Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors-Reference-Cited by-同舟云学术

Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors

Published:2018-08-31 Issue:6405 Volume:361 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Anderson Nathaniel D.¹²^ORCID,de Borja Richard¹^ORCID,Young Matthew D.³^ORCID,Fuligni Fabio¹,Rosic Andrej¹^ORCID,Roberts Nicola D.³^ORCID,Hajjar Simon¹,Layeghifard Mehdi¹^ORCID,Novokmet Ana¹,Kowalski Paul E.¹,Anaka Matthew¹,Davidson Scott⁴^ORCID,Zarrei Mehdi⁵,Id Said Badr¹^ORCID,Schreiner L. Christine¹^ORCID,Marchand Remi¹^ORCID,Sitter Joseph¹^ORCID,Gokgoz Nalan⁶^ORCID,Brunga Ledia¹^ORCID,Graham Garrett T.⁷^ORCID,Fullam Anthony³^ORCID,Pillay Nischalan⁸⁹^ORCID,Toretsky Jeffrey A.⁷^ORCID,Yoshida Akihiko¹⁰,Shibata Tatsuhiro¹¹¹²,Metzler Markus¹³^ORCID,Somers Gino R.²¹⁴,Scherer Stephen W.¹⁵¹⁵¹⁶^ORCID,Flanagan Adrienne M.⁹¹⁰,Campbell Peter J.³¹⁷,Schiffman Joshua D.¹⁸^ORCID,Shago Mary²⁴^ORCID,Alexandrov Ludmil B.¹⁹^ORCID,Wunder Jay S.²⁰²¹^ORCID,Andrulis Irene L.⁶¹⁵^ORCID,Malkin David¹²²²³^ORCID,Behjati Sam³²⁴^ORCID,Shlien Adam¹²⁴^ORCID

Affiliation:

1. Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.

2. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.

3. Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK.

4. Department of Paediatric Laboratory Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada.

5. The Centre for Applied Genomics, The Hospital for Sick Children, Toronto, Ontario, Canada.

6. Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada.

7. Department of Oncology and Pediatrics, Georgetown University, Washington, DC, USA.

8. University College London Cancer Institute, Huntley Street, London, UK.

9. Histopathology, Royal National Orthopaedic Hospital NHS Trust, Stanmore, Middlesex, UK.

10. Department of Pathology and Clinical Laboratories, National Cancer Center Hospital, Tokyo, Japan.

11. Division of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.

12. Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Sciences, The University of Tokyo, Minato-ku, Tokyo, Japan.

13. Department of Pediatrics and Adolescent Medicine, University Hospital Erlangen, Erlangen, Germany.

14. Department of Pathology, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.

15. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.

16. The McLaughlin Centre, University of Toronto, Toronto, Ontario, Canada.

17. Department of Haematology, University of Cambridge, Cambridge, UK.

18. Departments of Pediatrics and Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.

19. Department of Cellular and Molecular Medicine and Department of Bioengineering and Moores Cancer Center, University of California, La Jolla, San Diego, CA, USA.

20. University Musculoskeletal Oncology Unit, Mount Sinai Hospital, Toronto, Ontario, Canada.

21. Division of Orthopaedic Surgery, Department of Surgery, University of Toronto, Toronto, Ontario, Canada.

22. Division of Hematology-Oncology, The Hospital for Sick Children, Toronto, Ontario, Canada.

23. Department of Pediatrics, University of Toronto, Ontario, Canada.

24. Department of Paediatrics, University of Cambridge, Cambridge, UK.

Abstract

Looping together genes in cancer A subset of human cancers are characterized by aberrant fusion of two specific genes. In some cases, the activity of the resultant fusion protein drives tumor growth. Most fusion genes in cancer appear to arise from simple reciprocal chromosomal translocations. Anderson et al. found that the characteristic fusion gene in a bone and soft tissue tumor called Ewing sarcoma is produced by a far more complicated mechanism (see the Perspective by Imielinski and Ladanyi). In nearly half of the tumors examined, the fusion gene was created by the formation of dramatic genomic loops that disrupt multiple genes. These complex rearrangements occur in early replicating and transcriptionally active regions of the genome and are associated with poor prognosis. Science , this issue p. eaam8419 ; see also p. 848

Funder

SickKids Foundation

Garron Family Cancer Centre

The Ewings Cancer Foundation of Canada

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference43 articles.

1. Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development

2. Punctuated Evolution of Prostate Cancer Genomes

3. The impact of translocations and gene fusions on cancer causation