The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q– syndrome
Open accessAbstract
The identification of the genes associated with chromosomal translocation breakpoints has fundamentally changed understanding of the molecular basis of hematological malignancies. By contrast, the study of chromosomal deletions has been hampered by the large number of genes deleted and the complexity of their analysis. We report the generation of a mouse model for human 5q– syndrome using large-scale chromosomal engineering. Haploinsufficiency of the Cd74–Nid67 interval (containing Rps14, encoding the ribosomal protein S14) caused macrocytic anemia, prominent erythroid dysplasia and monolobulated megakaryocytes in the bone marrow. These effects were associated with defective bone marrow progenitor development, the appearance of bone marrow cells expressing high amounts of the tumor suppressor p53 and increased bone marrow cell apoptosis. Notably, intercrossing with p53-deficient mice completely rescued the progenitor cell defect, restoring common myeloid progenitor and megakaryocytic-erythroid progenitor, granulocyte-monocyte progenitor and hematopoietic stem cell bone marrow populations. This mouse model suggests that a p53-dependent mechanism underlies the pathophysiology of the 5q– syndrome.
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“In mouse models of Diamond Blackfan anemia, Treacher Collins syndrome craniofacial abnormalities and 5q syndrome macrocytic anemia, p53 activity is induced in response to mutations that cause ribosome dysfunction, precipitating either apoptotic or cell-cycle-arrest responses that result in the manifestations of the disease (Barlow et al., 2010; Jones et al., 2008; McGowan et al., 2008).”
From p53 at a glance (2010) · cites this paper as Barlow et al., 2010
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“inhibition of p53 activity with a small-molecule antagonist of p53, pifithrin-α, or by genetic ablation effectively diminished many of the symptoms in models of these p53-dependent diseases”
From p53 at a glance (2010) · cites this paper as Barlow et al., 2010
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Lenalidomide in the Myelodysplastic Syndrome with Chromosome 5q Deletion
List, A., Dewald, G., Bennett, J., Giagounidis, A., Raza, A., Feldman, E., Powell, B., Greenberg, P., Thomas, D., Stone, R., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa061292 · Cited by 1,319
Cited by
Frequent pathway mutations of splicing machinery in myelodysplasia
Yoshida, K., Sanada, M., Shiraishi, Y., Nowak, D., Nagata, Y., Yamamoto, R., Sato, Y., Sato-Otsubo, A., Kon, A., Nagasaki, M., et al. (2011) · Nature · doi:10.1038/nature10496 · Cited by 2,029
The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia
Sperling, A. S., Gibson, C. J., & Ebert, B. L. (2017) · Nature Reviews Cancer · doi:10.1038/nrc.2016.112 · Cited by 678
TP53 Mutations in Low-Risk Myelodysplastic Syndromes With del(5q) Predict Disease Progression
Jädersten, M., Saft, L., Smith, A., Kulasekararaj, A., Pomplun, S., Göhring, G., Hedlund, A., Hast, R., Schlegelberger, B., Porwit, A., et al. (2011) · Journal of Clinical Oncology · doi:10.1200/jco.2010.31.8576 · Cited by 463
Brady, C. A., & Attardi, L. D. (2010) · Journal of Cell Science · doi:10.1242/jcs.064501 · Cited by 403
The genetic basis of myelodysplasia and its clinical relevance
Cazzola, M., Della Porta, M. G., & Malcovati, L. (2013) · Blood · doi:10.1182/blood-2013-09-381665 · Cited by 346
Metadata
- Authors
- Barlow, J. L., Drynan, L. F., Hewett, D. R., Holmes, L. R., Lorenzo-Abalde, S., Lane, A. L., Jolin, H. E., Pannell, R., Middleton, A. J., Wong, S. H., Warren, A. J., Wainscoat, J. S., Boultwood, J., & McKenzie, A. N. J.
- Venue
- Nature Medicine
- Published
- 2009-11-22
- Volume
- 16
- Issue
- 1
- Pages
- 59-66
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2019828567
- Cited by
- 334
- References
- 2
- FWCI
- 22.19
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
