ArticleOncotarget2013
STAT6-mediated BCL6 repression in primary mediastinal B-cell lymphoma (PMBL).
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Revealing the promising therapeutic targets and prognostic markers of primary mediastinal large B-cell lymphoma.Discover oncology · 2026Review
- The CCL17-CCR4 Axis Is Critical for Mutant STAT6-Mediated Microenvironmental Remodeling and Therapeutic Resistance in Relapsed/Refractory Diffuse Large B-Cell Lymphoma.Cancer immunology research · 2026Article
- A first-in-class inhibitor of HSP110 to potentiate XPO1-targeted therapy in primary mediastinal B-cell lymphoma and classical Hodgkin lymphoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Altered pathways and targeted therapy in double hit lymphoma.Journal of hematology & oncology · 2022Review
- Apoptosis in inner ear sensory hair cells.Journal of otology · 2017Review
- Interferon γ is a STAT1-dependent direct inducer of BCL6 expression in imatinib-treated chronic myeloid leukemia cells.Oncogene · 2017Article
- Diffuse large B-cell lymphoma: can genomics improve treatment options for a curable cancer?Cold Spring Harbor molecular case studies · 2017Review
- BCL6 mRNA Expression Level in Invasive Duct Carcinoma not otherwise Specified.Journal of clinical and diagnostic research : JCDR · 2016Article
- Detection and prognostic value of recurrent exportin 1 mutations in tumor and cell-free circulating DNA of patients with classical Hodgkin lymphoma.Haematologica · 2016Article
- BCL6 is a negative prognostic factor and exhibits pro-oncogenic activity in ovarian cancer.American journal of cancer research · 2015Article
- Review
- Article
- Double-punching PMBL.Oncotarget · 2014Article
- Precision treatment of distinct molecular subtypes of diffuse large B-cell lymphoma: ascribing treatment based on the molecular phenotype.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Review
- Interleukin-32α downregulates the activity of the B-cell CLL/lymphoma 6 protein by inhibiting protein kinase Cε-dependent SUMO-2 modification.Oncotarget · 2014Article
- Targeting STAT6 in PMBL.Oncotarget · 2014Article
- Targeting primary mediastinal B-cell lymphoma.Oncotarget · 2014Article
- FOXO1 downregulation contributes to the oncogenic program of primary mediastinal B-cell lymphoma.Oncotarget · 2014Article
- Appropriate management of molecular subtypes of diffuse large B-cell lymphoma.Oncology (Williston Park, N.Y.) · 2014Review
- Targeting the intratumor heterogeneity in PMBL.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary mediastinal B-cell lymphoma (PMBL) is characterized by aberrant activation of JAK/STAT-signaling resulting in constitutive presence of phosphorylated STAT6 (pSTAT6). In primary PMBL samples pSTAT6 is only expressed in a sub-population of lymphoma cells in a pattern that is reminiscent of that of the BCL6 oncogene. Double-fluorescence staining was carried out to determine the association between these two proteins in ten primary PMBL cases and three available PMBL cell line models. Surprisingly, only a minute fraction of double-positive nuclei was observed, while each sample contained considerable fractions of single-positive pSTAT6 and BCL6 nuclei. The intratumoral coexistence of BCL6+/pSTAT6- and BCL6-/pSTAT6+ subpopulations suggests a negative interaction between these factors. In silico screening of the STAT6 /BCL6 promoters for DNA consensus binding sites identified five STAT-binding-sites in the BCL6 promoter. We confirmed STAT6 binding to the BCL6 promoter in vitro and in vivo by band shift / super shift assays and chromatin immunoprecipitations. Using BCL6 luciferase reporter assays, depletion of STAT6 by siRNA, and ectopic overexpression of a constitutive active STAT6 mutant, we proved that pSTAT6 is sufficient to transcriptionally repress BCL6. Recently developed small molecule inhibitors 79-6 and TG101348 that increases BCL6 target gene expression and decreases pSTAT6 levels, respectively, demonstrate that a combined targeting results in additive efficacy regarding their negative effect on cell viability. The delineated pSTAT6-mediated molecular repression mechanism links JAK/STAT to BCL6-signaling in PMBL and may carry therapeutic potential.
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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.