ArticleMolecular cancer therapeutics2015
CD30 Downregulation, MMAE Resistance, and MDR1 Upregulation Are All Associated with Resistance to Brentuximab Vedotin.
Article in Molecular cancer therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 204 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
- A phase 2 study of brentuximab vedotin in patients with CD30-positive advanced systemic mastocytosis.Blood advances · 2019Trial
- Treatment of CD30-Expressing Germ Cell Tumors and Sex Cord Stromal Tumors with Brentuximab Vedotin: Identification and Report of Seven Cases.The oncologist · 2018Trial
- Antibody-drug conjugates in gynaecological cancers: opportunities and challenges.Nature reviews. Clinical oncology · 2026Review
- Association between CD79B expression and polatuzumab vedotin efficacy, and therapy-induced changes in CD79B expression in diffuse large B-cell lymphoma.Virchows Archiv : an international journal of pathology · 2026Article
- Combining antibody conjugates with cytotoxic and immune-stimulating payloads maximizes anti-cancer activity.Molecular oncology · 2026Article
- Drug resistance to antibody-drug conjugates: mechanisms, challenges, and perspectives.Cancer biology & medicine · 2026Review
- Antibody-Drug Conjugates Targeting Resistance-Associated Signaling Pathways: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Overcoming resistance to antibody-drug conjugates: mechanisms and emerging strategies.The oncologist · 2026Review
- Antibody-drug conjugates in gynecologic malignancies: breakthroughs, challenges, and future directions.Frontiers in immunology · 2026Review
- Identification of antibody-drug conjugate payloads that are substrates of ATP-binding cassette drug efflux transporters.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- CD30 as a Target Molecule in the Diagnosis and Therapy of Lymphomas.American journal of hematology · 2026Review
- Mechanisms of resistance to trastuzumab deruxtecan in breast cancer elucidated by multi-omic molecular profiling.NPJ breast cancer · 2025Article
- HER2 expression in breast cancer: evidence gaps and challenges.NPJ precision oncology · 2025Review
- Mechanisms of resistance to antibody-drug conjugates in cancer: molecular barriers and pharmacological solutions.Cancer chemotherapy and pharmacology · 2025Review
- Targeted drug conjugates and molecular mechanisms in overcoming lung cancer drug resistance.Discover oncology · 2025Review
- Overcoming resistance to antibody-drug conjugates: from mechanistic insights to cutting-edge strategies.Journal of hematology & oncology · 2025Review
- Assessing efficacy of anti-glypican-1 antibody-drug conjugate as potential therapeutic approach for gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- Current Status of Molecularly Targeted Therapeutics in Blood Cancers.International journal of molecular sciences · 2025Review
- A Dual-Payload Bispecific ADC Improved Potency and Efficacy over Single-Payload Bispecific ADCs.Pharmaceutics · 2025Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Brentuximab vedotin (BV) is an antibody-drug conjugate that specifically delivers the potent cytotoxic drug monomethyl auristatin E (MMAE) to CD30-positive cells. BV is FDA approved for treatment of relapsed/refractory Hodgkin lymphoma and anaplastic large cell lymphoma (ALCL); however, many patients do not achieve complete remission and develop BV-resistant disease. We selected for BV-resistant Hodgkin lymphoma (L428) and ALCL (Karpas-299) cell lines using either constant (ALCL) or pulsatile (Hodgkin lymphoma) exposure to BV. We confirmed drug resistance by MTS assay and analyzed CD30 expression in resistant cells by flow cytometry, qRT-PCR, and Western blotting. We also measured drug exporter expression, MMAE resistance, and intracellular MMAE concentrations in BV-resistant cells. In addition, tissue biopsy samples from 10 Hodgkin lymphoma and 5 ALCL patients who had relapsed or progressed after BV treatment were analyzed by immunohistocytochemistry for CD30 expression. The resistant ALCL cell line, but not the Hodgkin lymphoma cell line, demonstrated downregulated CD30 expression compared with the parental cell line. In contrast, the Hodgkin lymphoma cell line, but not the ALCL cell line, exhibited MMAE resistance and increased expression of the MDR1 drug exporter compared with the parental line. For both Hodgkin lymphoma and ALCL, samples from patients relapsed/resistant on BV persistently expressed CD30 by immunohistocytochemistry. One Hodgkin lymphoma patient sample expressed MDR1 by immunohistocytochemistry. Although loss of CD30 expression is a possible mode of BV resistance in ALCL in vitro models, this has not been confirmed in patients. MMAE resistance and MDR1 expression are possible modes of BV resistance for Hodgkin lymphoma both in vitro and in patients.
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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.