ArticleOncotarget2014
The class-specific BCR tonic signal modulates lymphomagenesis in a c-myc deregulation transgenic model.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Eμ and 3'RR transcriptional enhancers of the IgH locus cooperate to promote c-myc-induced mature B-cell lymphomas.Blood advances · 2020Article
- Mouse Models ofFrontiers in immunology · 2020Review
- Review
- Efficient role of IgH 3' regulatory region deficient B-cells in the development of oil granulomas.Oncotarget · 2016Article
- Simple and rapid determination of homozygous transgenic mice via in vivo fluorescence imaging.Oncotarget · 2015Article
- Article
- Pre-germinal center origin for mature mouse B cell lymphomas: a major discrepancy with human mature lymphomas.Cell cycle (Georgetown, Tex.) · 2015Article
- A new 3'RR regulatory role during lymphomagenesis.Cell cycle (Georgetown, Tex.) · 2015Article
- Targeting the oncogene B lymphoma deregulator IgH 3' regulatory region does not impede the in vivo inflammatory response in mice.Oncoscience · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulation of c-myc by translocation onto immunoglobulin (Ig) loci can promote B cell malignant proliferations with phenotypes as diverse as acute lymphoid leukemia, Burkitt lymphoma, diffuse large B cell lymphoma, myeloma... The B cell receptor (BCR) normally providing tonic signals for cell survival and mitogenic responses to antigens, can also contribute to lymphomagenesis upon sustained ligand binding or activating mutations. BCR signaling varies among cell compartments and BCR classes. For unknown reasons, some malignancies associate with expression of either IgM or class-switched Ig. We explored whether an IgA BCR, with strong tonic signaling, would affect lymphomagenesis in c-myc IgH 3'RR transgenic mice prone to lymphoproliferations. Breeding c-myc transgenics in a background where IgM expression was replaced with IgA delayed lymphomagenesis. By comparison to single c-myc transgenics, lymphomas from double mutant animals were more differentiated and less aggressive, with an altered transcriptional program. Larger tumor cells more often expressed CD43 and CD138, which culminated in a plasma cell phenotype in 10% of cases. BCR class-specific signals thus appear to modulate lymphomagenesis and may partly explain the observed association of specific Ig classes with human B cell malignancies of differential phenotype, progression and prognosis.
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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.