Recurrent Somatic Structural Variations Contribute to Tumorigenesis in Pediatric Osteosarcoma
Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor sa...
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| Vydáno v: | Cell reports (Cambridge) Ročník 7; číslo 1; s. 104 - 112 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
Elsevier
01.04.2014
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| Témata: | |
| ISSN: | 2211-1247, 2211-1247 |
| On-line přístup: | Získat plný text |
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| Abstract | Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. |
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| AbstractList | Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. Osteosarcoma is a neoplasm of mesenchymal origin with features of osteogenic differentiation. Patients with recurrent or metastatic disease have a very poor prognosis. To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue (obtained from 19 patients) in the discovery cohort as well as 14 samples from 13 patients in the validation cohort. Our results demonstrate that pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). Moreover, single nucleotide variations (SNVs) exhibit a pattern of localized hypermutation called “kataegis” in 50% of the tumors. Despite these regions of kataegis across the osteosarcoma genomes, we detected relatively few recurrent SNVs, and only when SVs were included did we identify the major pathways that are mutated in osteosarcoma. We identified p53 pathway lesions in all 19 patient’s tumors in the discovery cohort, 9 of which were translocations in the first intron of the TP53 gene, leading to gene inactivation. This mechanism of p53 gene inactivation is unique to osteosarcoma among pediatric cancers. In an additional cohort of 32 patients, TP53 gene alterations were identified in 29 of those tumors. Beyond TP53, the RB1, ATRX and DLG2 genes showed recurrent somatic alterations (SNVs and/or SVs) in 29–53% of the tumors. These data highlight the power of whole-genome sequencing in identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods.Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. |
| Author | Mulder, Heather Ellison, David Lu, Charles Mardis, Elaine R. Mao, Shenghua Edmonson, Michael Bahrami, Armita Easton, John Qu, Chunxu Zhang, Jinghui Nagahawatte, Panduka Wu, Jianrong Dalton, James Navid, Fariba Wilson, Richard K. Wang, Jianmin Wu, Gang Ding, Li Shurtleff, Sheila Rusch, Michael Wei, Lei Yergeau, Donald Dyer, Michael A. Downing, James R. Chen, Xiang Li, Yongjin Daw, Najat C. Parker, Matthew Boggs, Kristy Pappo, Alberto Hedlund, Erin |
| AuthorAffiliation | 4 Department of Biostatistics, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA 10 Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA 7 Department of Genetics, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA 6 The Genome Institute, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA 8 Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA 11 Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA 3 Department of Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA 2 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA 1 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA 9 Siteman Cancer Center, Washington University School of Medicine in St. Louis, St. Louis, Mi |
| AuthorAffiliation_xml | – name: 2 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA – name: 3 Department of Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA – name: 4 Department of Biostatistics, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA – name: 1 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA – name: 6 The Genome Institute, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA – name: 9 Siteman Cancer Center, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA – name: 7 Department of Genetics, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA – name: 10 Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA – name: 11 Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA – name: 8 Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri 63108, USA |
| Author_xml | – sequence: 1 givenname: Xiang surname: Chen fullname: Chen, Xiang – sequence: 2 givenname: Armita surname: Bahrami fullname: Bahrami, Armita – sequence: 3 givenname: Alberto surname: Pappo fullname: Pappo, Alberto – sequence: 4 givenname: John surname: Easton fullname: Easton, John – sequence: 5 givenname: James surname: Dalton fullname: Dalton, James – sequence: 6 givenname: Erin surname: Hedlund fullname: Hedlund, Erin – sequence: 7 givenname: David surname: Ellison fullname: Ellison, David – sequence: 8 givenname: Sheila surname: Shurtleff fullname: Shurtleff, Sheila – sequence: 9 givenname: Gang surname: Wu fullname: Wu, Gang – sequence: 10 givenname: Lei surname: Wei fullname: Wei, Lei – sequence: 11 givenname: Matthew surname: Parker fullname: Parker, Matthew – sequence: 12 givenname: Michael surname: Rusch fullname: Rusch, Michael – sequence: 13 givenname: Panduka surname: Nagahawatte fullname: Nagahawatte, Panduka – sequence: 14 givenname: Jianrong surname: Wu fullname: Wu, Jianrong – sequence: 15 givenname: Shenghua surname: Mao fullname: Mao, Shenghua – sequence: 16 givenname: Kristy surname: Boggs fullname: Boggs, Kristy – sequence: 17 givenname: Heather surname: Mulder fullname: Mulder, Heather – sequence: 18 givenname: Donald surname: Yergeau fullname: Yergeau, Donald – sequence: 19 givenname: Charles surname: Lu fullname: Lu, Charles – sequence: 20 givenname: Li surname: Ding fullname: Ding, Li – sequence: 21 givenname: Michael surname: Edmonson fullname: Edmonson, Michael – sequence: 22 givenname: Chunxu surname: Qu fullname: Qu, Chunxu – sequence: 23 givenname: Jianmin surname: Wang fullname: Wang, Jianmin – sequence: 24 givenname: Yongjin surname: Li fullname: Li, Yongjin – sequence: 25 givenname: Fariba surname: Navid fullname: Navid, Fariba – sequence: 26 givenname: Najat C. surname: Daw fullname: Daw, Najat C. – sequence: 27 givenname: Elaine R. surname: Mardis fullname: Mardis, Elaine R. – sequence: 28 givenname: Richard K. surname: Wilson fullname: Wilson, Richard K. – sequence: 29 givenname: James R. surname: Downing fullname: Downing, James R. – sequence: 30 givenname: Jinghui surname: Zhang fullname: Zhang, Jinghui – sequence: 31 givenname: Michael A. surname: Dyer fullname: Dyer, Michael A. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24703847$$D View this record in MEDLINE/PubMed |
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| Snippet | Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To... Osteosarcoma is a neoplasm of mesenchymal origin with features of osteogenic differentiation. Patients with recurrent or metastatic disease have a very poor... |
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| SubjectTerms | Adolescent Bone Neoplasms - genetics Bone Neoplasms - pathology Carcinogenesis - genetics Carcinogenesis - pathology Child Child, Preschool Disease Progression DNA Copy Number Variations DNA, Neoplasm - genetics Genome, Human Humans Mutation Neoplasm Metastasis Osteosarcoma - genetics Osteosarcoma - pathology Polymorphism, Single Nucleotide |
| Title | Recurrent Somatic Structural Variations Contribute to Tumorigenesis in Pediatric Osteosarcoma |
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