ArticleThe American journal of pathology2008
CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 69 citations in OpenAlex.
- CD30 as a Target Molecule in the Diagnosis and Therapy of Lymphomas.American journal of hematology · 2026Review
- Anti-Cancer Potential of a new Derivative of Caffeic Acid Phenethyl Ester targeting the Centrosome.Redox biology · 2025Article
- Chimeric Antigen Receptor T Cells in Hodgkin and T-Cell Lymphomas.Hematology/oncology clinics of North America · 2023Review
- CD30 induces Reed-Sternberg cell-like morphology and chromosomal instability in classic Hodgkin lymphoma cell lines.Cancer science · 2023Article
- AuNP Aptasensor for Hodgkin Lymphoma Monitoring.Biosensors · 2022Article
- Molecular biology of Hodgkin lymphoma.Leukemia · 2021Review
- Humanized anti-CD123 antibody facilitates NK cell antibody-dependent cell-mediated cytotoxicity (ADCC) of Hodgkin lymphoma targets via ARF6/PLD-1.Blood cancer journal · 2019Article
- Brentuximab vedotin: clinical updates and practical guidance.Blood research · 2017Review
- Understanding CD30 biology and therapeutic targeting: a historical perspective providing insight into future directions.Blood cancer journal · 2017Review
- TCGA: Increased oncoprotein coding region mutations correlate with a greater expression of apoptosis-effector genes and a positive outcome for stomach adenocarcinoma.Cell cycle (Georgetown, Tex.) · 2016Article
- Tumor suppressor genes are larger than apoptosis-effector genes and have more regions of active chromatin: Connection to a stochastic paradigm for sequential gene expression programs.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- TRAF2 recruitment via T61 in CD30 drives NFκB activation and enhances hESC survival and proliferation.Molecular biology of the cell · 2015Article
- Management of relapsed or refractory hodgkin lymphoma with second-generation antibody-drug conjugates: focus on brentuximab vedotin.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2014Review
- Molecular genetics of peripheral T-cell lymphomas.International journal of hematology · 2014Review
- Article
- Notch is an essential upstream regulator of NF-κB and is relevant for survival of Hodgkin and Reed-Sternberg cells.Leukemia · 2012Article
- Detection of nuclear and membrane antigens by liquid-based cytology following long-term storage of d1 cells, karpas cells, and peripheral blood mononuclear cells.Annals of clinical and laboratory science · 2011Article
- Article
- CD30+ lymphoproliferative disorders.Haematologica · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High CD30 expression in classical Hodgkin's lymphoma and anaplastic large cell lymphoma (ALCL) suggests an important pathogenic role of this cytokine receptor. To test this hypothesis, we investigated CD30 signaling in Hodgkin's and ALCL cell lines by different approaches: 1) CD30 stimulation, 2) CD30 down-regulation, and 3) a combination of both. The effects were determined at the RNA (microarray and real-time quantitative RT-PCR), protein (electrophoretic mobility shift analysis, immunoblot, and flow cytometry), and cellular/functional (proliferation and apoptosis) levels. We demonstrate that Hodgkin's cells are virtually CD30 unresponsive. Neither CD30 stimulation nor CD30 silencing of Hodgkin's cells had any significant effect. In contrast, CD30 stimulation of ALCL cells activated nuclear transcription factor-kappaB (NF-kappaB), induced major transcriptional changes, and decreased proliferation. These effects could be abrogated by down-regulation of CD30. Stimulation of CD30 in ALCL cells, stably transfected with a dominant-negative NF-kappaB inhibitor, induced pronounced caspase activation and massive apoptosis. Our data indicate that 1) CD30 signaling is not effective in Hodgkin's cell lines but is effective in ALCL cell lines, 2) CD30 is probably not significantly involved in the pathogenesis of classical Hodgkin's lymphoma, and 3) CD30 stimulation triggers two competing effects in ALCL cells, namely activation of caspases and NF-kappaB-mediated survival. These data suggest that CD30-targeted therapy in ALCL should be combined with NF-kappaB inhibitors to induce effective cell killing.
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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.