ArticleThe Journal of clinical investigation2007
B cell activator PAX5 promotes lymphomagenesis through stimulation of B cell receptor signaling.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- DNA methylation and gene expression signatures are associated with ataxia-telangiectasia phenotype.Scientific reports · 2020Trial
- Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis.Nature immunology · 2026Article
- Rack1 regulates B-cell development and function by binding to and stabilizing the transcription factor Pax5.Cellular & molecular immunology · 2024Article
- PAX5 aberrant expression incorporated in MIPI-SP risk scoring system exhibits additive value in mantle cell lymphoma.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Sellar B lymphoblastic lymphoma mimics pituitary apoplexy with newly discovered gene mutations in TP53 and PAX5: A case report.Frontiers in oncology · 2023Article
- The Pleiotropy ofInternational journal of molecular sciences · 2022Review
- Prognostic significance of copy number variation in B-cell acute lymphoblastic leukemia.Frontiers in oncology · 2022Review
- Core regulatory circuitries in defining cancer cell identity across the malignant spectrum.Open biology · 2020Review
- Enhancer Architecture and Essential Core Regulatory Circuitry of Chronic Lymphocytic Leukemia.Cancer cell · 2018Article
- [Significance of PAX5 deletion in childhood B-lineage acute lymphoblastic leukemia without reproducible chromosomal abnormalities].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- CD19 chimeric antigen receptor (CD19 CAR)-redirected adoptive T-cell immunotherapy for the treatment of relapsed or refractory B-cell Non-Hodgkin's Lymphomas.American journal of cancer research · 2016Review
- Convergence of Acquired Mutations and Alternative Splicing of CD19 Enables Resistance to CART-19 Immunotherapy.Cancer discovery · 2015Article
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- CD19 is a major B cell receptor-independent activator of MYC-driven B-lymphomagenesis.The Journal of clinical investigation · 2012Article
- Murine models of B-cell lymphomas: promising tools for designing cancer therapies.Advances in hematology · 2012Article
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- PAX5 activates the transcription of the human telomerase reverse transcriptase gene in B cells.The Journal of pathology · 2010Article
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Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
The presumed involvement of paired box gene 5 (PAX5) in B-lymphomagenesis is based largely on the discovery of Pax5-specific translocations and somatic hypermutations in non-Hodgkin lymphomas. Yet mechanistically, the contribution of Pax5 to neoplastic growth remains undeciphered. Here we used 2 Myc-induced mouse B lymphoma cell lines, Myc5-M5 and Myc5-M12, which spontaneously silence Pax5. Reconstitution of these cells with Pax5-tamoxifen receptor fusion protein (Pax5ER(TAM)) increased neoplastic growth in a hormone-dependent manner. Conversely, expression of dominant-negative Pax5 in murine lymphomas and Pax5 knockdown in human lymphomas negatively affected cell expansion. Expression profiling revealed that Pax5 was required to maintain mRNA levels of several crucial components of B cell receptor (BCR) signaling, including CD79a, a protein with the immunoreceptor tyrosine-based activation motif (ITAM). In contrast, expression of 2 known ITAM antagonists, CD22 and PIR-B, was suppressed. The key role of BCR/ITAM signaling in Pax5-dependent lymphomagenesis was corroborated in Syk, an ITAM-associated tyrosine kinase. Moreover, we observed consistent expression of phosphorylated BLNK, an activated BCR adaptor protein, in human B cell lymphomas. Thus, stimulation of neoplastic growth by Pax5 occurs through BCR and is sensitive to genetic and pharmacological inhibitors of this pathway.
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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.