Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms

The myelodysplastic/myeloproliferative diseases (MDS/MPDs) are a heterogeneous group of myeloid neoplasms that share characteristics with chronic myeloproliferative diseases and myelodysplastic syndromes. The broad spectrum of clinical manifestations makes MDS/MPDs extremely difficult to diagnose an...

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Autores: Fütterer, Agnes, Campanero, Miguel R., Leonardo, Esther, Criado, Luis M., Hernández, Jesús M., San Miguel, Jesús F., Martínez-Alonso, Carlos
Tipo de recurso: artículo
Fecha de publicación:2005
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/3603
Acceso en línea:http://hdl.handle.net/10261/3603
Access Level:acceso abierto
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spelling Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasmsFütterer, AgnesCampanero, Miguel R.Leonardo, EstherCriado, Luis M.Hernández, Jesús M.San Miguel, Jesús F.Martínez-Alonso, CarlosThe myelodysplastic/myeloproliferative diseases (MDS/MPDs) are a heterogeneous group of myeloid neoplasms that share characteristics with chronic myeloproliferative diseases and myelodysplastic syndromes. The broad spectrum of clinical manifestations makes MDS/MPDs extremely difficult to diagnose and treat, with a median survival time of 1–5 years. No single gene defect has been firmly associated with MDS/MPDs, and no animal models have been developed for these diseases. The association of deletions on chromosome 20q with myeloid malignancies suggests the presence of unidentified tumor suppressor genes in this region. Here we show that the recently identified death inducer–obliterator (Dido) gene gives rise to at least 3 polypeptides (Dido1, Dido2, and Dido3) through alternative splicing, and we map the human gene to the long arm of chromosome 20. We found that targeting of murine Dido caused a transplantable disease whose symptoms and signs suggested MDS/MPDs. Furthermore, 100% of human MDS/MPD patients analyzed showed Dido expression abnormalities, which we also found in other myeloid but not lymphoid neoplasms or in healthy donors. Our findings suggest that Dido might be one of the tumor suppressor genes at chromosome 20q and that the Dido-targeted mouse may be a suitable model for studying MDS/MPD diseases and testing new approaches to their diagnosis and treatment.Peer reviewedAmerican Society for Clinical Investigation200820082005info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_65011817533 bytesapplication/pdfhttp://hdl.handle.net/10261/3603reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttp://dx.doi.org/10.1172/JCI24177info:eu-repo/semantics/openAccessoai:digital.csic.es:10261/36032026-05-22T06:33:51Z
dc.title.none.fl_str_mv Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
title Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
spellingShingle Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
Fütterer, Agnes
title_short Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
title_full Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
title_fullStr Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
title_full_unstemmed Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
title_sort Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
dc.creator.none.fl_str_mv Fütterer, Agnes
Campanero, Miguel R.
Leonardo, Esther
Criado, Luis M.
Hernández, Jesús M.
San Miguel, Jesús F.
Martínez-Alonso, Carlos
author Fütterer, Agnes
author_facet Fütterer, Agnes
Campanero, Miguel R.
Leonardo, Esther
Criado, Luis M.
Hernández, Jesús M.
San Miguel, Jesús F.
Martínez-Alonso, Carlos
author_role author
author2 Campanero, Miguel R.
Leonardo, Esther
Criado, Luis M.
Hernández, Jesús M.
San Miguel, Jesús F.
Martínez-Alonso, Carlos
author2_role author
author
author
author
author
author
description The myelodysplastic/myeloproliferative diseases (MDS/MPDs) are a heterogeneous group of myeloid neoplasms that share characteristics with chronic myeloproliferative diseases and myelodysplastic syndromes. The broad spectrum of clinical manifestations makes MDS/MPDs extremely difficult to diagnose and treat, with a median survival time of 1–5 years. No single gene defect has been firmly associated with MDS/MPDs, and no animal models have been developed for these diseases. The association of deletions on chromosome 20q with myeloid malignancies suggests the presence of unidentified tumor suppressor genes in this region. Here we show that the recently identified death inducer–obliterator (Dido) gene gives rise to at least 3 polypeptides (Dido1, Dido2, and Dido3) through alternative splicing, and we map the human gene to the long arm of chromosome 20. We found that targeting of murine Dido caused a transplantable disease whose symptoms and signs suggested MDS/MPDs. Furthermore, 100% of human MDS/MPD patients analyzed showed Dido expression abnormalities, which we also found in other myeloid but not lymphoid neoplasms or in healthy donors. Our findings suggest that Dido might be one of the tumor suppressor genes at chromosome 20q and that the Dido-targeted mouse may be a suitable model for studying MDS/MPD diseases and testing new approaches to their diagnosis and treatment.
publishDate 2005
dc.date.none.fl_str_mv 2005
2008
2008
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/3603
url http://hdl.handle.net/10261/3603
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv http://dx.doi.org/10.1172/JCI24177
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1817533 bytes
application/pdf
dc.publisher.none.fl_str_mv American Society for Clinical Investigation
publisher.none.fl_str_mv American Society for Clinical Investigation
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
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