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New Target Found for Treating Acute Myeloid Leukemia: Presented at ASH
By Mike Fillon
ATLANTA, GA -- December 14, 2005 -- New research shows that a novel antibody could target the specific cells that lead to acute myeloid leukemia (AML).
Results of the study were presented here December 11th at the 47th Annual Meeting of the American Society of Hematology (ASH).
James N. George, MD, professor of medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, and President of ASH said the study "provides important new insights for further improving our ability to treat this once inevitably fatal disease."
AML results when maverick stem cells in the bone marrow produce unchecked numbers of immature white blood cells, called myeloid cells. Nearly 12,000 new cases of AML have been diagnosed in the United States this year.
Senior study author Gerrit Jan Schuurhuis, PhD, associate professor, VU University Medical Center, Amsterdam, The Netherlands, noted that different kinds of stem cells can be distinguished by different molecular markers on their surface. Stem cells characterized by the presence of the CD34 marker and the absence of the CD38 marker (CD34+CD38-) appear to be the initiation point for AML. Sometimes these cells can survive even under intense chemotherapy, and, when found in high frequency after treatment, correlate to a return of the cancer and high mortality.
However, as stem cells are rare, they are hard to find. Previous research indicated that myeloid cells have a marker on their surface called CLL-1 that could be detected by a particular protein called anti-CLL-1 antibody.
To see if this antibody could also detect hidden bastions of the CD34+CD38- stem cells in AML patients in remission, Dr. George's team conducted a study that enrolled 89 patients with AML..
In the study, the antibody detected CD34+CD38- stem cells in 77 out of 89 AML patients at the time of diagnosis. CLL-1 expression in CD34+CD38- cells of control bone marrows was virtually absent. For those AML patients in remission who were CLL-1 positive, the ratio of CLL-1-positive AML stem cells to normal (CLL-1-negative) stem cells correlated to the probability of relapse. Therefore, patients in remission who are found to have dormant CD34+CD38- cells in their marrow are ideal candidates for antibody therapy.
Dr. Schuurhuis said the data provides strong evidence that a large CD34+CD38- population at diagnosis reflects a higher percentage of chemotherapy-resistant cells, which, in remission, will lead to the outgrowth of minimal residual disease, thereby affecting clinical outcome.
"The reliability of this antibody to detect and quantify the particular stem cells that foreshadow a poor prognosis for AML patients in remission means that scientists may now have the ability to hone in on these specific cells and target them for treatment," Dr. Schuurhuis said.
[Presentation title: The Novel AML Stem Cell Associated Antigen CLL-1 Discriminates Between Normal and Leukemic Stem Cells. Abstract 4]
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