ArticleCancer medicine2015
P-glycoprotein is expressed and causes resistance to chemotherapy in EBV-positive T-cell lymphoproliferative diseases.
Article in Cancer medicine, 2015. 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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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Efficacy of Brentuximab Vedotin in Relapsed or Refractory High-CD30-Expressing Non-Hodgkin Lymphomas: Results of a Multicenter, Open-Labeled Phase II Trial.Cancer research and treatment · 2020Trial
- NEK2 drives pathogenesis, drug resistance, and LMP1 expression in EBV-positive non-Hodgkin lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- How Oncovirus Affects Drug Resistance in Cancer Cells.Recent patents on anti-cancer drug discovery · 2026Review
- P-Glycoprotein as a Therapeutic Target in Hematological Malignancies: A Challenge to Overcome.International journal of molecular sciences · 2025Review
- Discovery of drug transporter inhibitors tied to long noncoding RNA in resistant cancer cells; a computational model -in silico- study.Frontiers in immunology · 2025Review
- Article
- Tumour Derived Extracellular Vesicles: Challenging Target to Blunt Tumour Immune Evasion.Cancers · 2022Review
- Refractory Hydroa Vacciniforme-like Lymphoma: Biological Insights from Morphoproteomic Analysis.International journal of hematology-oncology and stem cell research · 2022Article
- Chronic active Epstein-Barr virus infection treated with PEG-aspargase: A case report.World journal of clinical cases · 2021Article
- Latent Membrane Protein 1 Promotes Tumorigenesis Through Upregulation of PGC1β Signaling Pathway.Stem cell reviews and reports · 2021Article
- Simultaneous intraocular and cutaneous extranodal NK/T-cell lymphoma refractory to multiple therapies including pembrolizumab.Clinical case reports · 2021Article
- Chronic Active Epstein-Barr Virus Infection: The Elucidation of the Pathophysiology and the Development of Therapeutic Methods.Microorganisms · 2021Review
- BCL-XL inhibition by BH3-mimetic drugs induces apoptosis in models of Epstein-Barr virus-associated T/NK-cell lymphoma.Blood advances · 2020Article
- Clinical relevance of multi-drug resistance gene C3435T polymorphism in diffuse large B-cell lymphoma in Xinjiang.Medicine · 2020Observational
- Perplexing Role of P-Glycoprotein in Tumor Microenvironment.Frontiers in oncology · 2020Review
- Review
- Cancer stem cell populations in lymphoma in dogs and impact of cytotoxic chemotherapy.Veterinary and comparative oncology · 2019Article
- Down-regulation of intracellular reactive oxygen species attenuates P-glycoprotein-associated chemoresistance in Epstein-Barr virus-positive NK/T-cell lymphoma.American journal of translational research · 2019Article
- STAT3 is constitutively activated in chronic active Epstein-Barr virus infection and can be a therapeutic target.Oncotarget · 2018Article
- Celecoxib enhances sensitivity to chemotherapy drugs of T-cell lymphoma.Oncology letters · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus-positive T-cell lymphoproliferative diseases (EBV-T-LPDs) are rare lymphomas with poor prognosis. Although chemotherapeutic strategies such as CHOP have been often selected, they have exhibited only limited efficacy. To clarify the mechanism of chemoresistance, we examined P-glycoprotein (P-gp) expression. P-gp acts as an energy-dependent efflux pump that excretes drugs from the cytoplasm, resulting in low-intracellular drug concentrations and poor sensitivity to chemotherapy. We examined P-gp expression in EBV-positive cells by immunohistochemistry staining in three patients of EBV-T-LPDs and the expression was detected in all patients. We also examined mdr1 mRNA expression by reverse-transcriptase polymerase-chain reaction (RT-PCR) in EBV-positive tumor cells from these patients and additional three patients. The expression was detected in all examined patients. In five EBV-T-LPDs patients, P-gp function was detected by Rhodamine-123 efflux assay in these cells. The efflux was inhibited by treatment with a P-gp inhibitor, cyclosporine A (CsA). We also examined and detected P-gp expression in EBV-positive T-cell lines SNT8 and SNT16 established from EBV-T-LPDs patients, by RT-PCR and western blotting. The function was also detected by Rhodamine-123 efflux in these cell lines. Inhibition and knock down of P-gp by CsA and siRNA, respectively, enhanced etoposide- and doxorubicin-induced cell death in the EBV-positive T-cell lines. Finally, we infected the T-cell line MOLT4 with EBV, and found that mdr1 mRNA expression and Rhodamine 123 efflux were upregulated after infection. These results indicated that enhanced P-gp expression contributed to the chemoresistance of EBV-T-LPDs.
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