A recurrent point mutation in PRKCA is a hallmark of chordoid gliomas

Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kin...

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Published inNature communications Vol. 9; no. 1; pp. 2371 - 9
Main Authors Rosenberg, Shai, Simeonova, Iva, Bielle, Franck, Verreault, Maite, Bance, Bertille, Le Roux, Isabelle, Daniau, Mailys, Nadaradjane, Arun, Gleize, Vincent, Paris, Sophie, Marie, Yannick, Giry, Marine, Polivka, Marc, Figarella-Branger, Dominique, Aubriot-Lorton, Marie-Hélène, Villa, Chiara, Vasiljevic, Alexandre, Lechapt-Zalcman, Emmanuèle, Kalamarides, Michel, Sharif, Ariane, Mokhtari, Karima, Pagnotta, Stefano Maria, Iavarone, Antonio, Lasorella, Anna, Huillard, Emmanuelle, Sanson, Marc
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 18.06.2018
Nature Publishing Group
Nature Portfolio
Subjects
13/106
38/109
38/88
45
45/23
45/70
45/77
631/114/2410
631/208/68
631/67/395
82/29
Adult
Aged
Astrocytes
Brain tumors
Cell Proliferation
Cells, Cultured
Cerebral Ventricle Neoplasms - genetics
Cerebral Ventricle Neoplasms - metabolism
Female
Gene sequencing
Glioma
Glioma - genetics
Glioma - metabolism
Humanities and Social Sciences
Humans
Kinases
Life Sciences
Male
Middle Aged
multidisciplinary
Mutation
Point Mutation
Protein kinase C
Protein Kinase C-alpha - genetics
Protein Kinase C-alpha - metabolism
Proteins
Ribonucleic acid
RNA
Science
Science (multidisciplinary)
Tanycytes
Translation initiation
Tumorigenesis
Tumors
Cancer genetics
OncogenesProtein
function predictions
Online AccessGet full text

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Abstract Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA D463H mutation was not described in other tumors. PRKC A D463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCα D463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCα D463H is less stable than the PCKα WT protein. Compared to PCKα WT , the PKCα D463H protein is depleted from the cell membrane. The PKCα D463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis. Chordoid glioma is a slow growing diencephalic tumor whose mutational landscape is poorly characterized. Here, the authors perform whole-exome and RNA-sequencing and find that 15 of 16 chordoid glioma cases studied harbor the same PRKCA mutation which results in enhanced proliferation.
AbstractList Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA$^{D463H}$ mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKC$\alpha$) and is mutated in a wide range of human cancers. However the hot spot PRKCA$^{D463H}$ mutation was not described in other tumors. PRKCA$^{D463H}$ is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKC$\alpha$$^{D463H}$ mRNA levels are more abundant than wild-type PKC$\alpha$ transcripts, whilePKC$\alpha$$^{D463H}$ is less stable than the PCK$\alpha$WT protein. Compared to PCK$\alpha$WT, the PKC$\alpha$$^{D463H}$ protein is depleted from the cell membrane. The PKC$\alpha$$^{D463H}$ mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.
Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA D463H mutation was not described in other tumors. PRKC A D463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCα D463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCα D463H is less stable than the PCKα WT protein. Compared to PCKα WT , the PKCα D463H protein is depleted from the cell membrane. The PKCα D463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis. Chordoid glioma is a slow growing diencephalic tumor whose mutational landscape is poorly characterized. Here, the authors perform whole-exome and RNA-sequencing and find that 15 of 16 chordoid glioma cases studied harbor the same PRKCA mutation which results in enhanced proliferation.
Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCAD463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCAD463H mutation was not described in other tumors. PRKCAD463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCαD463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCαD463H is less stable than the PCKαWT protein. Compared to PCKαWT, the PKCαD463H protein is depleted from the cell membrane. The PKCαD463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.
Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA D463H mutation was not described in other tumors. PRKC A D463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCα D463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCα D463H is less stable than the PCKα WT protein. Compared to PCKα WT , the PKCα D463H protein is depleted from the cell membrane. The PKCα D463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.
Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA mutation was not described in other tumors. PRKCA is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCα mRNA levels are more abundant than wild-type PKCα transcripts, while PKCα is less stable than the PCKα protein. Compared to PCKα , the PKCα protein is depleted from the cell membrane. The PKCα mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.
Chordoid glioma is a slow growing diencephalic tumor whose mutational landscape is poorly characterized. Here, the authors perform whole-exome and RNA-sequencing and find that 15 of 16 chordoid glioma cases studied harbor the same PRKCA mutation which results in enhanced proliferation.
Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA D463H mutation was not described in other tumors. PRKCA D463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCαD463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCαD463H is less stable than the PCKαWT protein. Compared to PCKαWT, the PKCαD463H protein is depleted from the cell membrane. The PKCαD463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the analysis of 16 ChG by whole-exome and RNA-sequencing. We found that 15 ChG harbor the same PRKCA D463H mutation. PRKCA encodes the Protein kinase C (PKC) isozyme alpha (PKCα) and is mutated in a wide range of human cancers. However the hot spot PRKCA D463H mutation was not described in other tumors. PRKCA D463H is strongly associated with the activation of protein translation initiation (EIF2) pathway. PKCαD463H mRNA levels are more abundant than wild-type PKCα transcripts, while PKCαD463H is less stable than the PCKαWT protein. Compared to PCKαWT, the PKCαD463H protein is depleted from the cell membrane. The PKCαD463H mutant enhances proliferation of astrocytes and tanycytes, the cells of origin of ChG. In conclusion, our study identifies the hallmark mutation for chordoid gliomas and provides mechanistic insights on ChG oncogenesis.
ArticleNumber 2371
Author Gleize, Vincent
Lasorella, Anna
Aubriot-Lorton, Marie-Hélène
Rosenberg, Shai
Daniau, Mailys
Bance, Bertille
Figarella-Branger, Dominique
Iavarone, Antonio
Paris, Sophie
Vasiljevic, Alexandre
Pagnotta, Stefano Maria
Simeonova, Iva
Giry, Marine
Mokhtari, Karima
Sharif, Ariane
Marie, Yannick
Bielle, Franck
Villa, Chiara
Huillard, Emmanuelle
Sanson, Marc
Le Roux, Isabelle
Kalamarides, Michel
Nadaradjane, Arun
Verreault, Maite
Polivka, Marc
Lechapt-Zalcman, Emmanuèle
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/29915258$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Cancer genetics
OncogenesProtein
function predictions
Language English
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Snippet Chordoid glioma (ChG) is a characteristic, slow growing, and well-circumscribed diencephalic tumor, whose mutational landscape is unknown. Here we report the...
Chordoid glioma is a slow growing diencephalic tumor whose mutational landscape is poorly characterized. Here, the authors perform whole-exome and...
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Title A recurrent point mutation in PRKCA is a hallmark of chordoid gliomas
URI https://link.springer.com/article/10.1038/s41467-018-04622-w
https://www.ncbi.nlm.nih.gov/pubmed/29915258
https://www.proquest.com/docview/2056747934
https://www.proquest.com/docview/2057115362
https://amu.hal.science/hal-01858239
https://pubmed.ncbi.nlm.nih.gov/PMC6006150
https://doaj.org/article/47f7d121d4304c4ca98cb2dbb0a6edde
Volume 9
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