Leukemia Research
Volume 25, Issue 12 , Pages 1115-1125, December 2001

Direct effect of bispecific anti-CD33×anti-CD64 antibody on proliferation and signaling in myeloid cells

  • Larisa Balaian

      Affiliations

    • Department of Medicine and Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA
    • ,
  • Edward D. Ball

      Affiliations

    • Blood and Marrow Transplantation Division, University of California, 9500 Gilman Drive, San Diego, La Jolla, CA 92093-0960, USA
    • Corresponding Author InformationCorresponding author. Tel.: +1-858-657-7053; fax: +1-858-657-6837

Received 22 January 2001; accepted 27 April 2001.

Abstract 

Bispecific anti-CD33×anti-CD64 antibody (BsAb) directly inhibited proliferation and colony formation of human acute myeloid leukemia cell lines, without affecting the function of normal monocytes. Addition of BsAb to normal monocytes induced tyrosine phosphorylation of Cbl and Vav, association of these molecules with CD33, and downstream signaling. In leukemia cells that were insensitive to BsAb treatment, Vav and Cbl were constitutively phosphorylated and, therefore, constitutively associated with CD33. Direct growth inhibition is an additional mechanism by which BsAb may be useful in the therapy of AML.

Keywords:  Myeloid leukemia, Fc receptors, Monocytes, Bispecific antibodies

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PII: S0145-2126(01)00084-4

Leukemia Research
Volume 25, Issue 12 , Pages 1115-1125, December 2001

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