File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Large recurrent microdeletions associated with schizophrenia
  • Basic View
  • Metadata View
  • XML View
TitleLarge recurrent microdeletions associated with schizophrenia
 
AuthorsStefansson, H23
Rujescu, D2
Cichon, S4
Pietiläinen, OPH18
Ingason, A23
Steinberg, S23
Fossdal, R23
Sigurdsson, E9
Sigmundsson, T9
BuizerVoskamp, JE28
Hansen, T1 7
Jakobsen, KD1 7
Muglia, P12
Francks, C12
Matthews, PM6
Gylfason, A23
Halldorsson, BV23
Gudbjartsson, D23
Thorgeirsson, TE23
Sigurdsson, A23
Jonasdottir, A23
Jonasdottir, A23
Bjornsson, A23
Mattiasdottir, S23
Blondal, T23
Haraldsson, M9
Magnusdottir, BB9
Giegling, I2
Möller, HJ2
Hartmann, A2
Shianna, KV25
Ge, D25
Need, AC25
Crombie, C5
Fraser, G5
Walker, N19
Lonnqvist, J18
Suvisaari, J18
TuulioHenriksson, A18
Paunio, T18
Toulopoulou, T3
Bramon, E3
Di Forti, M3
Murray, R3
Ruggeri, M26
Vassos, E3
Tosato, S26
Walshe, M3
Li, T3 27
Vasilescu, C4
Mühleisen, TW4
Wang, AG1
Ullum, H1
Djurovic, S21 10
Melle, I10
Olesen, J14
Kiemeney, LA22
Franke, B22
Sabatti, C24
Freimer, NB13
Gulcher, JR23
Thorsteinsdottir, U23
Kong, A23
Andreassen, OA21 10
Ophoff, RA28 13
Georgi, A15
Rietschel, M15
Werge, T1
Petursson, H9
Goldstein, DB25
Nöthen, MM4
Peltonen, L17 18 29
Collier, DA3 27
St Clair, D5
Stefansson, K23 16
Kahn, RS28
Linszen, DH8
Van Os, J20
Wiersma, D11
Bruggeman, R11
Cahn, W28
De Haan, L8
Krabbendam, L20
MyinGermeys, I20
 
KeywordsReferences (31) View In Table Layout
 
Issue Date2008
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nature
 
CitationNature, 2008, v. 455 n. 7210, p. 232-236 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nature07229
 
AbstractReduced fecundity, associated with severe mental disorders, places negative selection pressure on risk alleles and may explain, in part, why common variants have not been found that confer risk of disorders such as autism, schizophrenia and mental retardation. Thus, rare variants may account for a larger fraction of the overall genetic risk than previously assumed. In contrast to rare single nucleotide mutations, rare copy number variations (CNVs) can be detected using genome-wide single nucleotide polymorphism arrays. This has led to the identification of CNVs associated with mental retardation and autism. In a genome-wide search for CNVs associating with schizophrenia, we used a population-based sample to identify de novo CNVs by analysing 9,878 transmissions from parents to offspring. The 66 de novo CNVs identified were tested for association in a sample of 1,433 schizophrenia cases and 33,250 controls. Three deletions at 1q21.1, 15q11.2 and 15q13.3 showing nominal association with schizophrenia in the first sample (phase I) were followed up in a second sample of 3,285 cases and 7,951 controls (phase II). All three deletions significantly associate with schizophrenia and related psychoses in the combined sample. The identification of these rare, recurrent risk variants, having occurred independently in multiple founders and being subject to negative selection, is important in itself. CNV analysis may also point the way to the identification of additional and more prevalent risk variants in genes and pathways involved in schizophrenia. ©2008 Macmillan Publishers Limited. All rights reserved.
 
ISSN0028-0836
2013 Impact Factor: 42.351
 
DOIhttp://dx.doi.org/10.1038/nature07229
 
PubMed Central IDPMC2687075
 
ISI Accession Number IDWOS:000259090800049
Funding AgencyGrant Number
EU grantLSHM-CT-2006-037761 ( Project SGENE)
Simons Foundation
NIMHR01 MH078075
Chinese National Natural Science Foundation
National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF)
Alfried Krupp von Bohlen und Halbach-Stiftung
R01MH71425-01A1
Funding Information:

We want to thank the subjects and their relatives and staff at the recruitment centres. This work was sponsored by EU grant LSHM-CT-2006-037761 ( Project SGENE), Simons Foundation and R01MH71425-01A1. Genotyping of the Dutch samples was sponsored by NIMH funding, R01 MH078075. This work was also supported by the Chinese National Natural Science Foundation and the National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF). M.M.N. received support from the Alfried Krupp von Bohlen und Halbach-Stiftung. We are grateful to S. Schreiber and M. Krawczak for providing genotype data for PopGen controls, and to K.- H. Jockel and R. Erbel for providing control individuals from the Heinz Nixdorf Recall Study. We thank L. Priebe and M. Alblas for technical assistance and analysis of CNV data from Bonn.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorStefansson, H
 
dc.contributor.authorRujescu, D
 
dc.contributor.authorCichon, S
 
dc.contributor.authorPietiläinen, OPH
 
dc.contributor.authorIngason, A
 
dc.contributor.authorSteinberg, S
 
dc.contributor.authorFossdal, R
 
dc.contributor.authorSigurdsson, E
 
dc.contributor.authorSigmundsson, T
 
dc.contributor.authorBuizerVoskamp, JE
 
dc.contributor.authorHansen, T
 
dc.contributor.authorJakobsen, KD
 
dc.contributor.authorMuglia, P
 
dc.contributor.authorFrancks, C
 
dc.contributor.authorMatthews, PM
 
dc.contributor.authorGylfason, A
 
dc.contributor.authorHalldorsson, BV
 
dc.contributor.authorGudbjartsson, D
 
dc.contributor.authorThorgeirsson, TE
 
dc.contributor.authorSigurdsson, A
 
dc.contributor.authorJonasdottir, A
 
dc.contributor.authorJonasdottir, A
 
dc.contributor.authorBjornsson, A
 
dc.contributor.authorMattiasdottir, S
 
dc.contributor.authorBlondal, T
 
dc.contributor.authorHaraldsson, M
 
dc.contributor.authorMagnusdottir, BB
 
dc.contributor.authorGiegling, I
 
dc.contributor.authorMöller, HJ
 
dc.contributor.authorHartmann, A
 
dc.contributor.authorShianna, KV
 
dc.contributor.authorGe, D
 
dc.contributor.authorNeed, AC
 
dc.contributor.authorCrombie, C
 
dc.contributor.authorFraser, G
 
dc.contributor.authorWalker, N
 
dc.contributor.authorLonnqvist, J
 
dc.contributor.authorSuvisaari, J
 
dc.contributor.authorTuulioHenriksson, A
 
dc.contributor.authorPaunio, T
 
dc.contributor.authorToulopoulou, T
 
dc.contributor.authorBramon, E
 
dc.contributor.authorDi Forti, M
 
dc.contributor.authorMurray, R
 
dc.contributor.authorRuggeri, M
 
dc.contributor.authorVassos, E
 
dc.contributor.authorTosato, S
 
dc.contributor.authorWalshe, M
 
dc.contributor.authorLi, T
 
dc.contributor.authorVasilescu, C
 
dc.contributor.authorMühleisen, TW
 
dc.contributor.authorWang, AG
 
dc.contributor.authorUllum, H
 
dc.contributor.authorDjurovic, S
 
dc.contributor.authorMelle, I
 
dc.contributor.authorOlesen, J
 
dc.contributor.authorKiemeney, LA
 
dc.contributor.authorFranke, B
 
dc.contributor.authorSabatti, C
 
dc.contributor.authorFreimer, NB
 
dc.contributor.authorGulcher, JR
 
dc.contributor.authorThorsteinsdottir, U
 
dc.contributor.authorKong, A
 
dc.contributor.authorAndreassen, OA
 
dc.contributor.authorOphoff, RA
 
dc.contributor.authorGeorgi, A
 
dc.contributor.authorRietschel, M
 
dc.contributor.authorWerge, T
 
dc.contributor.authorPetursson, H
 
dc.contributor.authorGoldstein, DB
 
dc.contributor.authorNöthen, MM
 
dc.contributor.authorPeltonen, L
 
dc.contributor.authorCollier, DA
 
dc.contributor.authorSt Clair, D
 
dc.contributor.authorStefansson, K
 
dc.contributor.authorKahn, RS
 
dc.contributor.authorLinszen, DH
 
dc.contributor.authorVan Os, J
 
dc.contributor.authorWiersma, D
 
dc.contributor.authorBruggeman, R
 
dc.contributor.authorCahn, W
 
dc.contributor.authorDe Haan, L
 
dc.contributor.authorKrabbendam, L
 
dc.contributor.authorMyinGermeys, I
 
dc.date.accessioned2011-09-27T03:03:09Z
 
dc.date.available2011-09-27T03:03:09Z
 
dc.date.issued2008
 
dc.description.abstractReduced fecundity, associated with severe mental disorders, places negative selection pressure on risk alleles and may explain, in part, why common variants have not been found that confer risk of disorders such as autism, schizophrenia and mental retardation. Thus, rare variants may account for a larger fraction of the overall genetic risk than previously assumed. In contrast to rare single nucleotide mutations, rare copy number variations (CNVs) can be detected using genome-wide single nucleotide polymorphism arrays. This has led to the identification of CNVs associated with mental retardation and autism. In a genome-wide search for CNVs associating with schizophrenia, we used a population-based sample to identify de novo CNVs by analysing 9,878 transmissions from parents to offspring. The 66 de novo CNVs identified were tested for association in a sample of 1,433 schizophrenia cases and 33,250 controls. Three deletions at 1q21.1, 15q11.2 and 15q13.3 showing nominal association with schizophrenia in the first sample (phase I) were followed up in a second sample of 3,285 cases and 7,951 controls (phase II). All three deletions significantly associate with schizophrenia and related psychoses in the combined sample. The identification of these rare, recurrent risk variants, having occurred independently in multiple founders and being subject to negative selection, is important in itself. CNV analysis may also point the way to the identification of additional and more prevalent risk variants in genes and pathways involved in schizophrenia. ©2008 Macmillan Publishers Limited. All rights reserved.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationNature, 2008, v. 455 n. 7210, p. 232-236 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nature07229
 
dc.identifier.citeulike3066975
 
dc.identifier.doihttp://dx.doi.org/10.1038/nature07229
 
dc.identifier.eissn1476-4687
 
dc.identifier.epage236
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.f10001118982
 
dc.identifier.isiWOS:000259090800049
Funding AgencyGrant Number
EU grantLSHM-CT-2006-037761 ( Project SGENE)
Simons Foundation
NIMHR01 MH078075
Chinese National Natural Science Foundation
National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF)
Alfried Krupp von Bohlen und Halbach-Stiftung
R01MH71425-01A1
Funding Information:

We want to thank the subjects and their relatives and staff at the recruitment centres. This work was sponsored by EU grant LSHM-CT-2006-037761 ( Project SGENE), Simons Foundation and R01MH71425-01A1. Genotyping of the Dutch samples was sponsored by NIMH funding, R01 MH078075. This work was also supported by the Chinese National Natural Science Foundation and the National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF). M.M.N. received support from the Alfried Krupp von Bohlen und Halbach-Stiftung. We are grateful to S. Schreiber and M. Krawczak for providing genotype data for PopGen controls, and to K.- H. Jockel and R. Erbel for providing control individuals from the Heinz Nixdorf Recall Study. We thank L. Priebe and M. Alblas for technical assistance and analysis of CNV data from Bonn.

 
dc.identifier.issn0028-0836
2013 Impact Factor: 42.351
 
dc.identifier.issue7210
 
dc.identifier.pmcidPMC2687075
 
dc.identifier.pmid18668039
 
dc.identifier.scopuseid_2-s2.0-49949085933
 
dc.identifier.spage232
 
dc.identifier.urihttp://hdl.handle.net/10722/141844
 
dc.identifier.volume455
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nature
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofNature
 
dc.relation.referencesReferences in Scopus
 
dc.subjectReferences (31) View In Table Layout
 
dc.titleLarge recurrent microdeletions associated with schizophrenia
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Stefansson, H</contributor.author>
<contributor.author>Rujescu, D</contributor.author>
<contributor.author>Cichon, S</contributor.author>
<contributor.author>Pietil&#228;inen, OPH</contributor.author>
<contributor.author>Ingason, A</contributor.author>
<contributor.author>Steinberg, S</contributor.author>
<contributor.author>Fossdal, R</contributor.author>
<contributor.author>Sigurdsson, E</contributor.author>
<contributor.author>Sigmundsson, T</contributor.author>
<contributor.author>BuizerVoskamp, JE</contributor.author>
<contributor.author>Hansen, T</contributor.author>
<contributor.author>Jakobsen, KD</contributor.author>
<contributor.author>Muglia, P</contributor.author>
<contributor.author>Francks, C</contributor.author>
<contributor.author>Matthews, PM</contributor.author>
<contributor.author>Gylfason, A</contributor.author>
<contributor.author>Halldorsson, BV</contributor.author>
<contributor.author>Gudbjartsson, D</contributor.author>
<contributor.author>Thorgeirsson, TE</contributor.author>
<contributor.author>Sigurdsson, A</contributor.author>
<contributor.author>Jonasdottir, A</contributor.author>
<contributor.author>Jonasdottir, A</contributor.author>
<contributor.author>Bjornsson, A</contributor.author>
<contributor.author>Mattiasdottir, S</contributor.author>
<contributor.author>Blondal, T</contributor.author>
<contributor.author>Haraldsson, M</contributor.author>
<contributor.author>Magnusdottir, BB</contributor.author>
<contributor.author>Giegling, I</contributor.author>
<contributor.author>M&#246;ller, HJ</contributor.author>
<contributor.author>Hartmann, A</contributor.author>
<contributor.author>Shianna, KV</contributor.author>
<contributor.author>Ge, D</contributor.author>
<contributor.author>Need, AC</contributor.author>
<contributor.author>Crombie, C</contributor.author>
<contributor.author>Fraser, G</contributor.author>
<contributor.author>Walker, N</contributor.author>
<contributor.author>Lonnqvist, J</contributor.author>
<contributor.author>Suvisaari, J</contributor.author>
<contributor.author>TuulioHenriksson, A</contributor.author>
<contributor.author>Paunio, T</contributor.author>
<contributor.author>Toulopoulou, T</contributor.author>
<contributor.author>Bramon, E</contributor.author>
<contributor.author>Di Forti, M</contributor.author>
<contributor.author>Murray, R</contributor.author>
<contributor.author>Ruggeri, M</contributor.author>
<contributor.author>Vassos, E</contributor.author>
<contributor.author>Tosato, S</contributor.author>
<contributor.author>Walshe, M</contributor.author>
<contributor.author>Li, T</contributor.author>
<contributor.author>Vasilescu, C</contributor.author>
<contributor.author>M&#252;hleisen, TW</contributor.author>
<contributor.author>Wang, AG</contributor.author>
<contributor.author>Ullum, H</contributor.author>
<contributor.author>Djurovic, S</contributor.author>
<contributor.author>Melle, I</contributor.author>
<contributor.author>Olesen, J</contributor.author>
<contributor.author>Kiemeney, LA</contributor.author>
<contributor.author>Franke, B</contributor.author>
<contributor.author>Sabatti, C</contributor.author>
<contributor.author>Freimer, NB</contributor.author>
<contributor.author>Gulcher, JR</contributor.author>
<contributor.author>Thorsteinsdottir, U</contributor.author>
<contributor.author>Kong, A</contributor.author>
<contributor.author>Andreassen, OA</contributor.author>
<contributor.author>Ophoff, RA</contributor.author>
<contributor.author>Georgi, A</contributor.author>
<contributor.author>Rietschel, M</contributor.author>
<contributor.author>Werge, T</contributor.author>
<contributor.author>Petursson, H</contributor.author>
<contributor.author>Goldstein, DB</contributor.author>
<contributor.author>N&#246;then, MM</contributor.author>
<contributor.author>Peltonen, L</contributor.author>
<contributor.author>Collier, DA</contributor.author>
<contributor.author>St Clair, D</contributor.author>
<contributor.author>Stefansson, K</contributor.author>
<contributor.author>Kahn, RS</contributor.author>
<contributor.author>Linszen, DH</contributor.author>
<contributor.author>Van Os, J</contributor.author>
<contributor.author>Wiersma, D</contributor.author>
<contributor.author>Bruggeman, R</contributor.author>
<contributor.author>Cahn, W</contributor.author>
<contributor.author>De Haan, L</contributor.author>
<contributor.author>Krabbendam, L</contributor.author>
<contributor.author>MyinGermeys, I</contributor.author>
<date.accessioned>2011-09-27T03:03:09Z</date.accessioned>
<date.available>2011-09-27T03:03:09Z</date.available>
<date.issued>2008</date.issued>
<identifier.citation>Nature, 2008, v. 455 n. 7210, p. 232-236</identifier.citation>
<identifier.issn>0028-0836</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/141844</identifier.uri>
<description.abstract>Reduced fecundity, associated with severe mental disorders, places negative selection pressure on risk alleles and may explain, in part, why common variants have not been found that confer risk of disorders such as autism, schizophrenia and mental retardation. Thus, rare variants may account for a larger fraction of the overall genetic risk than previously assumed. In contrast to rare single nucleotide mutations, rare copy number variations (CNVs) can be detected using genome-wide single nucleotide polymorphism arrays. This has led to the identification of CNVs associated with mental retardation and autism. In a genome-wide search for CNVs associating with schizophrenia, we used a population-based sample to identify de novo CNVs by analysing 9,878 transmissions from parents to offspring. The 66 de novo CNVs identified were tested for association in a sample of 1,433 schizophrenia cases and 33,250 controls. Three deletions at 1q21.1, 15q11.2 and 15q13.3 showing nominal association with schizophrenia in the first sample (phase I) were followed up in a second sample of 3,285 cases and 7,951 controls (phase II). All three deletions significantly associate with schizophrenia and related psychoses in the combined sample. The identification of these rare, recurrent risk variants, having occurred independently in multiple founders and being subject to negative selection, is important in itself. CNV analysis may also point the way to the identification of additional and more prevalent risk variants in genes and pathways involved in schizophrenia. &#169;2008 Macmillan Publishers Limited. All rights reserved.</description.abstract>
<language>eng</language>
<publisher>Nature Publishing Group. The Journal&apos;s web site is located at http://www.nature.com/nature</publisher>
<relation.ispartof>Nature</relation.ispartof>
<subject>References (31) View In Table Layout</subject>
<title>Large recurrent microdeletions associated with schizophrenia</title>
<type>Article</type>
<description.nature>link_to_OA_fulltext</description.nature>
<identifier.doi>10.1038/nature07229</identifier.doi>
<identifier.pmid>18668039</identifier.pmid>
<identifier.pmcid>PMC2687075</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-49949085933</identifier.scopus>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-49949085933&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>455</identifier.volume>
<identifier.issue>7210</identifier.issue>
<identifier.spage>232</identifier.spage>
<identifier.epage>236</identifier.epage>
<identifier.eissn>1476-4687</identifier.eissn>
<identifier.isi>WOS:000259090800049</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.f1000>1118982</identifier.f1000>
<identifier.citeulike>3066975</identifier.citeulike>
<bitstream.url>http://hub.hku.hk/bitstream/10722/141844/1/re01.htm</bitstream.url>
</item>
Author Affiliations
  1. Copenhagen University Hospital
  2. Ludwig-Maximilians-Universität München
  3. King's College London
  4. Universität Bonn
  5. University of Aberdeen
  6. Hammersmith Hospital
  7. Københavns Universitet
  8. Academic Medical Centre, University of Amsterdam
  9. National University Hospital Reykjavik
  10. Ulleval University Hospital
  11. Universitair Medisch Centrum Groningen
  12. GlaxoSmithKline
  13. UCLA Medical Center
  14. Amtssygehuset i Glostrup
  15. Universität Heidelberg
  16. University of Iceland
  17. Wellcome Trust Sanger Institute
  18. Kansanterveyslaitos
  19. Ravenscraig Hospital
  20. Maastricht University
  21. Universitetet i Oslo
  22. Radboud University Nijmegen Medical Centre
  23. CNS Division
  24. University of California, Los Angeles
  25. Duke Institute for Genome Sciences &amp; Policy
  26. Università degli Studi di Verona
  27. Sichuan University
  28. University Medical Center Utrecht
  29. Broad Institute