ReviewExperimental hematology2014
Murine xenogeneic models of myelodysplastic syndrome: an essential role for stroma cells.
Review in Experimental hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 22 citations in OpenAlex.
- Engraftment characterization of risk-stratified AML in NSGS mice.Blood advances · 2021Article
- The functional interplay of transcription factors and cell adhesion molecules in experimental myelodysplasia including hematopoietic stem progenitor compartment.Molecular and cellular biochemistry · 2021Article
- Screening differentially expressed proteins from co-cultured hematopoietic cells and bone marrow-derived stromal cells by quantitative proteomics (SILAC) method.Clinical proteomics · 2019Article
- The bone-marrow niche in MDS and MGUS: implications for AML and MM.Nature reviews. Clinical oncology · 2018Review
- Preclinical modeling of myelodysplastic syndromes.Leukemia · 2017Article
- The microenvironment in myelodysplastic syndromes: Niche-mediated disease initiation and progression.Experimental hematology · 2017Review
- Mesenchymal Stem and Progenitor Cells in Normal and Dysplastic Hematopoiesis-Masters of Survival and Clonality?International journal of molecular sciences · 2016Review
- Blockade of BCL-2 proteins efficiently induces apoptosis in progenitor cells of high-risk myelodysplastic syndromes patients.Leukemia · 2016Article
- Review
- Biology of BM failure syndromes: role of microenvironment and niches.Hematology. American Society of Hematology. Education Program · 2014Review
- Biology of the bone marrow microenvironment and myelodysplastic syndromes.Molecular genetics and metabolismReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The objective of is this article is to review murine xenotransplantation models for myelodysplastic syndromes (MDS). The difficulties in achieving sustained engraftment of MDS cells in immunodeficient mice may lie in innate characteristics of the MDS clones and microenvironmental factors. Engraftment of very low numbers of CD45(+) clonal MDS cells has been achieved with intravenous injection; higher rates of engraftment are obtained via the intramedullary route. Coinjection of certain stroma components with hematopoietic cells overcomes limitations of intravenous (IV) administration, allowing for engraftment of high proportions of human CD45(+) cells in mouse spleen and marrow. Expression of CD146 on stroma cells conveys an engraftment-facilitating effect. Clonal MDS cells have been propagated for periods beyond 6 months and have been transplanted successfully into secondary recipients. Engraftment of human clonal MDS cells with stem cell characteristics in immunodeficient mice is greatly facilitated by coinjection of stroma/mesenchymal cells, particularly with IV administration. CD146 expression on stroma is an essential factor; however, no model develops the laboratory and clinical features of human MDS. Additional work is needed to determine cellular and noncellular factors required for the full evolution of MDS.
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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.