ArticleCancers2018
IRF4 Mediates the Oncogenic Effects of STAT3 in Anaplastic Large Cell Lymphomas.
Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 36 citations in OpenAlex.
- CircZBTB46, a promising therapeutic target in crizotinib resistant ALK-positive T lymphomas.Leukemia · 2026Article
- The IL-1R and NFKBIZ pathway mediates immunoregulatory responses and immunotherapy efficacy in anaplastic large cell lymphoma.Leukemia · 2026Article
- Single mutation tunes IRF4 function and mediates B cell character to ameliorate murine lupus.iScience · 2025Article
- STAT3 couples activated tyrosine kinase signaling to the oncogenic core transcriptional regulatory circuitry of anaplastic large cell lymphoma.Cell reports. Medicine · 2024Article
- Analysis and therapeutic targeting of the IL-1R pathway in anaplastic large cell lymphoma.Blood · 2023Article
- Patient-derived xenograft models of ALK+ ALCL reveal preclinical promise for therapy with brigatinib.British journal of haematology · 2023Article
- Gene-Function-Based Clusters Explore Intricate Networks of Gene Expression of Circulating Tumor Cells in Patients with Colorectal Cancer.Biomedicines · 2023Article
- IRF4 as an Oncogenic Master Transcription Factor.Cancers · 2022Review
- Downregulation of STAT3 in Epstein-Barr Virus-Positive Hodgkin Lymphoma.Biomedicines · 2022Article
- Review
- Requirement of DNMT1 to orchestrate epigenomic reprogramming for NPM-ALK-driven lymphomagenesis.Life science alliance · 2021Article
- NOTCH4 Exhibits Anti-Inflammatory Activity in Activated Macrophages by Interfering With Interferon-γ and TLR4 Signaling.Frontiers in immunology · 2021Article
- Article
- The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL).Oncotarget · 2020Article
- Peripheral T cell lymphomas: from the bench to the clinic.Nature reviews. Cancer · 2020Review
- Emerging strategies in peripheral T-cell lymphoma.Hematology. American Society of Hematology. Education Program · 2019Article
- STAT3 Dysregulation in Mature T and NK Cell Lymphomas.Cancers · 2019Review
- Article
- Identification of lenalidomide resistance pathways in myeloma and targeted resensitization using cereblon replacement, inhibition of STAT3 or targeting of IRF4.Blood cancer journal · 2019Article
- Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic anaplastic large cell lymphomas (ALCL) are a category of T-cell non-Hodgkin's lymphomas which can be divided into anaplastic lymphoma kinase (ALK) positive and ALK negative subgroups, based on ALK gene rearrangements. Among several pathways aberrantly activated in ALCL, the constitutive activation of signal transducer and activator of transcription 3 (STAT3) is shared by all ALK positive ALCL and has been detected in a subgroup of ALK negative ALCL. To discover essential mediators of STAT3 oncogenic activity that may represent feasible targets for ALCL therapies, we combined gene expression profiling analysis and RNA interference functional approaches. A shRNA screening of STAT3-modulated genes identified interferon regulatory factor 4 (IRF4) as a key driver of ALCL cell survival. Accordingly, ectopic IRF4 expression partially rescued STAT3 knock-down effects. Treatment with immunomodulatory drugs (IMiDs) induced IRF4 down regulation and resulted in cell death, a phenotype rescued by IRF4 overexpression. However, the majority of ALCL cell lines were poorly responsive to IMiDs treatment. Combination with JQ1, a bromodomain and extra-terminal (BET) family antagonist known to inhibit MYC and IRF4, increased sensitivity to IMiDs. Overall, these results show that IRF4 is involved in STAT3-oncogenic signaling and its inhibition provides alternative avenues for the design of novel/combination therapies of ALCL.
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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.