The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma
Suzanne Baker, Jinghui Zhang and colleagues report the identification of recurrent somatic mutations in the bone morphogenetic protein (BMP) receptor ACVR1 in 32% of diffuse intrinsic pontine gliomas. Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 yea...
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| Vydáno v: | Nature genetics Ročník 46; číslo 5; s. 444 - 450 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
New York
Nature Publishing Group US
01.05.2014
Nature Publishing Group |
| Témata: | |
| ISSN: | 1061-4036, 1546-1718, 1546-1718 |
| On-line přístup: | Získat plný text |
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| Abstract | Suzanne Baker, Jinghui Zhang and colleagues report the identification of recurrent somatic mutations in the bone morphogenetic protein (BMP) receptor
ACVR1
in 32% of diffuse intrinsic pontine gliomas.
Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis
1
. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in
ACVR1
exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes,
TP53
and
ATRX
, in both DIPGs and NBS-HGGs
2
,
3
,
4
,
5
. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes
NTRK1, NTRK2
and
NTRK3
in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase–RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. |
|---|---|
| AbstractList | Suzanne Baker, Jinghui Zhang and colleagues report the identification of recurrent somatic mutations in the bone morphogenetic protein (BMP) receptor
ACVR1
in 32% of diffuse intrinsic pontine gliomas.
Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis
1
. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in
ACVR1
exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes,
TP53
and
ATRX
, in both DIPGs and NBS-HGGs
2
,
3
,
4
,
5
. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes
NTRK1, NTRK2
and
NTRK3
in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase–RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. [PUBLICATION ABSTRACT] Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis (1). We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs (2-5). Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. Pediatric high-grade glioma (HGG) is a devastating disease with a two-year survival of less than 20%1. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs) by whole genome, whole exome, and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPG (32%), in addition to the previously reported frequent somatic mutations in histone H3, TP53 and ATRX in both DIPG and NBS-HGGs2-5. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, 2, or 3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase/RAS/PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59%, respectively, of pediatric HGGs, including DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem.Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. |
| Audience | Academic |
| Author | Wilson, Richard K Lu, Charles Pounds, Stanley Ma, Xiaotu Taylor, Michael R Edmonson, Michael Jones, Chris Baker, Suzanne J Onar-Thomas, Arzu Boop, Frederick A Easton, John Qu, Chunxu Vadodaria, Bhavin Zhang, Jinghui Nagahawatte, Panduka Mardis, Elaine R Zhang, Junyuan Ju, Bensheng Wetmore, Cynthia Kriwacki, Richard Fulton, Robert S Becksfort, Jared Wu, Gang Ding, Li Mulder, Heather L Huether, Robert Lin, Tong Ochoa, Kerri Diaz, Alexander K Paugh, Barbara S Fulton, Lucinda L Downing, James R Rusch, Michael Russell, Jake C Wei, Lei Yergeau, Donald Gajjar, Amar Gupta, Pankaj Li, Yongjin Chen, Xiang Broniscer, Alberto Rankin, Sherri L Parker, Matthew Ellison, David W Boggs, Kristy Zhu, Xiaoyan Hedlund, Erin |
| AuthorAffiliation | 3 Integrated Biomedical Sciences Program, University of Tennessee Health Science Center, Memphis, TN 38163 7 Department of Biostatistics, St. Jude Children’s Research Hospital, Memphis, TN 38105 8 Department of Structural Biology, St. Jude Children’s Research Hospital, Memphis, TN 38105 10 Division of Molecular Pathology, Institute for Cancer Research, London, UK SM2 5NG 6 The Genome Institute, Washington University, 633108 14 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN 38105 12 Department of Surgery, St. Jude Children’s Research Hospital, Memphis, TN 38105 2 Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis, TN 38105 4 Department of Chemical Biology and Therapeutics, St. Jude Children’s Research Hospital, Memphis, TN 38105 1 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN 38105 5 Department of Pediatric Cancer Genome Project, St. Jude Children’s Research Hospital, Memphis, TN 38105 9 Bi |
| AuthorAffiliation_xml | – name: 11 Division of Cancer Therapeutics, Institute for Cancer Research, London, UK SM2 5NG – name: 8 Department of Structural Biology, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 7 Department of Biostatistics, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 5 Department of Pediatric Cancer Genome Project, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 4 Department of Chemical Biology and Therapeutics, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 1 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 9 Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Buffalo, NY 14263 – name: 13 Department of Oncology, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 10 Division of Molecular Pathology, Institute for Cancer Research, London, UK SM2 5NG – name: 2 Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 6 The Genome Institute, Washington University, 633108 – name: 12 Department of Surgery, St. Jude Children’s Research Hospital, Memphis, TN 38105 – name: 3 Integrated Biomedical Sciences Program, University of Tennessee Health Science Center, Memphis, TN 38163 – name: 14 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN 38105 |
| Author_xml | – sequence: 1 givenname: Gang surname: Wu fullname: Wu, Gang organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 2 givenname: Alexander K surname: Diaz fullname: Diaz, Alexander K organization: Integrated Biomedical Sciences Program, University of Tennessee Health Science Center, Memphis, TN 38163 – sequence: 3 givenname: Barbara S surname: Paugh fullname: Paugh, Barbara S organization: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 4 givenname: Sherri L surname: Rankin fullname: Rankin, Sherri L organization: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 5 givenname: Bensheng surname: Ju fullname: Ju, Bensheng organization: Department of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 6 givenname: Yongjin surname: Li fullname: Li, Yongjin organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 7 givenname: Xiaoyan surname: Zhu fullname: Zhu, Xiaoyan organization: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 8 givenname: Chunxu surname: Qu fullname: Qu, Chunxu organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 9 givenname: Xiang surname: Chen fullname: Chen, Xiang organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 10 givenname: Junyuan surname: Zhang fullname: Zhang, Junyuan organization: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 11 givenname: John surname: Easton fullname: Easton, John organization: Department of Pediatric Cancer Genome Project, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 12 givenname: Michael surname: Edmonson fullname: Edmonson, Michael organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 13 givenname: Xiaotu surname: Ma fullname: Ma, Xiaotu organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 14 givenname: Charles surname: Lu fullname: Lu, Charles organization: The Genome Institute, Washington University, 633108 – sequence: 15 givenname: Panduka surname: Nagahawatte fullname: Nagahawatte, Panduka organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 16 givenname: Erin surname: Hedlund fullname: Hedlund, Erin organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 17 givenname: Michael surname: Rusch fullname: Rusch, Michael organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 18 givenname: Stanley surname: Pounds fullname: Pounds, Stanley organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 19 givenname: Tong surname: Lin fullname: Lin, Tong organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 20 givenname: Arzu surname: Onar-Thomas fullname: Onar-Thomas, Arzu organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 21 givenname: Robert surname: Huether fullname: Huether, Robert organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 22 givenname: Richard surname: Kriwacki fullname: Kriwacki, Richard organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 23 givenname: Matthew surname: Parker fullname: Parker, Matthew organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 24 givenname: Pankaj surname: Gupta fullname: Gupta, Pankaj organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 25 givenname: Jared surname: Becksfort fullname: Becksfort, Jared organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 26 givenname: Lei surname: Wei fullname: Wei, Lei organization: Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Buffalo, NY 14263 – sequence: 27 givenname: Heather L surname: Mulder fullname: Mulder, Heather L organization: Department of Pediatric Cancer Genome Project, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 28 givenname: Kristy surname: Boggs fullname: Boggs, Kristy organization: Department of Pediatric Cancer Genome Project, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 29 givenname: Bhavin surname: Vadodaria fullname: Vadodaria, Bhavin organization: Department of Pediatric Cancer Genome Project, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 30 givenname: Donald surname: Yergeau fullname: Yergeau, Donald organization: Department of Pediatric Cancer Genome Project, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 31 givenname: Jake C surname: Russell fullname: Russell, Jake C organization: Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 32 givenname: Kerri surname: Ochoa fullname: Ochoa, Kerri organization: The Genome Institute, Washington University, 633108 – sequence: 33 givenname: Robert S surname: Fulton fullname: Fulton, Robert S organization: The Genome Institute, Washington University, 633108 – sequence: 34 givenname: Lucinda L surname: Fulton fullname: Fulton, Lucinda L organization: The Genome Institute, Washington University, 633108 – sequence: 35 givenname: Chris surname: Jones fullname: Jones, Chris organization: Division of Cancer Therapeutics, Institute for Cancer Research, London, UK SM2 5NG – sequence: 36 givenname: Frederick A surname: Boop fullname: Boop, Frederick A organization: Department of Surgery, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 37 givenname: Alberto surname: Broniscer fullname: Broniscer, Alberto organization: Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 38 givenname: Cynthia surname: Wetmore fullname: Wetmore, Cynthia organization: Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 39 givenname: Amar surname: Gajjar fullname: Gajjar, Amar organization: Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 40 givenname: Li surname: Ding fullname: Ding, Li organization: The Genome Institute, Washington University, 633108 – sequence: 41 givenname: Elaine R surname: Mardis fullname: Mardis, Elaine R organization: The Genome Institute, Washington University, 633108 – sequence: 42 givenname: Richard K surname: Wilson fullname: Wilson, Richard K organization: The Genome Institute, Washington University, 633108 – sequence: 43 givenname: Michael R surname: Taylor fullname: Taylor, Michael R organization: Department of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 44 givenname: James R surname: Downing fullname: Downing, James R organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 45 givenname: David W surname: Ellison fullname: Ellison, David W organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 46 givenname: Jinghui surname: Zhang fullname: Zhang, Jinghui organization: Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105 – sequence: 47 givenname: Suzanne J surname: Baker fullname: Baker, Suzanne J organization: Integrated Biomedical Sciences Program, University of Tennessee Health Science Center, Memphis, TN 38163 |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24705251$$D View this record in MEDLINE/PubMed |
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| Snippet | Suzanne Baker, Jinghui Zhang and colleagues report the identification of recurrent somatic mutations in the bone morphogenetic protein (BMP) receptor
ACVR1
in... Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs,... Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis (1). We analyzed 127 pediatric HGGs,... Pediatric high-grade glioma (HGG) is a devastating disease with a two-year survival of less than 20%1. We analyzed 127 pediatric HGGs, including diffuse... |
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| Title | The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma |
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