ArticleBlood2008
IRF-4 functions as a tumor suppressor in early B-cell development.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 58 citations in OpenAlex.
- IRF-4-mediated CIITA transcription is blocked by KSHV encoded LANA to inhibit MHC II presentation.PLoS pathogens · 2013Trial
- Advancing the genetic engineering toolbox by combining AsCas12a knock-in mice with ultra-compact screening.Nature communications · 2025Article
- DFF-ChIP: a method to detect and quantify complex interactions between RNA polymerase II, transcription factors, and chromatin.Nucleic acids research · 2024Article
- IRF4 Participates in Pulmonary Fibrosis Induced by Silica Particles through Regulating Macrophage Polarization and Fibroblast Activation.Inflammation · 2024Article
- Integrative alternative splicing analysis reveals new prognosis signature in B-cell acute lymphoblastic leukemia.International journal of biological sciences · 2024Article
- The dynamic functions of IRF4 in B cell malignancies.Clinical and experimental medicine · 2023Review
- A multimorphic mutation in IRF4 causes human autosomal dominant combined immunodeficiency.Science immunology · 2023Article
- A pilot study of the use of dynamic analysis of cell-free DNA from aqueous humor and vitreous fluid for the diagnosis and treatment monitoring of vitreoretinal lymphomas.Haematologica · 2022Article
- IRF4 drives clonal evolution and lineage choice in a zebrafish model of T-cell lymphoma.Nature communications · 2022Article
- Overexpression of IRF3 Predicts Poor Prognosis in Clear Cell Renal Cell Carcinoma.International journal of general medicine · 2021Article
- Genome-Wide Association Analyses Identify Variants inFrontiers in genetics · 2021Article
- Inhibition of DNMT1 and ERRα crosstalk suppresses breast cancer via derepression of IRF4.Oncogene · 2020Article
- Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-cell Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Article
- Germline Risk Contribution to Genomic Instability in Multiple Myeloma.Frontiers in genetics · 2019Review
- Spontaneous loss of B lineage transcription factors leads to pre-B leukemia in Ebf1Oncogenesis · 2017Article
- Article
- Dual mechanisms by which miR-125b represses IRF4 to induce myeloid and B-cell leukemias.Blood · 2014Article
- IRF4 and IRF8: Governing the virtues of B Lymphocytes.Frontiers in biology · 2014Article
- Kaposi's sarcoma-associated herpesvirus viral interferon regulatory factor 4 (vIRF4) targets expression of cellular IRF4 and the Myc gene to facilitate lytic replication.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interferon regulatory factor-4 (IRF-4) is a hematopoietic cell-restricted transcription factor important for hematopoietic development and immune response regulation. It was also originally identified as the product of a proto-oncogene involved in chromosomal translocations in multiple myeloma. In contrast to its oncogenic function in late stages of B lymphopoiesis, expression of IRF-4 is down-regulated in certain myeloid and early B-lymphoid malignancies. In this study, we found that the IRF-4 protein levels are increased in lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhibitor imatinib. We further found that IRF-4 deficiency enhances BCR/ABL transformation of B-lymphoid progenitors in vitro and accelerates disease progression of BCR/ABL-induced acute B-lymphoblastic leukemia (B-ALL) in mice, whereas forced expression of IRF-4 potently suppresses BCR/ABL transformation of B-lymphoid progenitors in vitro and BCR/ABL-induced B-ALL in vivo. Further analysis showed that IRF-4 inhibits growth of BCR/ABL+ B lymphoblasts primarily through negative regulation of cell-cycle progression. These results demonstrate that IRF-4 functions as tumor suppressor in early B-cell development and may allow elucidation of new molecular pathways significant to the lymphoid leukemogenesis by BCR/ABL. The context dependent roles of IRF-4 in oncogenesis should be an important consideration in developing cancer therapies targeting IRF-4.
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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.