ReviewBlood2015
Revisiting the case for genetically engineered mouse models in human myelodysplastic syndrome research.
Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed.
- The differentiation of myeloid progenitors is effected by cascading waves of coordinated gene expression that remodel cellular physiology in a characteristic sequence.PLoS computational biology · 2026Article
- Humanized mouse models in MDS.Cell death & disease · 2025Review
- Evi1 governs Kdm6b-mediated histone demethylation to regulate the Laptm4b-driven mTOR pathway in hematopoietic progenitor cells.The Journal of clinical investigation · 2024Article
- Review
- CAR virus receptor mediates erythroid differentiation and migration and is downregulated in MDS.Leukemia · 2023Article
- Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs.The Journal of experimental medicine · 2023Article
- PI3-kinase deletion promotes myelodysplasia by dysregulating autophagy in hematopoietic stem cells.Science advances · 2023Article
- Article
- Transforming growth factor-β signaling modifies the hematopoietic acute inflammatory response to drive bone marrow failure.Haematologica · 2022Article
- RNPS1 inhibits excessive tumor necrosis factor/tumor necrosis factor receptor signaling to support hematopoiesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS.The Journal of experimental medicine · 2021Review
- Summary of animal models of myelodysplastic syndrome.Animal models and experimental medicine · 2021Review
- Overexpression of Hmga2 activates Igf2bp2 and remodels transcriptional program of Tet2-deficient stem cells in myeloid transformation.Oncogene · 2021Article
- Mitotic Errors Promote Genomic Instability and Leukemia in a Novel Mouse Model of Fanconi Anemia.Frontiers in oncology · 2021Article
- Inducible expression of a disease-associatedThe Journal of biological chemistry · 2020Article
- Targeting Aberrant Splicing in Myelodysplastic Syndromes: Biologic Rationale and Clinical Opportunity.Hematology/oncology clinics of North America · 2020Review
- Myelodysplastic syndrome patient-derived xenografts: from no options to many.Haematologica · 2020Article
- Energy metabolism and drug response in myeloid leukaemic stem cells.British journal of haematology · 2019Review
- A highly efficient and faithful MDS patient-derived xenotransplantation model for pre-clinical studies.Nature communications · 2019Article
- Increased Ripk1-mediated bone marrow necroptosis leads to myelodysplasia and bone marrow failure in mice.Blood · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Much-needed attention has been given of late to diseases specifically associated with an expanding elderly population. Myelodysplastic syndrome (MDS), a hematopoietic stem cell-based blood disease, is one of these. The lack of clear understanding of the molecular mechanisms underlying the pathogenesis of this disease has hampered the development of efficacious therapies, especially in the presence of comorbidities. Mouse models could potentially provide new insights into this disease, although primary human MDS cells grow poorly in xenografted mice. This makes genetically engineered murine models a more attractive proposition, although this approach is not without complications. In particular, it is unclear if or how myelodysplasia (abnormal blood cell morphology), a key MDS feature in humans, presents in murine cells. Here, we evaluate the histopathologic features of wild-type mice and 23 mouse models with verified myelodysplasia. We find that certain features indicative of myelodysplasia in humans, such as Howell-Jolly bodies and low neutrophilic granularity, are commonplace in healthy mice, whereas other features are similarly abnormal in humans and mice. Quantitative hematopoietic parameters, such as blood cell counts, are required to distinguish between MDS and related diseases. We provide data that mouse models of MDS can be genetically engineered and faithfully recapitulate human disease.
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What OpenQuestion holds
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.