ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016
Lenalidomide, Thalidomide, and Pomalidomide Reactivate the Epstein-Barr Virus Lytic Cycle through Phosphoinositide 3-Kinase Signaling and Ikaros Expression.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Ubiquitination dynamics in human tumour viruses: Viral infection, oncogenesis and antiviral therapy.The FEBS journal · 2026Review
- Novel Cereblon-Binding Immunomodulators Have Increased Potency Against Gammaherpesvirus- Associated Lymphomas In Vitro.Journal of medical virology · 2025Article
- Novel PI3Kδ inhibitor exerts antitumor activity in Burkitt lymphoma by inducing ROS-dependent apoptosis.Medical oncology (Northwood, London, England) · 2025Article
- Targeting Ikaros and Aiolos with pomalidomide fails to reactivate or induce apoptosis of the latent HIV reservoir.Journal of virology · 2025Article
- Characteristics and outcomes of secondary acute lymphoblastic leukemia (sALL) after multiple myeloma (MM): SEER data analysis in a single-center institution.Cancer pathogenesis and therapy · 2025Article
- Single-cell transcriptional profile of CD34+ hematopoietic progenitor cells from del(5q) myelodysplastic syndromes and impact of lenalidomide.Nature communications · 2024Article
- Development of Epstein-Barr virus-associated lymphoproliferative disorder and hemophagocytic lymphohistiocytosis during long-term lenalidomide maintenance therapy in multiple myeloma.International journal of hematology · 2023Article
- Clinical Characteristics and Prognosis of Secondary Acute Lymphoblastic Leukemia in Patients with Multiple Myeloma during Long-Term Thalidomide Maintenance.Journal of personalized medicine · 2023Article
- Epstein-Barr Virus Driven Hodgkin's Lymphoma after a Short Course of Daratumumab Treatment for Relapsed Multiple Myeloma.Case reports in hematology · 2023Article
- Inhibitory effect and related mechanism of decitabine combined with gemcitabine on proliferation of NK/T cell lymphoma cells.Frontiers in pharmacology · 2023Article
- G protein-coupled receptor 183 mediates the sensitization of Burkitt lymphoma tumors to CD47 immune checkpoint blockade by anti-CD20/PI3Kδi dual therapy.Frontiers in immunology · 2023Article
- Review
- Post-marketing safety of immunomodulatory drugs in multiple myeloma: A pharmacovigilance investigation based on the FDA adverse event reporting system.Frontiers in pharmacology · 2022Article
- Bystander Memory T Cells and IMiD/Checkpoint Therapy in Multiple Myeloma: A Dangerous Tango?Frontiers in immunology · 2021Review
- Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2.PLoS pathogens · 2021Article
- First reported case of secondary mixed phenotype acute leukemia after multiple myeloma.American journal of blood research · 2021Article
- Promising Response to Lenalidomide-Combination Therapy in a Discordant Lymphoma Consisting of EBV-Positive Diffuse Large B-Cell Lymphoma and Angioimmunoblastic T-Cell Lymphoma: A Case Report.OncoTargets and therapy · 2021Article
- EBV-related lymphoma after long-term daratumumab treatment: a case report.Blood cancer journal · 2020Article
- ARID2 is a pomalidomide-dependent CRL4Nature chemical biology · 2020Article
- Lytic Induction Therapy against Epstein-Barr Virus-Associated Malignancies: Past, Present, and Future.Cancers · 2020Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
purposeLenalidomide, thalidomide, and pomalidomide (LTP) are immunomodulatory agents approved for use in multiple myeloma, but in some settings, especially with alkylating agents, an increase in Hodgkin lymphoma and other secondary primary malignancies (SPM) has been noted. Some of these malignancies have been linked to Epstein-Barr virus (EBV), raising the possibility that immunomodulatory drugs disrupt latent EBV infection. EXPERIMENTAL
designWe studied the ability of LTP to reactivate latently infected EBV-positive cell lines in vitro and in vivo, and evaluated the EBV viral load in archived serum samples from patients who received a lenalidomide, thalidomide, and dexamethasone (LTD) combination.
resultsTreatment of EBV-infected B-cell lines with LTP at physiologically relevant concentrations induced the immediate early gene BZLF1, the early gene BMRF1, and the late proteins VCA and BCFR1. This occurred in the potency order pomalidomide > lenalidomide > thalidomide, and the nucleoside analogue ganciclovir enhanced the cytotoxic effects of lenalidomide and pomalidomide in Burkitt lymphoma cells in vitro and in vivo EBV reactivation was related to PI3K stimulation and Ikaros suppression, and blocked by the PI3Kδ inhibitor idelalisib. Combinations of lenalidomide with dexamethasone or rituximab increased EBV reactivation compared with lenalidomide alone and, importantly, lenalidomide with melphalan produced even greater reactivation.
conclusionsWe conclude LTP may reactivate EBV-positive resting memory B cells thereby enhancing EBV lytic cycle and host immune suppression. Clin Cancer Res; 22(19); 4901-12. ©2016 AACR.
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