ArticleProceedings of the National Academy of Sciences of the United States of America2013
Conditional inactivation of p53 in mature B cells promotes generation of nongerminal center-derived B-cell lymphomas.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis.Nature immunology · 2026Article
- Mouse models of B cell lymphomas on the basis of genetic features.Frontiers in immunology · 2026Review
- In vivo CRISPR screening reveals cooperation of KMT2D and TP53 deficiencies in B-cell lymphomagenesis.Blood advances · 2025Article
- Risk of lymphoid malignancy associated with cancer predisposition genes.Blood cancer journal · 2025Article
- Molecular mechanisms insulating proliferation from genotoxic stress in B lymphocytes.Trends in immunology · 2023Review
- Distinct oncogenic phenotypes in hematopoietic specific deletions of Trp53.Scientific reports · 2023Article
- Review
- SETD2 Haploinsufficiency Enhances Germinal Center-Associated AICDA Somatic Hypermutation to Drive B-cell Lymphomagenesis.Cancer discovery · 2022Article
- The Eµ-hnRNP K Murine Model of Lymphoma: Novel Insights into the Role of hnRNP K in B-Cell Malignancies.Frontiers in immunology · 2021Review
- RASSF10 is frequently epigenetically inactivated in kidney cancer and its knockout promotes neoplasia in cancer prone mice.Oncogene · 2020Article
- Article
- Insights into the genomic landscape of MYD88 wild-type Waldenström macroglobulinemia.Blood advances · 2018Article
- Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.Nature communications · 2017Article
- CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas.Cancer discovery · 2017Article
- Transgenic mouse model of IgMBlood cancer journal · 2016Article
- Mdm2 overexpression and p73 loss exacerbate genomic instability and dampen apoptosis, resulting in B-cell lymphoma.Oncogene · 2016Article
- Combined deletion of Xrcc4 and Trp53 in mouse germinal center B cells leads to novel B cell lymphomas with clonal heterogeneity.Journal of hematology & oncology · 2016Article
- The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development.Nature medicine · 2015Article
- Illuminating p53 function in cancer with genetically engineered mouse models.Seminars in cell & developmental biology · 2014Review
- Effects of prostaglandin E2 on p53 mRNA transcription and p53 mutagenesis during T-cell-independent human B-cell clonal expansion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor exerts a central role in protecting cells from oncogenic transformation. Accordingly, the p53 gene is mutated in a large number of human cancers. In mice, germ-line inactivation of p53 confers strong predisposition to development of different types of malignancies, but the early onset of thymic lymphomas in the majority of the animals prevents detailed studies of tumorigenesis in other tissues. Here, we use the Cre/Lox approach to inactivate p53 in mature B cells in mice (referred to as "CP" B cells) and find that such p53 inactivation results in the routine development of IgM-positive CP peripheral B-cell lymphomas. The CP lymphomas generally appear to arise, even in mice subjected to immunization protocols to activate germinal center reaction, from naive B cells that had not undergone immunoglobulin (Ig) heavy chain gene class switching or somatic hypermutation. In contrast to thymic lymphomas that arise in p53-deficient mice, which generally lack clonal translocations, nearly all analyzed CP B-cell tumors carried clonal translocations. However, in contrast to spontaneous translocations in other mouse B-cell tumor models, CP B-cell tumor translocations were not recurrent and did not involve Ig loci. Therefore, CP tumors might provide models for human lymphomas lacking Ig translocations, such as splenic marginal zone B-cell lymphoma or Waldenstrom macroglobulinemia. Our studies indicate that deletion of p53 is sufficient to trigger transformation of mature B cells and support the notion that p53 deficiency may allow accumulation of oncogenic translocations in B cells.
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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.