Scientists presented data here today at the 40th Annual Meeting of the American Society of Hematology (ASH), demonstrating how a breakthrough new experimental compound, known as CMA-676, uses an antibody connected to chemotherapy molecules to help patients fight a virulent and often fatal form of cancer - acute myelogenous leukemia (AML). The data appeared to confirm that this novel treatment method -- "antibody-targeted chemotherapy" -- shows promising efficacy and a more tolerable side effect profile than current chemotherapy treatments.
AML is a life-threatening disease in which certain white blood cells become cancerous and rapidly replace and destroy normal bone marrow and blood cells. AML is among the most serious forms of adult leukemia, with a relatively high fatality rate. Most patients require intensive chemotherapy to achieve complete remission, and some also must undergo bone marrow transplants. Up to half of patients with AML, even after such intensive treatment, have residual leukemic cells or experience a relapse.
Because current chemotherapy drugs to treat AML are non-specific - harming good as well as bad cells - patients who are receiving standard chemotherapy become very sick. Researchers at the Fred Hutchinson Cancer Research Center, in collaboration with scientists from thirteen leading leukemia centers including, University of Chicago Medical Center, MD Anderson Cancer Center and The University of Pennsylvania Cancer Center, are working with Wyeth-Ayerst Research and Celltech PLC to study CMA-676, an antibody-drug conjugate that delivers treatment directly to the leukemia cells.
The antibody is engineered to carry just a few molecules of a new and extremely
potent chemotherapy agent - from the calicheamicin family -- to selectively
destroy leukemic blast cells. This approach may spare primary and vital bone
marrow cells that are responsible for regenerating normal blood cells once the
leukemia cells are destr
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Contact: Susan Edmonds
sedmonds@fhcrc.org
206-667-2896
Fred Hutchinson Cancer Research Center
7-Dec-1998