ArticleThe Journal of experimental medicine2007
AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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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.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Phenotypical Characterization and Clinical Outcome of Canine Burkitt-Like Lymphoma.Frontiers in veterinary science · 2021Article
- UnAIDed Class Switching in Activated B-Cells Reveals Intrinsic Features of a Self-Cleaving IgH Locus.Frontiers in immunology · 2021Article
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- Article
- 3'Oncotarget · 2018Article
- Cooperative Targets of Combined mTOR/HDAC Inhibition Promote MYC Degradation.Molecular cancer therapeutics · 2017Article
- Associations of Autoimmunity, Immunodeficiency, Lymphomagenesis, and Gut Microbiota in Mice with Knockins for a Pathogenic Autoantibody.The American journal of pathology · 2017Article
- Transgenic mouse model of IgMBlood cancer journal · 2016Article
- Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.Nature reviews. Immunology · 2016Review
- Article
- AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway.EMBO molecular medicine · 2015Article
- Article
- Epigenetic function of activation-induced cytidine deaminase and its link to lymphomagenesis.Frontiers in immunology · 2014Review
- Waldenström macroglobulinemia: clinical and immunological aspects, natural history, cell of origin, and emerging mouse models.ISRN hematology · 2013Review
- B cell-specific deficiencies in mTOR limit humoral immune responses.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Mechanisms and impacts of chromosomal translocations in cancers.Frontiers of medicine · 2012Review
- Oncogenic Myc translocations are independent of chromosomal location and orientation of the immunoglobulin heavy chain locus.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Mouse model of endemic Burkitt translocations reveals the long-range boundaries of Ig-mediated oncogene deregulation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- UNG shapes the specificity of AID-induced somatic hypermutation.The Journal of experimental medicine · 2012Article
- Decrease in topoisomerase I is responsible for activation-induced cytidine deaminase (AID)-dependent somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
Abstract
Activation-induced cytidine deaminase (AID) is required for immunoglobulin (Ig) class switch recombination and somatic hypermutation, and has also been implicated in translocations between Ig switch regions and c-Myc in plasma cell tumors in mice. We asked if AID is required for accelerated tumor development in pristane-treated Bcl-xL transgenic BALB/c mice deficient in AID (pBxAicda-/-). pBxAicda-/- mice developed tumors with a lower frequency (24 vs. 62%) and a longer mean latency (108 vs. 36 d) than AID-sufficient mice. The tumors appeared in oil granuloma tissue and did not form ascites. By interphase fluorescence in situ hybridization, six out of nine pBxAicda-/- primary tumors had T(12;15) and one had T(6;15) chromosomal translocations. Two tumors were transplantable and established as stable cell lines. Molecular and cytogenetic analyses showed that one had an unusual unbalanced T(12;15) translocation, with IgH Cmu and Pvt-1 oriented head to tail at the breakpoint, resulting in an elevated expression of c-Myc. In contrast, the second was T(12;15) negative, but had an elevated N-Myc expression caused by a paracentric inversion of chromosome 12. Thus, novel mechanisms juxtapose Ig and Myc-family genes in AID-deficient plasma cell tumors.
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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.