ArticleOncotarget2016
A strong host response and lack of MYC expression are characteristic for diffuse large B cell lymphoma transformed from nodular lymphocyte predominant Hodgkin lymphoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation of incidence and outcomes of transformed nodular lymphocyte predominant Hodgkin Lymphoma in the United States: a population-based cohort study.Blood cancer journal · 2026Article
- The HBP Pathway Inhibitor FR054 Enhances Temozolomide Sensitivity in Glioblastoma Cells by Promoting Ferroptosis and Inhibiting O-GlcNAcylation.CNS neuroscience & therapeutics · 2025Article
- Specific Polo-Like Kinase 1 Expression in Nodular Lymphocyte-Predominant Hodgkin Lymphoma Suggests an Intact Immune Surveillance Program.The American journal of pathology · 2024Article
- Review
- 3D analyses reveal T cells with activated nuclear features in T-cell/histiocyte-rich large B-cell lymphoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- Review
- Article
- Tumor immunotherapy: drug-induced neoantigens (xenogenization) and immune checkpoint inhibitors.Oncotarget · 2017Review
- [Update on nodular lymphocyte predominant Hodgkin's lymphoma and related lesions].Der Pathologe · 2017Review
- Dose-dependent effects of gamma radiation on the early zebrafish development and gene expression.PloS one · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is an indolent lymphoma, but can transform into diffuse large B cell lymphoma (DLBCL), showing a more aggressive clinical behavior. Little is known about these cases on the molecular level. Therefore, the aim of the present study was to characterize DLBCL transformed from NLPHL (LP-DLBCL) by gene expression profiling (GEP). GEP revealed an inflammatory signature pinpointing to a specific host response. In a coculture model resembling this host response, DEV tumor cells showed an impaired growth behavior. Mechanisms involved in the reduced tumor cell proliferation included a downregulation of MYC and its target genes. Lack of MYC expression was also confirmed in 12/16 LP-DLBCL by immunohistochemistry. Furthermore, CD274/PD-L1 was upregulated in DEV tumor cells after coculture with T cells or monocytes and its expression was validated in 12/19 cases of LP-DLBCL. Thereby, our data provide new insights into the pathogenesis of LP-DLBCL and an explanation for the relatively low tumor cell content. Moreover, the findings suggest that treatment of these patients with immune checkpoint inhibitors may enhance an already ongoing host response in these patients.
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