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

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dc.creator Fütterer, Agnes
dc.creator Campanero, Miguel R.
dc.creator Leonardo, Esther
dc.creator Criado, Luis M.
dc.creator Hernández, Jesús M.
dc.creator San Miguel, Jesús F.
dc.creator Martínez-Alonso, Carlos
dc.date 2008-04-16T07:55:58Z
dc.date 2008-04-16T07:55:58Z
dc.date 2005-09
dc.date.accessioned 2017-01-31T01:02:25Z
dc.date.available 2017-01-31T01:02:25Z
dc.identifier The Journal of Clinical Investigation, Volume 115, Number 9, September 2005, pp. 2351-2362
dc.identifier 0021-9738
dc.identifier http://hdl.handle.net/10261/3603
dc.identifier 10.1172/JCI24177
dc.identifier.uri http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3603
dc.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.
dc.description Peer reviewed
dc.format 1817533 bytes
dc.format application/pdf
dc.language eng
dc.publisher American Society for Clinical Investigation
dc.relation http://dx.doi.org/10.1172/JCI24177
dc.rights openAccess
dc.title Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms
dc.type Artículo


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