ArticleThe Journal of clinical investigation2005
Dido gene expression alterations are implicated in the induction of hematological myeloid neoplasms.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- The Coming of Age of Preclinical Models of MDS.Frontiers in oncology · 2022Pooled it
- Domain acquisition enabled functional expansion of the TFIIS transcription factor family.Cell & bioscience · 2025Review
- The chromatin reader Dido3 is a regulator of the gene network that controls B cell differentiation.Cell & bioscience · 2025Article
- DIDO is necessary for the adipogenesis that promotes diet-induced obesity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation.Nature communications · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- Hepatitis, testicular degeneration, and ataxia in DIDO3-deficient mice with altered mRNA processing.Cell & bioscience · 2022Article
- Nuclear Morphological Abnormalities in Cancer: A Search for Unifying Mechanisms.Results and problems in cell differentiation · 2022Article
- CircDIDO1 inhibits gastric cancer progression by encoding a novel DIDO1-529aa protein and regulating PRDX2 protein stability.Molecular cancer · 2021Article
- Impaired stem cell differentiation and somatic cell reprogramming in DIDO3 mutants with altered RNA processing and increased R-loop levels.Cell death & disease · 2021Article
- Splicing Anomalies in Myeloproliferative Neoplasms: Paving the Way for New Therapeutic Venues.Cancers · 2020Review
- High-throughput gene screen reveals modulators of nuclear shape.Molecular biology of the cell · 2020Article
- Role of DIDO1 in Progression of Esophageal Squamous Cell Carcinoma.Journal of gastrointestinal cancer · 2020Article
- BAP1 maintains chromosome stability by stabilizing DIDO1 in renal cell carcinoma.American journal of cancer research · 2020Article
- Dido3-dependent SFPQ recruitment maintains efficiency in mammalian alternative splicing.Nucleic acids research · 2019Article
- Whole‑exome sequencing analysis of products of conception identifies novel mutations associated with missed abortion.Molecular medicine reports · 2018Article
- A Unique pH-Dependent Recognition of Methylated Histone H3K4 by PPS and DIDO.Structure (London, England : 1993) · 2017Article
- Turning the tide in myelodysplastic/myeloproliferative neoplasms.Nature reviews. Cancer · 2017Review
- Exploring genetic associations with ceRNA regulation in the human genome.Nucleic acids research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.