ArticleCancer research2011
Human CD59 inhibitor sensitizes rituximab-resistant lymphoma cells to complement-mediated cytolysis.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 87 citations in OpenAlex.
- Increased CD59 protein expression is associated with the outcome of patients with diffuse large B-cell lymphoma treated with R-CHOP.Medical oncology (Northwood, London, England) · 2014Trial
- Induced resistance to ofatumumab-mediated cell clearance mechanisms, including complement-dependent cytotoxicity, in chronic lymphocytic leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- CD59 silencing enhances doxorubicin sensitivity in DLBCL cells and is associated with poor prognosis in patients treated with CHOP regimen.Clinical and experimental medicine · 2026Article
- Complement system in tumor growth and metastases.British journal of cancer · 2026Review
- Macrocyclic Peptide Probes for Immunomodulatory Protein CD59: Potent Modulators of Bacterial Toxin Activity and Antibody-Dependent Cytotoxicity.Angewandte Chemie (International ed. in English) · 2025Article
- Potassium/sodium cation carriers robustly upregulate CD20 antigen by targeting MYC, and synergize with anti- CD20 immunotherapies to eliminate malignant B cells.Haematologica · 2025Article
- Anti-HER2 Cancer-Specific mAb, HInternational journal of molecular sciences · 2024Article
- Emerging role of complement in COVID-19 and other respiratory virus diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Unveiling CD59-Antibody Interactions to Design Paratope-Mimicking Peptides for Complement Modulation.International journal of molecular sciences · 2023Article
- Exploring complement-dependent cytotoxicity by rituximab isotypes in 2D and 3D-cultured B-cell lymphoma.BMC cancer · 2022Article
- NANOG confers resistance to complement-dependent cytotoxicity in immune-edited tumor cells through up-regulating CD59.Scientific reports · 2022Article
- Determinants of response to daratumumab in Epstein-Barr virus-positive natural killer and T-cell lymphoma.Journal for immunotherapy of cancer · 2021Article
- Review
- Herbal NF-κB Inhibitors Sensitize Rituximab-Resistant B Lymphoma Cells to Complement-Mediated Cytolysis.Frontiers in oncology · 2021Article
- Complement Activation in the Treatment of B-Cell Malignancies.Antibodies (Basel, Switzerland) · 2020Review
- The Role of Complement in the Mechanism of Action of Therapeutic Anti-Cancer mAbs.Antibodies (Basel, Switzerland) · 2020Review
- Drivers and regulators of humoral innate immune responses to infection and cancer.Molecular immunology · 2020Review
- Review
- Surfaceome interrogation using an RNA-seq approach highlights leukemia initiating cell biomarkers in an LMO2 T cell transgenic model.Scientific reports · 2019Article
- Overexpression of CD59 inhibits apoptosis of T-acute lymphoblastic leukemia via AKT/Notch1 signaling pathway.Cancer cell international · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Rituximab efficacy in cancer therapy depends in part on induction of complement-dependent cytotoxicity (CDC). Human CD59 (hCD59) is a key complement regulatory protein that restricts the formation of the membrane attack complex, thereby inhibiting induction of CDC. hCD59 is highly expressed in B-cell non-Hodgkin's lymphoma (NHL), and upregulation of hCD59 is an important determinant of the sensitivity of NHL cells to rituximab treatment. Here, we report that the potent hCD59 inhibitor rILYd4 enhances CDC in vitro and in vivo, thereby sensitizing rituximab-resistant lymphoma cells and primary chronic lymphocytic leukemia cells (CLL) to rituximab treatment. By defining pharmcokinetic/pharmacodynamic profiles of rILYd4 in mice, we showed that by itself rILYd4 does not adversely mediate in vivo hemolysis of hCD59-expressing erythrocytes. Increasing expression levels of the complement regulators CD59 and CD55 in rituximab-resistant cells occur due to selection of preexisting clones rather than de novo induction of these proteins. Moreover, lymphoma cells overexpressing CD59 were directly responsible for the resistance to rituximab-mediated CDC therapy. Our results rationalize the use of rILYd4 as a therapeutic adjuvant for rituximab treatment of rituximab-resistant lymphoma and CLL. Furthermore, they suggest that preemptive elimination of CD59-overexpressing subpopulations along with rituximab treatment may be a useful approach to ablate or conquer rituximab resistance.
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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.