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  • CD62L as a therapeutic target in chronic lymphocytic leukemia

    Author(s)
    Burgess, Melinda
    Gill, Devinder
    Singhania, Richa
    Cheung, Catherine
    Chambers, Lynne
    Renyolds, Brent A
    Smith, Louise
    Mollee, Peter
    Saunders, Nicholas
    McMillan, Nigel AJ
    Griffith University Author(s)
    McMillan, Nigel
    Year published
    2013
    Metadata
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    Abstract
    Purpose: Despite advances in the treatment of chronic lymphocytic leukemia (CLL), the disease remains incurable with standard therapies and relapse is inevitable. A growing body of evidence indicates that alterations in the adhesion properties of neoplastic cells play a pivotal role in the development and progression of CLL. Experimental Design: The expression of 71 cell surface molecules was examined on CLL peripheral blood mononuclear cells (PBMCs) over 3 weeks in culture. The most highly upregulated marker, CD62L, was examined further for expression on CD5+/CD19+ CLL cells in vitro and in lymph node and bone marrow ...
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    Purpose: Despite advances in the treatment of chronic lymphocytic leukemia (CLL), the disease remains incurable with standard therapies and relapse is inevitable. A growing body of evidence indicates that alterations in the adhesion properties of neoplastic cells play a pivotal role in the development and progression of CLL. Experimental Design: The expression of 71 cell surface molecules was examined on CLL peripheral blood mononuclear cells (PBMCs) over 3 weeks in culture. The most highly upregulated marker, CD62L, was examined further for expression on CD5+/CD19+ CLL cells in vitro and in lymph node and bone marrow biopsies. The prosurvival role of CD62L was examined using a functional blocking antibody and therapeutic potential evaluated by comparison with current chemotherapy agents. Results: Blocking CD62L resulted in apoptosis of CLL cells but not PBMCs from healthy donors suggesting a novel role for CD62L in CLL cell survival. The beneficial effect of coculturing CLL cells with bone marrow stromal cells or endothelial cells does not protect CLL cells from anti-CD62L-related toxicity. Moreover, combining fludarabine or mafosfamide with the anti-CD62L in vitro produced an additive effect both with and without stromal cells. Conclusion: This is the first reported data showing that blocking the activation and homing marker, CD62L, regulates CLL cell survival in vitro. These data also suggest that therapeutic antibodies against CD62L may provide additional clinical benefit to patients with CLL receiving current standard chemotherapy protocols.
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    Journal Title
    Clinical Cancer Research
    Volume
    19
    Issue
    20
    DOI
    https://doi.org/10.1158/1078-0432.CCR-13-1037
    Subject
    Cellular Immunology
    Oncology and Carcinogenesis
    Publication URI
    http://hdl.handle.net/10072/57754
    Collection
    • Journal articles

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