ArticleLeukemia2005
STAT3 is essential for Hodgkin lymphoma cell proliferation and is a target of tyrphostin AG17 which confers sensitization for apoptosis.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 94 citations in OpenAlex.
- The antitumor mechanism of oclacitinib in canine lymphoma.Scientific reports · 2026Article
- Integrative bioinformatics and machine learning identify key crosstalk genes and immune interactions in head and neck cancer and Hodgkin lymphoma.Scientific reports · 2025Article
- GATA3 Immunohistochemical Staining in Classical Hodgkin Lymphoma and Its Diagnostic Utility in Differential DiagnosisTurkish journal of haematology : official journal of Turkish Society of Haematology · 2025Article
- Research landmarks on the 60th anniversary of Epstein-Barr virus.Science China. Life sciences · 2025Review
- Mechanisms of lymphoma-stromal interactions focusing on tumor-associated macrophages, fibroblastic reticular cells, and follicular dendritic cells.Journal of clinical and experimental hematopathology : JCEH · 2024Review
- Discovery of novel predisposing coding and noncoding variants in familial Hodgkin lymphoma.Blood · 2023Article
- Article
- PD-1/PD-L1 Pathway: A Therapeutic Target in CD30+ Large Cell Lymphomas.Biomedicines · 2022Review
- Role and Mechanisms of Tumor-Associated Macrophages in Hematological Malignancies.Frontiers in oncology · 2022Review
- Review
- Revisiting IL-6 expression in the tumor microenvironment of classical Hodgkin lymphoma.Blood advances · 2021Article
- The polymorphisms of IL-6/STAT3 signaling pathway may contribute to cutaneous T-cell lymphomas susceptibility.Archives of dermatological research · 2021Observational
- The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics.Frontiers in genetics · 2021Review
- Epstein Barr Virus: Development of Vaccines and Immune Cell Therapy for EBV-Associated Diseases.Frontiers in immunology · 2021Review
- Heat Shock Proteins in Lymphoma Immunotherapy.Frontiers in immunology · 2021Review
- Autocrine IL-6/STAT3 signaling aids development of acquired drug resistance in Group 3 medulloblastoma.Cell death & disease · 2020Article
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- Phospho-valproic acid (MDC-1112) suppresses glioblastoma growth in preclinical models through the inhibition of STAT3 phosphorylation.Carcinogenesis · 2019Article
- Co-Expression of the Epstein-Barr Virus-Encoded Latent Membrane Proteins and the Pathogenesis of Classic Hodgkin Lymphoma.Cancers · 2018Review
- Tyrphostin AG17 inhibits adipocyte differentiation in vivo and in vitro.Lipids in health and disease · 2018Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical Hodgkin lymphoma (cHL) is a distinct malignancy of the immune system. Despite the progress made in the understanding of the biology of cHL, the transforming events remain to be elucidated. Recently, we demonstrated that the Janus kinase inhibitor AG490 blocked cellular proliferation and STAT3 phosphorylation in cHL. To explore the potential of constitutively activated STAT3 as a drug target and its role in cHL pathogenesis, different cHL cell lines were analyzed. Treatment of cHL cells by the protein tyrosine kinase inhibitor AG17 was associated with inhibition of cellular proliferation and cell cycle arrest. AG17 treatment was accompanied by decreased levels of STAT3 phosphorylation, whereas NF-kappaB and p38/SAPK2 signaling were not inhibited. Incubation with AG17 or AG490 sensitized cHL cells to CD95/Fas/Apo-1 or staurosporine-mediated apoptosis. Coincubation of tyrphostins with staurosporine was accompanied by rapid complete inhibition of STAT3 phosphorylation. RNA interference directed against STAT3 in L428 and L1236 cHL cells demonstrated that STAT3 is essential for cell proliferation of these cHL cells. In conclusion, these findings support the concept that STAT3 signaling is important in the pathogenesis of cHL and tyrphostins are agents for developing new therapeutic strategies.
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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.