721466
Volume 15
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