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 in | Cancer cell Vol. 15; no. 6; pp. 514 - 526 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
02.06.2009
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Subjects | |
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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. |
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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 |
AuthorAffiliation_xml | – name: 1 Division of Molecular Medicine and Genetics, Department of Internal Medicine and Cell & Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109 – name: 3 Departments of Developmental and Cell Biology and Biological Chemistry, University of California, Irvine, CA 92697 – name: 2 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109 |
Author_xml | – sequence: 1 givenname: Yuan surname: Wang fullname: Wang, Yuan organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 2 givenname: Jiong surname: Yang fullname: Yang, Jiong organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 3 givenname: Huarui surname: Zheng fullname: Zheng, Huarui organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 4 givenname: Gerald J. surname: Tomasek fullname: Tomasek, Gerald J. organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 5 givenname: Peng surname: Zhang fullname: Zhang, Peng organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 6 givenname: Paul E. surname: McKeever fullname: McKeever, Paul E. organization: Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA – sequence: 7 givenname: Eva Y.-H.P. surname: Lee fullname: Lee, Eva Y.-H.P. organization: Department of Developmental and Cell Biology, University of California, Irvine, Irvine, CA 92697, USA – sequence: 8 givenname: Yuan surname: Zhu fullname: Zhu, Yuan email: yuanzhu@umich.edu organization: Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19477430$$D View this record in MEDLINE/PubMed |
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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 |
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