ArticleLeukemia2002
CD20-induced B cell death can bypass mitochondria and caspase activation.
Article in Leukemia, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 84 citations in OpenAlex.
- Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia.Drugs · 2003Trial
- Rituximab in Connective Tissue Disease-Associated Interstitial Lung Disease: From Immunopathogenesis to Therapeutic Implications.International journal of molecular sciences · 2025Review
- CD3xCD19 DART molecule treatment induces non-apoptotic killing and is efficient against high-risk chemotherapy and venetoclax-resistant chronic lymphocytic leukemia cells.Journal for immunotherapy of cancer · 2020Article
- Mechanisms of Resistance to Monoclonal Antibodies (mAbs) in Lymphoid Malignancies.Current hematologic malignancy reports · 2019Review
- Association of rituximab with graphene oxide confers direct cytotoxicity for CD20-positive lymphoma cells.Oncotarget · 2016Article
- POLYMERIC BIOMATERIALS AND NANOMEDICINES.Journal of drug delivery science and technology · 2015Article
- Antitumor activity of an anti-CD98 antibody.International journal of cancer · 2015Article
- Drug-Free Macromolecular Therapeutics--A New Paradigm in Polymeric Nanomedicines.Biomaterials science · 2015Article
- The status of radioimmunotherapy in CD20+ non-Hodgkin's lymphoma.Targeted oncology · 2015Review
- A Two-Step Pretargeted Nanotherapy for CD20 Crosslinking May Achieve Superior Anti-Lymphoma Efficacy to Rituximab.Theranostics · 2015Article
- Reformatting Rituximab into Human IgG2 and IgG4 Isotypes Dramatically Improves Apoptosis Induction In Vitro.PloS one · 2015Article
- Drug-free macromolecular therapeutics induce apoptosis of patient chronic lymphocytic leukemia cells.Drug delivery and translational research · 2014Article
- Article
- Rituximab resistance.Best practice & research. Clinical haematology · 2011Review
- Article
- Molecular profiling of cytomegalovirus-induced human CD8+ T cell differentiation.The Journal of clinical investigation · 2010Article
- CD20 deficiency in humans results in impaired T cell-independent antibody responses.The Journal of clinical investigation · 2010Article
- Antibody and immunomodulatory agents in treatment of indolent non-Hodgkin's lymphoma.Current treatment options in oncology · 2006Review
- Rituximab induces different but overlapping sets of genes in human B-lymphoma cell lines.Cancer immunology, immunotherapy : CII · 2005Article
- Monoclonal antibody therapeutics and apoptosis.Oncogene · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The apoptotic pathway activated by chimeric anti-CD20 monoclonal antibodies (rituximab, IDEC.C2B8) was analyzed using the Burkitt lymphoma cell line Ramos. Crosslinking of CD20 (CD20XL) induced apoptosis in Ramos cells, which involved loss of mitochondrial membrane potential (Deltapsi(m)), the release of cytochrome-c (cyt-c), and activation of caspases-9 and -3. Nevertheless, several lines of evidence showed that the apoptotic outcome did not depend on these events. First, under circumstances where Ramos cells display resistance to either CD95- or B cell receptor (BCR)-induced apoptosis, CD20XL-induced apoptosis was not affected, pointing to a distinct pathway. Second, the broad-spectrum caspase inhibitor zVAD-fmk prevented processing of caspase-9, -3 and PARP as well as DNA fragmentation, but did not block apoptosis as measured by annexin V staining, cell size and membrane integrity. Lastly, Bcl-2 overexpression blocked cyt-c release and the decrease in Deltapsi(m), and completely prevented CD95- or BCR-mediated apoptosis; however, it did not affect CD20XL-induced cell death. We conclude that although CD20XL can initiate the mitochondrial apoptosis pathway, CD20-induced apoptosis does not necessarily require active caspases and cannot be blocked by Bcl-2. Since most chemotherapeutic drugs require the activation of caspases to exert their cytotoxicity, these findings provide an important rationale for the use of CD20 mAbs in chemoresistant malignancies.
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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.