ArticleCell cycle (Georgetown, Tex.)2012
Loss of p53 exacerbates multiple myeloma phenotype by facilitating the reprogramming of hematopoietic stem/progenitor cells to malignant plasma cells by MafB.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Adipose‑derived mesenchymal stem cell‑derived HCAR1 regulates immune response in the attenuation of sepsis.Molecular medicine reports · 2022Article
- Article
- Review
- The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival.The Journal of biological chemistry · 2020Article
- Lmo2 expression defines tumor cell identity during T-cell leukemogenesis.The EMBO journal · 2018Article
- Involvement of MAFB and MAFF in Retinoid-Mediated Suppression of Hepatocellular Carcinoma Invasion.International journal of molecular sciences · 2018Article
- Could Vitamin D Analogues Be Used to Target Leukemia Stem Cells?International journal of molecular sciences · 2016Review
- Is lineage decision-making restricted during tumoral reprograming of haematopoietic stem cells?Oncotarget · 2015Review
- MiR-223 targeting MAFB suppresses proliferation and migration of nasopharyngeal carcinoma cells.BMC cancer · 2015Article
- p53 abnormalities and potential therapeutic targeting in multiple myeloma.BioMed research international · 2014Review
- Somatic inactivation of Tp53 in hematopoietic stem cells or thymocytes predisposes mice to thymic lymphomas with clonal translocations.Cell cycle (Georgetown, Tex.) · 2013Article
- Genetic background affects susceptibility to tumoral stem cell reprogramming.Cell cycle (Georgetown, Tex.) · 2013Article
- Function of oncogenes in cancer development: a changing paradigm.The EMBO journal · 2013Review
- Polo-like kinase 1 inhibitors, mitotic stress and the tumor suppressor p53.Cell cycle (Georgetown, Tex.) · 2013Article
- The involvement of a Nanog, Klf4 and c-Myc transcriptional circuitry in the intertwining between neoplastic progression and reprogramming.Cell cycle (Georgetown, Tex.) · 2013Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple myeloma (MM) is a serious, mostly incurable human cancer of malignant plasma cells. Chromosomal translocations affecting MAFB are present in a significant percentage of multiple myeloma patients. Genetically engineered Sca1-MafB mice, in which MafB expression is limited to hematopoietic stem/progenitor cells (HS/P-Cs), display the phenotypic features of MM. Contrary to many other types of cancer, it is not yet known if the p53 gene plays any essential role in the pathogenesis of this disease. Here, we show, taking advantage of the Sca1-MafB MM mouse model, that loss of p53 does not rescue the multiple myeloma disease, but instead accelerates its development and exacerbates the MM phenotype. Therefore, the efficiency of the MafB-induced MM reprogramming of normal HS/P-Cs to terminally differentiated malignant plasma cells is enhanced by p53 deficiency, in analogy to what happens in reprogramming to pluripotency. These results raise caution about interfering with p53 function when treating multiple myeloma.
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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.