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Published in: Current Hematologic Malignancy Reports 1/2012

01-03-2012 | Acute Myelogenous Leukemia (EJ Feldman, Section Editor)

What Happened to Anti-CD33 Therapy for Acute Myeloid Leukemia?

Author: Joseph G. Jurcic

Published in: Current Hematologic Malignancy Reports | Issue 1/2012

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Abstract

CD33, a 67-kDa glycoprotein expressed on the majority of myeloid leukemia cells as well as on normal myeloid and monocytic precursors, has been an attractive target for monoclonal antibody (mAb)–based therapy of acute myeloid leukemia (AML). Lintuzumab, an unconjugated, humanized anti-CD33 mAb, has modest single-agent activity against AML but failed to improve patient outcomes in two randomized trials when combined with conventional chemotherapy. Gemtuzumab ozogamicin, an anti-CD33 mAb conjugated to the antitumor antibiotic calicheamicin, improved survival in a subset of AML patients when combined with standard chemotherapy, but safety concerns led to US marketing withdrawal. The activity of these agents confirms that CD33 remains a viable therapeutic target for AML. Strategies to improve the results of mAb-based therapies for AML include antibody engineering to enhance effector function, use of alternative drugs and chemical linkers to develop safer and more effective drug conjugates, and radioimmunotherapeutic approaches.
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Metadata
Title
What Happened to Anti-CD33 Therapy for Acute Myeloid Leukemia?
Author
Joseph G. Jurcic
Publication date
01-03-2012
Publisher
Current Science Inc.
Published in
Current Hematologic Malignancy Reports / Issue 1/2012
Print ISSN: 1558-8211
Electronic ISSN: 1558-822X
DOI
https://doi.org/10.1007/s11899-011-0103-0

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Disordered Epigenetic Regulation in the Pathophysiology of Myeloproliferative Neoplasms

Chronic Lymphocytic Leukemia (S O'Brien, Section Editor)

Treatment of Older Patients with Chronic Lymphocytic Leukemia

Chronic Lymphocytic Leukemia (S O’Brien, Section Editor)

Inhibiting B-Cell Receptor Signaling Pathways in Chronic Lymphocytic Leukemia

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