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The p53 pathway in hematopoiesis: lessons from mouse models, implications for humans
Open accessAbstract
Aberrations in the p53 tumor suppressor pathway are associated with hematologic malignancies. p53-dependent cell cycle control, senescence, and apoptosis functions are actively involved in maintaining hematopoietic homeostasis under normal and stress conditions. Whereas loss of p53 function promotes leukemia and lymphoma development in humans and mice, increased p53 activity inhibits hematopoietic stem cell function and results in myelodysplasia. Thus, exquisite regulation of p53 activity is critical for homeostasis. Most of our understanding of p53 function in hematopoiesis is derived from genetically engineered mice. Here we summarize some of these models, the various mechanisms that disrupt the regulation of p53 activity, and their relevance to human disease.
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“Indeed, constitutive p53 activity impairs hematopoietic homeostasis and causes HSC depletion (42).”
From Txnip Enhances Fitness of Dnmt3a -Mutant Hematopoietic Stem Cells via p21 (2022) · cites this paper as [42]
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Cites
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
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
Mdm2 promotes the rapid degradation of p53
Haupt, Y., Maya, R., Kazaz, A., & Oren, M. (1997) · Nature · doi:10.1038/387296a0 · Cited by 4,506
Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
Malkin, D., Li, F. P., Strong, L. C., Fraumeni, J. F., Nelson, C. E., Kim, D. H., Kassel, J., Gryka, M. A., Bischoff, F. Z., Tainsky, M. A., et al. (1990) · Science · doi:10.1126/science.1978757 · Cited by 3,765
Regulation of p53 stability by Mdm2
Kubbutat, M. H. G., Jones, S. N., & Vousden, K. H. (1997) · Nature · doi:10.1038/387299a0 · Cited by 3,312
Live or let die: the cell's response to p53
Vousden, K. H., & Lü, X. (2002) · Nature reviews. Cancer · doi:10.1038/nrc864 · Cited by 3,231
Kiel, M. J., Yilmaz, Ö. H., Iwashita, T., Yilmaz, O. H., Terhorst, C., & Morrison, S. J. (2005) · Cell · doi:10.1016/j.cell.2005.05.026 · Cited by 3,168
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Momand, J., Zambetti, G. P., Olson, D. C., George, D., & Levine, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90644-r · Cited by 3,113
p53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
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Palanichamy, J. K., Tran, T. M., King, J. K., Katzman, S. J., Ritter, A. J., Sharma, G., Tso, C., Contreras, J. R., Fernando, T. R., Sanford, J. R., et al. (2023) · Scientific Reports · doi:10.1038/s41598-023-33949-8 · Cited by 4
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Benedito, S. D. S., Bernardo, P. S., Martin, J., Marty, C., Plo, I., Antony‐Debré, I., & Monte-Mór, B. D. C. R. (2026) · HemaSphere · doi:10.1002/hem3.70332 · Cited by 2
Ines, A., Ekström, J., Tuomela, T., Rämet, M., Salminen, T. S., & Vesala, L. (2026) · PLoS Genetics · doi:10.1371/journal.pgen.1012094 · Cited by 2
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Yallowitz, A. R., Hanel, W. G., & Moll, U. M. (2015) · Cell Death and Differentiation · doi:10.1038/cdd.2015.63 · Cited by 1
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Gustafsson, B. M. (2015) · International Journal of Hematologic Oncology · doi:10.2217/ijh.15.10
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Liu, S., Feng, Z. J., Su, M., Liu, C., Xi, Y., Chen, H., Luo, L., Tian, X., Zhao, F., & Li, L. (2024) · Development · doi:10.1242/dev.202903
Hasanova, A., Asadov, C. D., Shirinova, A., Aliyeva, G., & Alimirzoyeva, Z. (2025) · Pathology - Research and Practice · doi:10.1016/j.prp.2025.155943
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Cardona, C. J., Young, M., & Montgomery, M. R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26178359
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Toufektchan, E. (2018) · theses.fr (ABES) · doi:10.70675/58dfec7cz94b0z449fz96a6z9051bf80c551
Rakotopare, J. (2024) · theses.fr (ABES) · doi:10.70675/cc79cc10zbaf8z4e88za003z8a8d37707576
Natsagdorj, M., Hara, H., Iida, K., Kashiwakura, Y., Baatartsogt, N., Ganzorig, E., Canarutto, D., Pinho, S., Naldini, L., Ohmori, T., et al. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2531364123
Metadata
- Authors
- Pant, V., Quintás-Cardama, A., & Lozano, G.
- Affiliations
- Departments of Genetics and
- Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2012-12-20
- Volume
- 120
- Issue
- 26
- Pages
- 5118-5127
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC3537308
- OpenAlex
- W1983610544
- Cited by
- 129
- References
- 147
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 10 · 2023: 11 · 2022: 5 · 2021: 13 · 2020: 11 · 2019: 7 · 2018: 10 · 2017: 10 · 2016: 8 · 2015: 13 · 2014: 8 · 2013: 9
- FWCI
- 0.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA47296, R01CA047296, P30CA016672)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- p53, hematopoiesis, hematologic malignancies, hematopoietic stem cells, myelodysplastic syndrome, leukemia, lymphoma, cell cycle regulation, senescence, apoptosis, hematopoietic homeostasis, genetically engineered mouse models, p53 regulation
- MeSH terms
- Animals, Hematologic Diseases, Hematopoiesis, Humans, Learning, Models, Biological, Signal Transduction, Tumor Suppressor Protein p53, Models, Animal, Mice
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